neuregulin1-erbb4-signaling-involved-acupuncture-promoting-myelin

Neuregulin1-ErbB4 Signaling Involved in Acupuncture Promoting Myelin Regeneration in Spinal Cord Injury Rats

Spinal cord injury (SCI) often results in severe neurological dysfunction, and myelin repair is a critical step in the recovery of neurological function. ...

aconitine-induces-myocardial-damage-rats-associated-with-activation

Aconitine Induces Myocardial Damage in Rats Associated With Activation of the JNK1/2 Signaling Pathway

Acute Aconitine (Acon) poisoning can cause arrhythmia and myocardial damage; however, the underlying mechanisms remain unclear. This study investigated ...

Kunming Medical University

First Affiliated Hospital, Kunming Medical University

Cognitive impairment in diabetes (CID) is a severe chronic complication of diabetes mellitus, and its pathogenesis has not yet been fully understood. Increasing evidence has shown that the distribution and expression of N-methyl-D-aspartame receptor (NMDAR) and subunits NR2A and NR2B, which all participated in the development of the central nervous system and formation of learning and memory, are correlated with the occurrence and development of CID.

[Association of NMDAR, NR2A, and NR2B with cognitive impairment in diabetic patients].

Cognitive impairment in diabetes (CID) is a severe chronic complication of diabetes mellitus (DM). It has been hypothesized that diabetes can lead to cognitive dysfunction due to expression changes of excitatory neurotransmission mediated by N-methyl-D-aspartate receptors (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR); however, the pathogenesis involved in this has not been fully understood, especially at early phase of DM. Here, we sought to determine the cognitive changes and aim to correlate this with the expression changes of NMDAR and AMPAR of glutamate signaling pathways in the rat hippocampus from early phase of DM and in the course of the disease progression. By Western blot analysis and immunofluorescence labeling, the hippocampus in diabetic rats showed a significant increase in protein expression NMDAR subunits NR1, NR2A and NR2B and AMPAR subunit GluR1. Along with this, behavioral test by Morris water maze showed a significant decline in their performance when compared with the control rats. It is suggested that NR1, NR2A, NR2B and GluR1are involved in learning and memory and that their expression alterations maybe correlated with the occurrence and development of CID in diabetic rats induced by streptozotocin.

Expression Changes of NMDA and AMPA Receptor Subunits in the Hippocampus in rats with Diabetes Induced by Streptozotocin Coupled with Memory Impairment.

Cognitive dysfunction is a very severe consequence of diabetes, but the underlying causes are still unclear. Recently, the cerebellum was reported to play an important role in learning and memory. Since long-term depression (LTD) is a primary cellular mechanism for cerebellar motor learning, we aimed to explore the role of cerebellar LTD pathways in diabetic rats and the therapeutic effect of gastrodin. Diabetes was induced by a single injection of streptozotocin into adult Sprague-Dawley rats. Motor learning ability was assessed by a beam walk test. Pathological changes of the cerebellum were assessed by Hematoxylin-Eosin (HE) and Nissl staining. Cellular apoptosis was assessed by anti-caspase-3 immunostaining. Protein expression levels of LTD pathway-related factors, including GluR2, protein kinase C (PKC), NR2A, and nNOS, in the cerebellar cortex were evaluated by western blotting and double immunofluorescence. The NO concentration was measured. The cellular degeneration and the apoptosis of Purkinje cells were evident in the cerebellum of diabetic rats. Protein expression levels of GluR2 (NC9W: 1.26 ± 0.12; DM9W + S: 0.81 ± 0.07), PKC (NC9W: 1.66 ± 0.10; DM9W + S: 0.58 ± 0.19), NR2A (NC9W: 1.40 ± 0.05; DM9W + S: 0.63 ± 0.06), nNOS (NC9W: 1.26 ± 0.12; DM9W + S: 0.68 ± 0.04), and NO (NC9W: 135.61 ± 31.91; DM9W + S: 64.06 ± 24.01) in the cerebellum were significantly decreased in diabetic rats. Following gastrodin intervention, the outcome of motor learning ability was significantly improved (NC9W: 6.70 ± 3.31; DM9W + S: 20.47 ± 9.43; DM9W + G: 16.04 ± 7.10). In addition, degeneration and apoptosis were ameliorated, and this was coupled with the elevation of the protein expression of the abovementioned biomarkers. Arising from the above, we concluded that gastrodin may contribute to the improvement of motor learning by protecting the LTD pathways in Purkinje cells.

Gastrodin Ameliorates Motor Learning Deficits Through Preserving Cerebellar Long-Term Depression Pathways in Diabetic Rats.

The mechanism of cognitive dysfunction in diabetes is still unclear. Recently, studies have shown that the cerebellum is involved in cognition. Furthermore, diabetes-induced cerebellar alterations is related to vascular changes. Therefore, we aimed to explore the roles of vascular function in diabetes-induced cerebellar damage and motor learning deficits. Type 1 diabetes was induced by a single injection of streptozotocin in Sprague-Dawley rats. Motor learning was assessed by beam walk test and beam balance test. The pathological changes of the cerebellum were assessed by Hematoxylin and eosin staining and Nissl staining. Apoptosis was evaluated by anti-caspase-3 immunostaining. Protein expression was evaluated by western blotting and double immunofluorescence. Our results have shown that motor learning was impaired in diabetic rats, coupled with damaged Purkinje cells and decreased capillary density in the cerebellum. In addition, the protein expression of neuronal NOS, inducible NOS, endothelial NOS, total nitric oxide, vascular endothelial growth factor and its cognate receptor Flk-1 was decreased in the cerebellum. Gastrodin treatment ameliorated neuronal damage and restored protein expression of relevant factors. Arising from the above, it is suggested that vascular dysfunction and NO signaling deficits in the cerebellum may be the underlying mechanism of early manifestations of cognitive impairment in diabetes, which could be ameliorated by gastrodin intervention.

Early Intervention of Gastrodin Improved Motor Learning in Diabetic Rats Through Ameliorating Vascular Dysfunction.

Traumatic brain injury (TBI) is a major cause of disability worldwide, without definitive and effective intervention. Dexmedetomidine (DEX) has a neuroprotective effect against TBI; however, the detailed mechanism underlying this effect remains unclear.

Identification of candidate genes and pathways in dexmedetomidine-induced neuroprotection in rats using RNA sequencing and bioinformatics analysis.

Aconitine is a crucial toxic component in Chinese herbal medicines such as Aconitum, Aconitum coreanum, and Aconitum soongaricum. The poisoning symptoms of the central nervous system and cardiovascular system caused by it are relatively common in China, and there are many studies on cardiovascular system diseases caused by aconitine. However, the specific mechanism of neurotoxicity induced by aconitine is still unclear. This study explored the effect and mechanism of mitochondrial calcium uniporter on mitochondrial energy metabolism disorder in aconitine poisoning hippocampal neurons. The results showed that after treatment with 400μmol/L aconitine, mitochondrial energy metabolism was abnormal in rat hippocampal neuron cells, the expression of MCU in mitochondria was up-regulated, calcium overload in mitochondria, ATP production decreased, and mitochondrial membrane potential Changes, increased expression of the apoptosis gene Cleaved-Caspase-3. After treatment with the MCU agonist spermine, mitochondrial energy metabolism was significantly abnormal, and cell apoptosis was increased considerably. However, pretreatment with calcium ion channel inhibitor Ruthenium Red (RR) effectively promoted the generation of ATP, thereby improving mitochondrial energy metabolism disorders and reducing cell apoptosis. These results suggest that aconitine induces mitochondrial energy metabolism dysfunction in hippocampal neurons, which may be related to the increased expression of MCU.

Mechanism of aconitine mediated neuronal apoptosis induced by mitochondrial calcium overload caused by MCU.

This study aims to investigate the role and regulatory mechanisms of PTP1B in acute pancreatitis.

Inhibition of PTP1B Through NADH Dehydrogenase Activity Reduces Acute Pancreatic Acinar Cell Pyroptosis by Inhibiting the ROS/TXNIP/NLRP3 Pathway.

The tree shrew (Tupaia belangeri) has become an ideal model for studying various neurological diseases. However, there is no stable tree shrew model of traumatic brain injury (TBI) at present. This study aimed to establish a tree shrew TBI model and clarify the expression characteristics of inflammatory factors after brain injury, as well as the polarization characteristics of glial cells.

ArticleTotal : 2	Year
Publication title	2026
Publication title	2026

Article	Year
[Association of NMDAR, NR2A, and NR2B with cognitive impairment in diabetic patients]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University\| PubMed ID: 24369260	2013
Expression Changes of NMDA and AMPA Receptor Subunits in the Hippocampus in rats with Diabetes Induced by Streptozotocin Coupled with Memory Impairment. Neurochemical research\| PubMed ID: 30747310	2019
Gastrodin Ameliorates Motor Learning Deficits Through Preserving Cerebellar Long-Term Depression Pathways in Diabetic Rats. Frontiers in neuroscience\| PubMed ID: 31824244	2019
Early Intervention of Gastrodin Improved Motor Learning in Diabetic Rats Through Ameliorating Vascular Dysfunction. Neurochemical research\| PubMed ID: 32415405	2020
Identification of candidate genes and pathways in dexmedetomidine-induced neuroprotection in rats using RNA sequencing and bioinformatics analysis. Annals of palliative medicine\| PubMed ID: 33545770	2021
Mechanism of aconitine mediated neuronal apoptosis induced by mitochondrial calcium overload caused by MCU. Toxicology letters\| PubMed ID: 37506855	2023
Inhibition of PTP1B Through NADH Dehydrogenase Activity Reduces Acute Pancreatic Acinar Cell Pyroptosis by Inhibiting the ROS/TXNIP/NLRP3 Pathway. Digestive diseases and sciences\| PubMed ID: 41051643	2025
A study on the establishment of a traumatic brain injury model of tree shrews and the observation of neuroinflammatory responses. IBRO neuroscience reports\| PubMed ID: 41280136	2025

Yongjie Huang

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