intracerebroventricular-delivery-gut-derived-microbial-metabolites

Intracerebroventricular Delivery of Gut-Derived Microbial Metabolites in Freely Moving Mice

The impact of gut microbiota and their metabolites on host physiology and behavior has been extensively investigated in this decade. Numerous studies have ...

National Cheng Kung University

Platelet plays a pivotal role in the pathogenesis of thrombotic cardiovascular diseases. Recently, the polymorphism of platelet glycoprotein (GP) genes has been reported to be associated with an increased risk for ischemic stroke. The purpose of this study is to evaluate the association between platelet GP genetic variants and ischemic stroke in young Taiwanese. We conducted a case-control study in 157 young ischemic stroke patients recruited between September 2001 and March 2003 and 157 age- and sex-matched controls. The genotypes of platelet GP Ia C807T, GP Ib C3550T, and GP IIIa Pl(A1/A2) polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism. Student's t-test, chi-square test, and logistic regression modeling were used for data analyses. The GP Ia C807T CC, CT and TT genotype frequencies were similar between patients (50.3%, 43.9%, 5.7%) and controls (53.5%, 38.9%, 7.6%; p=0.58). There were no significant differences in GP Ib C3550T CC and CT genotype distributions between patients (91.1%, 8.9%) and controls (91.7%, 8.3%; p=0.84). Of all subjects, none carries GP IIIa Pl(A2) mutation. In conclusion, platelet GP Ia C807T and GP Ib C3550T polymorphisms in our population are less common compared with Caucasians, and GP IIIa Pl(A1/A2) genetic mutation is not found, and all of them are not associated with ischemic stroke in young Taiwanese.

Platelet glycoprotein Ia C807T, Ib C3550T, and IIIa Pl(A1/A2) polymorphisms and ischemic stroke in young Taiwanese.

La principale fonction physiologique des mitochondries est de g&eacute;n&eacute;rer le triphosphate d&#39;ad&eacute;nosine par l&#39;interm&eacute;diaire de la phosphorylation oxydative par l&#39;interm&eacute;diaire de la cha&icirc;ne de transport d&#39;&eacute;lectrons. Surproduction d&#39;esp&egrave;ces oxyg&eacute;n&eacute;es r&eacute;actives (ROS) comme sous-produits produits des mitochondries ont &eacute;t&eacute; impliqu&eacute;s dans les blessures c&eacute;r&eacute;brales aigu&euml;s comme les accidents vasculaires c&eacute;r&eacute;braux de l&#39;isch&eacute;mie c&eacute;r&eacute;brale. Il a &eacute;t&eacute; bien document&eacute; que voie apoptotique d&eacute;pendante de mitochondries implique la liaison aux prot&eacute;ines pro - et anti-apoptotiques, lib&eacute;ration du cytochrome c, conduisant &agrave; la mort en fin de compte &agrave; neuronale. En revanche, mitochondries jouent &eacute;galement un r&ocirc;le pour contrer les effets n&eacute;gatifs induits par le stress oxydatif excessif. Des &eacute;tudes r&eacute;centes ont r&eacute;v&eacute;l&eacute; que le stress oxydatif et l&#39;&eacute;tat redox des neurones isch&eacute;miques sont &eacute;galement impliqu&eacute;s dans la voie de signalisation impliquant des peroxysomes prolif&eacute;rative activ&eacute;s r&eacute;cepteur-&gamma; (PPAR&gamma;) Co-activateur 1&alpha; (PGC1-&alpha;). PGC1-&alpha; est un ma&icirc;tre r&eacute;gulateur de ROS, nettoyage des enzymes dont le mangan&egrave;se superoxyde dismutase 2 et la prot&eacute;ine d&eacute;couplante 2, les deux sont des prot&eacute;ines mitochondriales et peuvent contribuer &agrave; la survie des neurones. PGC1-&alpha; est &eacute;galement impliqu&eacute; dans la biogen&egrave;se mitochondriale qui sont vitale pour la survie des cellules. Preuve exp&eacute;rimentale prend en charge les r&ocirc;les de dysfonctionnement mitochondrial et le stress oxydatif comme d&eacute;terminants de la mort neuronale, mais aussi des m&eacute;canismes endog&egrave;nes de protection apr&egrave;s un AVC. Cet examen a pour but de r&eacute;sumer les connaissances actuelles en mettant l&#39;accent sur les m&eacute;canismes mol&eacute;culaires qui sous-tendent l&#39;isch&eacute;mie c&eacute;r&eacute;brale impliquant ROS, dysfonctionnement mitochondrial, apoptose, prot&eacute;ines mitochondriales capables de ROS nettoyage et biogen&egrave;se mitochondriale.

R&ocirc;les du Stress oxydatif, l&#39;apoptose, PGC-1&alpha; et la biogen&egrave;se mitochondriale dans l&#39;isch&eacute;mie c&eacute;r&eacute;brale.

&#x7EBF;&#x7C92;&#x4F53;&#x7684;&#x4E3B;&#x8981;&#x751F;&#x7406;&#x529F;&#x80FD;&#x662F;&#x751F;&#x6210;&#x4E09;&#x78F7;&#x9178;&#x817A;&#x82F7;&#x901A;&#x8FC7;&#x6C27;&#x5316;&#x78F7;&#x9178;&#x5316;&#xFF0C;&#x901A;&#x8FC7;&#x7535;&#x5B50;&#x4F20;&#x9012;&#x94FE;&#x3002;&#x5982;&#x4ECE;&#x7F3A;&#x8840;&#x6027;&#x8111;&#x4E2D;&#x98CE;&#x7684;&#x6025;&#x6027;&#x9885;&#x8111;&#x635F;&#x4F24;&#x6709;&#x7275;&#x8FDE;&#x4F5C;&#x4E3A;&#x526F;&#x4EA7;&#x54C1;&#x4ECE;&#x7EBF;&#x7C92;&#x4F53;&#x751F;&#x6210;&#x6D3B;&#x6027;&#x6C27; (ROS) &#x751F;&#x4EA7;&#x8FC7;&#x5269;&#x3002;&#x5B83;&#x8BE6;&#x7EC6;&#x5730;&#x8BB0;&#x5F55;&#x4E86;&#x8FD9;&#x7EBF;&#x7C92;&#x4F53;&#x4F9D;&#x8D56;&#x6027;&#x51CB;&#x4EA1;&#x901A;&#x8DEF;&#x6D89;&#x53CA; pro &#x548C;&#x6297;&#x51CB;&#x4EA1;&#x86CB;&#x767D;&#x7ED3;&#x5408;&#xFF0C;&#x91CA;&#x653E;&#x7EC6;&#x80DE;&#x8272;&#x7D20; c&#x3001; &#x9886;&#x5148;&#x7684;&#x6700;&#x7EC8;&#x5230;&#x795E;&#x7ECF;&#x5143;&#x6B7B;&#x4EA1;&#x3002;&#x53E6;&#x4E00;&#x65B9;&#x9762;&#xFF0C;&#x7EBF;&#x7C92;&#x4F53;&#x4E5F;&#x53D1;&#x6325;&#x4F5C;&#x7528;&#x6765;&#x62B5;&#x6D88;&#x8BF1;&#x53D1;&#x8FC7;&#x5EA6;&#x6C27;&#x5316;&#x5E94;&#x6FC0;&#x7684;&#x4E0D;&#x5229;&#x5F71;&#x54CD;&#x3002;&#x6700;&#x8FD1;&#x7684;&#x7814;&#x7A76;&#x8868;&#x660E;&#x6C27;&#x5316;&#x5E94;&#x6FC0;&#x4E0E;&#x7F3A;&#x8840;&#x6027;&#x795E;&#x7ECF;&#x5143;&#x7684;&#x6C27;&#x5316;&#x8FD8;&#x539F;&#x72B6;&#x6001;&#x4E5F;&#x5377;&#x5165;&#x6D89;&#x53CA;&#x8FC7;&#x6C27;&#x5316;&#x7269;&#x9176;&#x4F53;&#x589E;&#x6B96;&#x6FC0;&#x6D3B;&#x53D7;&#x4F53;-&gamma; (PPAR&gamma;) &#x6210;&#x866B; 1&alpha; &#x7684;&#x4FE1;&#x53F7;&#x8F6C;&#x5BFC;&#x9014;&#x5F84; &#xFF08;PGC1-&alpha;)&#x3002;PGC1-&alpha; &#x662F;&#x6D3B;&#x6027;&#x6C27;&#x6E05;&#x9664;&#x9176;&#x5305;&#x62EC;&#x9530;&#x8D85;&#x6C27;&#x5316;&#x7269;&#x6B67;&#x5316;&#x9176; 2 &#x4E3B;&#x8C03;&#x8282;&#x5668;&#x53CA;&#x89E3;&#x5076;&#x8054;&#x86CB;&#x767D; 2&#xFF0C;&#x65E2;&#x662F;&#x7EBF;&#x7C92;&#x4F53;&#x86CB;&#x767D;&#x8D28;&#xFF0C;&#x5E76;&#x53EF;&#x80FD;&#x4F1A;&#x6709;&#x52A9;&#x4E8E;&#x795E;&#x7ECF;&#x7EC6;&#x80DE;&#x7684;&#x751F;&#x5B58;&#x3002;PGC1-&alpha; &#x4E5F;&#x53C2;&#x4E0E;&#x7EBF;&#x7C92;&#x4F53;&#x751F;&#x7269;&#x53D1;&#x751F;&#x5B66;&#xFF0C;&#x5BF9;&#x7EC6;&#x80DE;&#x7684;&#x751F;&#x5B58;&#x662F;&#x81F3;&#x5173;&#x91CD;&#x8981;&#x7684;&#x3002;&#x5B9E;&#x9A8C;&#x8BC1;&#x636E;&#x652F;&#x6301;&#x8111;&#x5352;&#x4E2D;&#x540E;&#x4F5C;&#x4E3A;&#x795E;&#x7ECF;&#x5143;&#x6B7B;&#x4EA1;&#x4EE5;&#x53CA;&#x5185;&#x6E90;&#x6027;&#x4FDD;&#x62A4;&#x673A;&#x5236;&#x7684;&#x51B3;&#x5B9A;&#x56E0;&#x7D20;&#x7684;&#x7EBF;&#x7C92;&#x4F53;&#x529F;&#x80FD;&#x969C;&#x788D;&#x53CA;&#x6C27;&#x5316;&#x5E94;&#x6FC0;&#x4F5C;&#x7528;&#x3002;&#x8FD9;&#x6B21;&#x5BA1;&#x67E5;&#x7684;&#x76EE;&#x7684;&#x662F;&#x603B;&#x7ED3;&#x7684;&#x91CD;&#x70B9;&#x653E;&#x5728;&#x57FA;&#x7840;&#x6D89;&#x53CA; ROS&#x3001; &#x7EBF;&#x7C92;&#x4F53;&#x7684;&#x529F;&#x80FD;&#x7D0A;&#x4E71;&#x3001; &#x7EC6;&#x80DE;&#x51CB;&#x4EA1;&#x7EBF;&#x7C92;&#x4F53;&#x86CB;&#x767D;&#x8D28;&#x80FD;&#x591F;&#x6E05;&#x9664;&#x6D3B;&#x6027;&#x6C27;&#x548C;&#x7EBF;&#x7C92;&#x4F53;&#x751F;&#x7269;&#x53D1;&#x751F;&#x5B66;&#x7684;&#x7F3A;&#x8840;&#x6027;&#x8111;&#x635F;&#x4F24;&#x7684;&#x5206;&#x5B50;&#x673A;&#x5236;&#x7684;&#x5F53;&#x524D;&#x77E5;&#x8BC6;&#x3002;

&#x6C27;&#x5316;&#x5E94;&#x6FC0;&#x3001; &#x7EC6;&#x80DE;&#x51CB;&#x4EA1;&#x3001; PGC 1&alpha; &#x5728;&#x7F3A;&#x8840;&#x6027;&#x8111;&#x635F;&#x4F24;&#x7EBF;&#x7C92;&#x4F53;&#x751F;&#x7269;&#x53D1;&#x751F;&#x5B66;&#x7684;&#x89D2;&#x8272;&#x3002;

The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as stroke from cerebral ischemia. It was well-documented that mitochondria-dependent apoptotic pathway involves pro- and anti-apoptotic protein binding, release of cytochrome c, leading ultimately to neuronal death. On the other hand, mitochondria also play a role to counteract the detrimental effects elicited by excessive oxidative stress. Recent studies have revealed that oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves peroxisome proliferative activated receptor-Î³ (PPARÎ³) co-activator 1Î± (PGC1-Î±). PGC1-Î± is a master regulator of ROS scavenging enzymes including manganese superoxide dismutase 2 and the uncoupling protein 2, both are mitochondrial proteins, and may contribute to neuronal survival. PGC1-Î± is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after stroke. This review aims to summarize the current knowledge focusing on the molecular mechanisms underlying cerebral ischemia involving ROS, mitochondrial dysfunction, apoptosis, mitochondrial proteins capable of ROS scavenging, and mitochondrial biogenesis.

Roles of Oxidative Stress, Apoptosis, PGC-1Î± and Mitochondrial Biogenesis in Cerebral Ischemia.

Die prim&auml;re physiologische Funktion der Mitochondrien soll Adenosintriphosphat durch Oxidative Phosphorylierung &uuml;ber die Atmungskette generieren. &Uuml;berproduktion von reaktive Sauerstoffspezies (ROS) als Nebenprodukte aus Mitochondrien erzeugt haben in akuten Gehirn Verletzungen wie z. B. Strich von zerebraler Isch&auml;mie verwickelt worden. Es wurde gut dokumentiert, dass Mitochondrien-abh&auml;ngige Apoptotic Weg beinhaltet Pro und Anti-Apoptotic Proteinbindung, Freisetzung von Cytochrom c, f&uuml;hrt letztlich zu neuronalen Tod. Auf der anderen Seite spielen Mitochondrien auch eine Rolle, um die sch&auml;dlichen Auswirkungen hervorgerufen durch &uuml;berm&auml;&szlig;ige oxidativen Stress entgegenzuwirken. J&uuml;ngste Studien haben gezeigt, dass oxidativer Stress und den Redox-Zustand des isch&auml;mischen Neuronen auch in den Signalweg verwickelt sind, bei der Peroxisom proliferative aktivierte Rezeptor-&gamma; (PPAR&gamma;) Coaktivator 1&alpha; (PGC1-&alpha;). PGC1-&alpha; ist ein master Regulator der Aufr&auml;umvorgang Enzyme darunter Mangan-Superoxid-Dismutase 2 ROS und das uncoupling Protein 2, mitochondriale Proteine sind sowohl zum neuronalen &uuml;berleben beitragen k&ouml;nnen. PGC1-&alpha; ist auch mitochondriale Biogenese beteiligt, die f&uuml;r Zelle &Uuml;berleben unerl&auml;sslich ist. Belege st&uuml;tzen die Rollen von mitochondriale Dysfunktion und oxidativer Stress als Determinanten der neuronalen Tod sowie endogenen Schutzmechanismen nach Schlaganfall. Diese Bewertung soll das aktuelle Wissen konzentriert sich auf die molekularen Mechanismen zerebrale Isch&auml;mie mit ROS aufr&auml;umen und mitochondriale Biogenese mitochondrialer Proteine, Apoptosis, mitochondriale Dysfunktion, ROS zusammenfassen.

Rollen des oxidativen Stress, Apoptosis, PGC-1&alpha; und Mitochondrial Biogenesis in zerebralen Isch&auml;mie.

La funzione fisiologica primaria dei mitocondri &egrave; generare trifosfato di adenosina attraverso fosforilazione ossidativa tramite la catena di trasporto degli elettroni. Sovrapproduzione di specie reattive dell&#39;ossigeno (ROS) come sottoprodotti generati dai mitocondri sono stati implicati nelle lesioni acute cerebrali come tratto da ischemia cerebrale. E &#39; stato ben documentato che via apoptotica mitocondrio-dipendente coinvolge il legame alle proteine pro - e anti-apoptotic, rilascio del citocromo c, portando la morte definitiva di un neurone. D&#39;altra parte, i mitocondri svolgono un ruolo per contrastare gli effetti dannosi, provocati dall&#39;eccessivo stress ossidativo. Recenti studi hanno rivelato che lo stress ossidativo e dello stato redox di neuroni ischemici sono anche implicati nella via di segnalazione che coinvolge peroxisome proliferative &gamma; del recettore attivato (PPAR) coattivatore 1&alpha; (PGC1-&alpha;). PGC1-&alpha; &egrave; un regolatore master di ROS scavenging enzimi tra cui manganese superossido dismutasi 2 e la proteina disgiungente 2, entrambe sono proteine mitocondriali e pu&ograve; contribuire alla sopravvivenza neuronale. PGC1-&alpha; &egrave; anche coinvolto nella biogenesi mitocondriale che sono vitale per la sopravvivenza delle cellule. Prove sperimentali supportano i ruoli di disfunzione mitocondriale e stress ossidativo come fattori determinanti della morte neuronale, nonch&eacute; meccanismi protettivi endogeni dopo ictus. Questa rassegna mira a riassumere le conoscenze attuali, concentrandosi sui meccanismi molecolari sottostante ischemia cerebrale che coinvolge la disfunzione mitocondriale, apoptosi, ROS, le proteine mitocondriali capaci di ROS scavenging e biogenesi mitocondriale.

Ruoli di Stress ossidativo, apoptosi, PGC-1&alpha; e biogenesi mitocondriale nell&#39;Ischemia cerebrale.

&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x306E;&#x4E3B;&#x306A;&#x751F;&#x7406;&#x7684;&#x6A5F;&#x80FD;&#x3092;&#x901A;&#x3058;&#x3066;&#x96FB;&#x5B50;&#x8F38;&#x9001;&#x30C1;&#x30A7;&#x30FC;&#x30F3;&#x3092;&#x4ECB;&#x3057;&#x3066;&#x306E;&#x9178;&#x5316;&#x7684;&#x30EA;&#x30F3;&#x9178;&#x5316;&#x30A2;&#x30C7;&#x30CE;&#x30B7;&#x30F3;&#x4E09;&#x30EA;&#x30F3;&#x9178;&#x3092;&#x751F;&#x6210;&#x3059;&#x308B;&#x305F;&#x3081;&#x3067;&#x3059;&#x3002;&#x904E;&#x5270;&#x6D3B;&#x6027;&#x9178;&#x7D20;&#x7A2E; (ROS) &#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x304B;&#x3089;&#x751F;&#x6210;&#x3055;&#x308C;&#x308B;&#x526F;&#x7523;&#x7269;&#x3068;&#x3057;&#x3066;&#x306E;&#x8133;&#x865A;&#x8840;&#x304B;&#x3089;&#x30B9;&#x30C8;&#x30ED;&#x30FC;&#x30AF;&#x306A;&#x3069;&#x306E;&#x6025;&#x6027;&#x8133;&#x50B7;&#x5BB3;&#x95A2;&#x4E0E;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;&#x305D;&#x308C;&#x306F;&#x5341;&#x5206;&#x306B;&#x6587;&#x66F8;&#x5316;&#x3055;&#x308C;&#x305F;&#x6700;&#x7D42;&#x7684;&#x306B;&#x795E;&#x7D4C;&#x7D30;&#x80DE;&#x6B7B;&#x3092;&#x5C0E;&#x304F;&#x30D7;&#x30ED;&#x304A;&#x3088;&#x3073;&#x6297;&#x30A2;&#x30DD;&#x30C8;&#x30FC;&#x30B7;&#x30B9;&#x86CB;&#x767D;&#x7D50;&#x5408;&#x3001;&#x30B7;&#x30C8;&#x30AF;&#x30ED;&#x30E0; c &#x306E;&#x30EA;&#x30EA;&#x30FC;&#x30B9;&#x305D;&#x306E;&#x4F9D;&#x5B58;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x3092;&#x4ECB;&#x3057;&#x305F;&#x30A2;&#x30DD;&#x30C8;&#x30FC;&#x30B7;&#x30B9;&#x7D4C;&#x8DEF;&#x3092;&#x4F34;&#x3044;&#x307E;&#x3059;&#x3002;&#x305D;&#x306E;&#x4E00;&#x65B9;&#x3067;&#x3001;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x3082;&#x904E;&#x5EA6;&#x306E;&#x9178;&#x5316;&#x30B9;&#x30C8;&#x30EC;&#x30B9;&#x306B;&#x3088;&#x308A;&#x8A98;&#x767A;&#x3055;&#x308C;&#x308B;&#x6709;&#x5BB3;&#x306A;&#x5F71;&#x97FF;&#x306B;&#x5BFE;&#x6297;&#x3059;&#x308B;&#x5F79;&#x5272;&#x3092;&#x679C;&#x305F;&#x3057;&#x307E;&#x3059;&#x3002;&#x6700;&#x8FD1;&#x306E;&#x7814;&#x7A76;&#x304C;&#x660E;&#x3089;&#x304B;&#x306B;&#x9178;&#x5316;&#x30B9;&#x30C8;&#x30EC;&#x30B9;&#x3068;&#x865A;&#x8840;&#x6027;&#x30CB;&#x30E5;&#x30FC;&#x30ED;&#x30F3;&#x306E;&#x9178;&#x5316;&#x9084;&#x5143;&#x72B6;&#x614B;&#x304C;&#x30DA;&#x30EB;&#x30AA;&#x30AD;&#x30B7;&#x30BD;&#x30FC;&#x30E0;&#x5897;&#x6B96;&#x6D3B;&#x6027;&#x5316;&#x53D7;&#x5BB9;&#x4F53; &gamma; (ppar &gamma;) &#x30B3;&#x30A2;&#x30AF;&#x30C1;&#x30D9;&#x30FC;&#x30BF;&#x30FC;-1 &alpha; &#x3092;&#x542B;&#x3080;&#x30B7;&#x30B0;&#x30CA;&#x30EB;&#x4F1D;&#x9054;&#x7D4C;&#x8DEF;&#x306B;&#x3082;&#x95A2;&#x4E0E;&#x3059;&#x308B;&#x3044;&#x308B;&#x3068; (PGC1 &alpha;)&#x3002;PGC1 &alpha; &#x30DE;&#x30F3;&#x30AC;&#x30F3; &#x30B9;&#x30FC;&#x30D1;&#x30FC;&#x30AA;&#x30AD;&#x30B7;&#x30C9;&#x30B8;&#x30B9;&#x30E0;&#x30BF;&#x30FC;&#x30BC; 2 &#x3092;&#x542B;&#x3080;&#x9175;&#x7D20;&#x6E05;&#x6383; ROS &#x306E;&#x30DE;&#x30B9;&#x30BF;&#x30FC;&#x8ABF;&#x7BC0;&#x56E0;&#x5B50;&#x3067;&#x3042;&#x308B;&#x3068;&#x8131;&#x5171;&#x5F79;&#x30BF;&#x30F3;&#x30D1;&#x30AF;&#x8CEA; 2&#x3001;&#x4E21;&#x65B9;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x86CB;&#x767D;&#x8CEA;&#x3001;&#x304A;&#x3088;&#x3073;&#x795E;&#x7D4C;&#x7D30;&#x80DE;&#x306E;&#x751F;&#x5B58;&#x306B;&#x8CA2;&#x732E;&#x3059;&#x308B;&#x304B;&#x3082;&#x3057;&#x308C;&#x306A;&#x3044;&#x3002;PGC1 &alpha; &#x306F;&#x307E;&#x305F;&#x7D30;&#x80DE;&#x306E;&#x751F;&#x5B58;&#x306B;&#x6B20;&#x304B;&#x305B;&#x306A;&#x3044;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x306E;&#x751F;&#x5408;&#x6210;&#x306B;&#x95A2;&#x4E0E;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;&#x5B9F;&#x9A13;&#x7684;&#x8A3C;&#x62E0;&#x8133;&#x5352;&#x4E2D;&#x5F8C;&#x306E;&#x5185;&#x56E0;&#x6027;&#x4FDD;&#x8B77;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x3068;&#x540C;&#x69D8;&#x306B;&#x795E;&#x7D4C;&#x7D30;&#x80DE;&#x6B7B;&#x306E;&#x898F;&#x5B9A;&#x56E0;&#x3068;&#x3057;&#x3066;&#x306E;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x6A5F;&#x80FD;&#x969C;&#x5BB3;&#x3068;&#x9178;&#x5316;&#x30B9;&#x30C8;&#x30EC;&#x30B9;&#x306E;&#x5F79;&#x5272;&#x3092;&#x30B5;&#x30DD;&#x30FC;&#x30C8;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;&#x3053;&#x306E;&#x30EC;&#x30D3;&#x30E5;&#x30FC;&#x306F;&#x8133;&#x865A;&#x8840;&#x306E; ROS&#x3001;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x6A5F;&#x80FD;&#x969C;&#x5BB3;, &#x30A2;&#x30DD;&#x30C8;&#x30FC;&#x30B7;&#x30B9;, &#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x86CB;&#x767D;&#x8CEA;&#x6E05;&#x6383;&#x3001;ROS &#x3068;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x306E;&#x751F;&#x5408;&#x6210;&#x80FD;&#x529B;&#x3092;&#x542B;&#x3080;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x306B;&#x7126;&#x70B9;&#x3092;&#x5F53;&#x3066;&#x3001;&#x73FE;&#x5728;&#x306E;&#x30CA;&#x30EC;&#x30C3;&#x30B8;&#x3092;&#x8981;&#x7D04;&#x3092;&#x76EE;&#x6307;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#x9178;&#x5316;&#x30B9;&#x30C8;&#x30EC;&#x30B9;&#x3001;&#x30A2;&#x30DD;&#x30C8;&#x30FC;&#x30B7;&#x30B9;&#x3001;PGC-1 &alpha; &#x3068;&#x8133;&#x865A;&#x8840;&#x306B;&#x304A;&#x3051;&#x308B;&#x30DF;&#x30C8;&#x30B3;&#x30F3;&#x30C9;&#x30EA;&#x30A2;&#x306E;&#x751F;&#x5408;&#x6210;&#x306E;&#x5F79;&#x5272;

&#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xC758; &#xAE30;&#xBCF8; &#xC0DD;&#xB9AC; &#xAE30;&#xB2A5; &#xC804;&#xC790; &#xC804;&#xC1A1; &#xCCB4;&#xC778;&#xC744; &#xD1B5;&#xD574; &#xC0B0;&#xD654; &#xC778; &#xC0B0;&#xD654;&#xB97C; &#xD1B5;&#xD574; &#xC544;&#xB370;&#xB178;&#xC2E0; &#xC0BC;&#xC778;&#xC0B0;&#xC744; &#xC0DD;&#xC131; &#xD558;&#xB294; &#xAC83;. &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xC5D0;&#xC11C; &#xC0DD;&#xC131; &#xB41C; &#xBD80;&#xC0B0;&#xBB3C;&#xC73C;&#xB85C; &#xBC18;&#xC751;&#xC131; &#xC0B0;&#xC18C; &#xC885; (&#xC120;&#xC0DD;&#xB2D8;)&#xC758; &#xACFC;&#xC789; &#xB300;&#xB1CC; &#xD5C8; &#xD608;&#xC5D0;&#xC11C; &#xB1CC;&#xC878;&#xC911; &#xB4F1; &#xAE09;&#xC131; &#xB1CC; &#xC190;&#xC0C1;&#xC5D0; &#xC5F0;&#xB8E8; &#xB418;&#xC5B4; &#xC788;&#xB2E4;. &#xADF8;&#xAC83;&#xC740; &#xC798; &#xBB38;&#xC11C;&#xD654;&#xB294; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xC5D0; &#xC885;&#xC18D;&#xC801;&#xC778; apoptotic &#xD1B5;&#xB85C; &#xD3EC;&#xD568; &#xD504;&#xB85C; &#xC548;&#xD2F0; apoptotic &#xB2E8;&#xBC31;&#xC9C8; &#xBC14;&#xC778;&#xB529;, &#xC2DC; &#xD1A0; &#xD06C;&#xB86C; c&#xC758; &#xCD9C;&#xC2DC;&#xC5D0; &#xC2E0;&#xACBD; &#xAD81;&#xADF9;&#xC801;&#xC73C;&#xB85C; &#xC8FD;&#xC74C;&#xC744; &#xC120;&#xB3C4;. &#xB2E4;&#xB978; &#xD55C;&#xD3B8;&#xC73C;&#xB85C;, &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544;&#xB3C4; &#xC5ED;&#xD560;&#xC744; &#xACFC;&#xB3C4; &#xD55C; &#xC0B0;&#xD654; &#xC2A4;&#xD2B8;&#xB808;&#xC2A4;&#xC5D0; &#xC758;&#xD574; elicited &#xD574;&#xB85C;&#xC6B4; &#xD6A8;&#xACFC; &#xC911;&#xD654;. &#xCD5C;&#xADFC; &#xC5F0;&#xAD6C;&#xB294; &#xC0B0;&#xD654; &#xC2A4;&#xD2B8;&#xB808;&#xC2A4;&#xC640; &#xD5C8; &#xD608; &#xC131; &#xC2E0;&#xACBD; &#xC138;&#xD3EC;&#xC758; redox &#xC2A4;&#xD14C;&#xC774;&#xD2B8; peroxisome &#xC99D;&#xC2DD; &#xD65C;&#xC131;&#xD654; &#xC218;&#xC6A9; &#xCCB4; &gamma; (PPAR&gamma;) &#xBC29;&#xC1A1; 1&alpha;&#xC744; &#xD3EC;&#xD568; &#xD558;&#xB294; &#xC2E0;&#xD638; &#xD1B5;&#xB85C;&#xC5D0; &#xC5F0;&#xB8E8; &#xB610;&#xD55C; &#xBC1D;&#xD600;&#xC84C;&#xB2E4; (PGC1-&alpha;). PGC1-&alpha; &#xD6A8;&#xC18C; &#xB9DD;&#xAC04; superoxide dismutase 2&#xB97C; &#xD3EC;&#xD568; &#xD558; &#xC5EC; &#xCCAD;&#xC18C; &#xD558;&#xB294; &#xC120;&#xC0DD;&#xB2D8;&#xC758; &#xB9C8;&#xC2A4;&#xD130; &#xB808; &#xADE4; &#xB808;&#xC774; &#xD130; &#xC774;&#xBA70;, uncoupling &#xB2E8;&#xBC31;&#xC9C8; 2&#xB294; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xB2E8;&#xBC31;&#xC9C8;&#xC640; &#xC2E0;&#xACBD; &#xC0DD;&#xC874;&#xC5D0; &#xAE30;&#xC5EC;&#xD560; &#xC218; &#xC788;&#xC2B5;&#xB2C8;&#xB2E4;. PGC1-&alpha;&#xB3C4;&#xC740; &#xC138;&#xD3EC; &#xC0DD;&#xC874;&#xC744; &#xC704;&#xD55C; &#xC911;&#xC694; &#xD55C; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xC18D;&#xC5D0; &#xCC38;&#xC5EC; &#xD558;&#xACE0;&#xC788;&#xB2E4;. &#xC2E4;&#xD5D8;&#xC801; &#xC99D;&#xAC70; &#xB1CC;&#xC878;&#xC911; &#xD6C4; &#xC2E0;&#xACBD; &#xC8FD;&#xC74C;&#xC73C;&#xB85C; &#xC0DD; &#xBCF4;&#xD638; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC758; &#xACB0;&#xC815; &#xC694;&#xC778;&#xC73C;&#xB85C; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC; &#xB9AC;&#xC544; &#xAE30;&#xB2A5; &#xC7A5;&#xC560; &#xBC0F; &#xC0B0;&#xD654; &#xC2A4;&#xD2B8;&#xB808;&#xC2A4;&#xC758; &#xC5ED;&#xD560;&#xC744; &#xC9C0;&#xC6D0;&#xD569;&#xB2C8;&#xB2E4;. &#xC774; &#xAC80;&#xD1A0; &#xC120;&#xC0DD;&#xB2D8;, &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC; &#xB9AC;&#xC544; &#xAE30;&#xB2A5; &#xC7A5;&#xC560;, apoptosis, &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xB2E8;&#xBC31;&#xC9C8; &#xCCAD;&#xC18C;, &#xC120;&#xC0DD;&#xB2D8; &#xD558; &#xACE0; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xC18D; &#xB300;&#xB1CC; &#xD5C8; &#xD608; &#xAE30;&#xBCF8; &#xBD84;&#xC790; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC5D0; &#xCD08;&#xC810;&#xC744; &#xB9DE;&#xCD94;&#xACE0; &#xD604;&#xC7AC;&#xC758; &#xC9C0;&#xC2DD;&#xC744; &#xC694;&#xC57D; &#xD558;&#xB294; &#xAC83;&#xC744; &#xBAA9;&#xD45C;&#xB85C;.

&#xC0B0;&#xD654; &#xC2A4;&#xD2B8;&#xB808;&#xC2A4;, Apoptosis, PGC 1&alpha; &#xBC0F; &#xB300;&#xB1CC; &#xAD6D; &#xC18C; &#xBE48; &#xD608;&#xC5D0; &#xBBF8;&#xD1A0; &#xCF58; &#xB4DC;&#xB9AC; &#xC544; &#xC18D;&#xC758; &#xC5ED;&#xD560;.

La principal funci&oacute;n fisiol&oacute;gica de las mitocondrias es generar trifosfato de adenosina a trav&eacute;s de la fosforilaci&oacute;n oxidativa mediante la cadena de transporte de electrones. Superproducci&oacute;n de especies reactivas del ox&iacute;geno (ROS) como subproductos generados a partir de las mitocondrias han sido implicados en lesiones cerebrales agudas tales como movimiento de la isquemia cerebral. Fue bien documentado que v&iacute;a apopt&oacute;tica de las mitocondrias-dependiente implica pro - y anti-apoptotic Uni&oacute;n a prote&iacute;nas, liberaci&oacute;n de citocromo c, llevando a la muerte en &uacute;ltima instancia a neuronal. Por otro lado, las mitocondrias tambi&eacute;n desempe&ntilde;an un papel para contrarrestar los efectos perjudiciales que provocada por el estr&eacute;s oxidativo excesivo. Estudios recientes han revelado que el estr&eacute;s oxidativo y el estado redox de neuronas isqu&eacute;micas tambi&eacute;n est&aacute;n implicados en la v&iacute;a de se&ntilde;alizaci&oacute;n que involucra peroxisoma activado proliferativa receptor-&gamma; (PPARy) coactivador 1&alpha; (PGC1-&alpha;). PGC1-&alpha; es un regulador principal de ROS borrado enzimas como la super&oacute;xido dismutasa de manganeso 2 y la prote&iacute;na desacoplar 2, ambos son prote&iacute;nas mitocondriales y puede contribuir a la supervivencia neuronal. PGC1-&alpha; tambi&eacute;n participa en la biog&eacute;nesis mitocondrial que es vital para la supervivencia celular. La evidencia experimental apoya las funciones de la disfunci&oacute;n mitocondrial y el estr&eacute;s oxidativo como determinantes de muerte neuronal, as&iacute; como mecanismos end&oacute;genos de protecci&oacute;n despu&eacute;s del accidente cerebrovascular. Esta revisi&oacute;n pretende resumir el conocimiento actual, centr&aacute;ndose en los mecanismos moleculares subyacentes de la isquemia cerebral que involucra la disfunci&oacute;n mitocondrial, apoptosis, ROS, prote&iacute;nas mitocondriales capaces de ROS borrado y la biog&eacute;nesis mitocondrial.

Papeles de estr&eacute;s oxidativo, Apoptosis, PGC-1&alpha; y biog&eacute;nesis mitocondrial en la isquemia Cerebral.

Recent studies showed that increased mitochondrial fission is an early event of cell death during cerebral ischemia and dynamin-related protein 1 (Drp1) plays an important role in mitochondrial fission, which may be regulated by PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase thought to protect cells from stress-induced mitochondrial dysfunction and regulate mitochondrial fission. However, the roles of PINK1 and Drp1 in hippocampal injury caused by transient global ischemia (TGI) remain unknown. We therefore tested the hypothesis that TGI may induce PINK1 causing downregulation of Drp1 phosphorylation to enhance hippocampal neuronal survival, thus functioning as an endogenous neuroprotective mechanism. We found progressively increased PINK1 expression in the hippocampal CA1 subfield1-48 h following TGI, reaching the maximal level at 4 h. Despite lack of changes in the expression level of total Drp1 and phosphor-Drp1 at Ser637, TGI induced a time-dependent increase of Drp1 phosphorlation at Ser616 that peaked after 24 h. Notably, PINK1-siRNA increased p-Drp1(Ser616) protein level in hippocampal CA1 subfield 24 h after TGI. The PINK1 siRNA also aggravated the TGI-induced oxidative DNA damage with an increased 8-hydroxy-deoxyguanosine (8-OHdG) content in hippocampal CA1 subfield. Furthermore, PINK1 siRNA also augmented TGI-induced apoptosis as evidenced by the increased numbers of TUNEL-positive staining and enhanced DNA fragmentation. These findings indicated that PINK1 is an endogenous protective mediator vital for neuronal survival under ischemic insult through regulating Drp1 phosphorylation at Ser616.

Roles of PTEN-induced putative kinase 1 and dynamin-related protein 1 in transient global ischemia-induced hippocampal neuronal injury.

The advantage of using a cytoplasmic hybrid (cybrid) model to study the genetic effects of mitochondria is that the cells have the same nuclear genomic background. We previously demonstrated the independent role of mitochondria in the pathogenesis of insulin resistance (IR) and pro-inflammation in type 2 diabetes. In this study, we compared mitochondrial dynamics and related physiological functions between cybrid cells harboring diabetes-susceptible (B4) and diabetes-protective (D4) mitochondrial haplogroups, especially the responses before and after insulin stimulation. Cybrid B4 showed a more fragmented mitochondrial network, impaired mitochondrial biogenesis and bioenergetics, increased apoptosis and ineffective mitophagy and a low expression of fusion-related molecules. Upon insulin stimulation, increases in network formation, mitochondrial DNA (mtDNA) content, and ATP production were observed only in cybrid D4. Insulin promoted a pro-fusion dynamic status in both cybrids, but the trend was greater in cybrid D4. In cybrid B4, the imbalance of mitochondrial dynamics and impaired biogenesis and bioenergetics, and increased apoptosis were significantly improved in response to antioxidant treatment. We concluded that diabetes-susceptible mtDNA variants are themselves resistant to insulin.

Altered mitochondrial dynamics and response to insulin in cybrid cells harboring a diabetes-susceptible mitochondrial DNA haplogroup.

Prolonged seizure activity may result in mitochondrial dysfunction and lead to cell death in the hippocampus. Mitochondrial fission may occur in an early stage of neuronal cell death. This study examined the role of the mitochondrial fission protein dynamin-related protein 1 (Drp1) in the hippocampus following status epilepticus.

Dynamin-Related Protein 1 Promotes Mitochondrial Fission and Contributes to The Hippocampal Neuronal Cell Death Following Experimental Status Epilepticus.

In Taiwan, the prevalence of hyperlipidemia increased due to lifestyle and dietary habit changes. Low density lipoprotein cholesterol (LDL-C) and non-high density lipoprotein cholesterol (non-HDL-C) are all significant predicting factors of coronary artery disease in Taiwan. We recognized that lipid control is especially important in patients with existed atherosclerotic cardiovascular diseases (ASCVD), including coronary artery disease (CAD), ischemic stroke and peripheral arterial disease (PAD). Because the risk of ASCVD is high in patients with diabetes mellitus (DM), chronic kidney disease (CKD) and familial hypercholesterolemia (FH), lipid control is also necessary in these patients. Lifestyle modification is the first step to control lipid. Weight reduction, regular physical exercise and limitation of alcohol intake all reduce triglyceride (TG) levels. Lipid-lowering drugs include HMG-CoA reductase inhibitors (statins), cholesterol absorption inhibitors (ezetimibe), proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, nicotinic acids (niacin), fibric acids derivatives (fibrates), and long-chain omega-3 fatty acids. Statin is usually the first line therapy. Combination therapy with statin and other lipid-lowering agents may be considered in some clinical settings. For patients with acute coronary syndrome (ACS) and stable CAD, LDL-C < 70 mg/dL is the major target. A lower target of LDL-C <55 mg/dL can be considered in ACS patients with DM. After treating LDL-C to target, non-HDL-C can be considered as a secondary target for patients with TG ≥ 200 mg/dL. The suggested non-HDL-C target is < 100 mg/dL in ACS and CAD patients. For patients with ischemic stroke or transient ischemic attack presumed to be of atherosclerotic origin, statin therapy is beneficial and LDL-C < 100 mg/dL is the suggested target. For patients with symptomatic carotid stenosis or intracranial arterial stenosis, in addition to antiplatelets and blood pressure control, LDL-C should be lowered to < 100 mg/dL. Statin is necessary for DM patients with CV disease and the LDL-C target is < 70 mg/dL. For diabetic patients who are ≥ 40 years of age, or who are < 40 years of age but have additional CV risk factors, the LDL-C target should be < 100 mg/dL. After achieving LDL-C target, combination of other lipid-lowering agents with statin is reasonable to attain TG < 150 mg/dL and HDL-C >40 in men and >50 mg/dL in women in DM. LDL-C increased CV risk in patients with CKD. In adults with glomerular filtration rate (GFR) < 60 mL/min/1.73m without chronic dialysis (CKD stage 3-5), statin therapy should be initiated if LDL-C ≥ 100 mg/dL. Ezetimibe can be added to statin to consolidate the CV protection in CKD patients. Mutations in LDL receptor, apolipoprotein B and PCSK9 genes are the common causes of FH. Diagnosis of FH usually depends on family history, clinical history of premature CAD, physical findings of xanthoma or corneal arcus and high levels of LDL-C. In addition to conventional lipid lowering therapies, adjunctive treatment with mipomersen, lomitapide, or PCSK9 inhibitors become necessary to further reduce LDL-C in patients with FH. Overall, these recommendations are to help the health care professionals in Taiwan to treat hyperlipidemia with current scientific evidences. We hope the prescription rate of lipid lowering drugs and control rate of hyperlipidemia in high risk patients could be increased by implementation of the clinical guidelines. The major purpose is to improve clinical outcomes of these high risk patients through the control of hyperlipidemia.

2017 Taiwan lipid guidelines for high risk patients.

'Corrigendum to "2017 Taiwan lipid guidelines for high risk patients" [Journal of the Formosan Medical Association (2017) [217-248]'.

This study is intended to explore the associations between nutritional status and molecular biomarkers and the clinical severity of Parkinson's disease (PD), as well as to examine the differences in related factors between PD patients with normal nutrition and those with at risk for malnutrition. A cross-sectional assessment of 82 consecutive outpatients with PD was conducted using the mini nutritional assessment (MNA), Unified Parkinson's Disease Rating Scale (UPDRS), and the Hoehn and Yahr scale to determine the nutritional status, the clinical severity of PD, and the stage of the disease. Recordings of blood samples collected after 12 h of overnight fasting were also assessed in terms of serum levels of glycated hemoglobin (HbA1c), blood urea nitrogen (BUN), creatinine, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), hemoglobin (Hgb), folate, and vitamin B12. All participants were divided into normal nutrition and malnutrition risk groups via the MNA scores to compare the above-mentioned parameters. The results showed that the total MNA score was significantly correlated with some parts of the UPDRS scale (e.g., Sections 1 and 2) and the levels of HbAlc in PD patients and those with risk for malnutrition, with significantly lower weight and body mass index (BMI), and with lower levels of Hgb and HDL. Higher levels of cholesterol were observed in the malnutrition risk group as compared with the normal nutrition group. The findings suggest that the clinical severity of PD is associated with nutritional status. Body weight, BMI, and the levels of Hgb, cholesterol, and HDL could be, at least partially, important biological markers to monitor malnutrition and the progression of the disease.

Nutritional Status Associated with Molecular Biomarkers, Physiological Indices, and Clinical Severity in Parkinson's Disease Patients.

Social interactions among animals mediate essential behaviours, including mating, nurturing, and defence. The gut microbiota contribute to social activity in mice, but the gut-brain connections that regulate this complex behaviour and its underlying neural basis are unclear. Here we show that the microbiome modulates neuronal activity in specific brain regions of male mice to regulate canonical stress responses and social behaviours. Social deviation in germ-free and antibiotic-treated mice is associated with elevated levels of the stress hormone corticosterone, which is primarily produced by activation of the hypothalamus-pituitary-adrenal (HPA) axis. Adrenalectomy, antagonism of glucocorticoid receptors, or pharmacological inhibition of corticosterone synthesis effectively corrects social deficits following microbiome depletion. Genetic ablation of glucocorticoid receptors in specific brain regions or chemogenetic inactivation of neurons in the paraventricular nucleus of the hypothalamus that produce corticotrophin-releasing hormone (CRH) reverse social impairments in antibiotic-treated mice. Conversely, specific activation of CRH-expressing neurons in the paraventricular nucleus induces social deficits in mice with a normal microbiome. Via microbiome profiling and in vivo selection, we identify a bacterial species, Enterococcus faecalis, that promotes social activity and reduces corticosterone levels in mice following social stress. These studies suggest that specific gut bacteria can restrain the activation of the HPA axis, and show that the microbiome can affect social behaviours through discrete neuronal circuits that mediate stress responses in the brain.

Microbiota regulate social behaviour via stress response neurons in the brain.

Anxiety is characterized by tension feelings and worried thoughts even in the absence of threatening stimulus. Pathological condition of anxiety elicits defensive behavior and aversive reaction ultimately impacting individuals and society. The gut microbiota has been shown to contribute to the modulation of anxiety-like behavior in rodents through the gut-brain axis. Several studies observed that germ-free (GF) and the broad spectrum of antibiotic cocktail (ABX)-treated rodents display lowered anxiety-like behavior. We speculate that gut microbial short-chain fatty acids (SCFA) modulate the innate anxiety response. Herein, we administered SCFA in the drinking water in adult mice treated with ABX to deplete the microbiota and tested their anxiety-like behaviors. To further augment the innate fear response, we enhanced the aversive stimulus of the anxiety-related behavior tests. Strikingly, we found that the anxiety-like behavior in ABX mice was not altered when enhanced aversive stimulus, while control and ABX mice supplemented with SCFA displayed increased anxiety-like behavior. Vagus nerve serves as a promising signaling pathway in the gut-brain axis. We determined the role of vagus nerve by subdiaphragmatic vagotomy (SDV) in ABX mice supplemented with SCFA. The restored anxiety-like behavior in ABX mice by SCFA was unaffected by SDV. These findings suggest that gut microbiota can regulate anxiety-like behavior through their fermentation products SCFA.

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Microbiota regulate social behaviour via stress response neurons in the brain. Nature\| PubMed ID: 34194038
Oral short-chain fatty acids administration regulates innate anxiety in adult microbiome-depleted mice. Neuropharmacology\| PubMed ID: 35613660	2022

Chia-Wei Liou

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