an-herbal-enema-formula-alleviates-ulcerative-colitis-inhibiting

An Herbal Enema Formula Alleviates Ulcerative Colitis by Inhibiting Enteric Glial Activation <em>via</em> the S100&#946;/RAGE/NF-&#954;B Pathway

Activation of enteric glial cells (EGCs) contributes to the pathogenesis of ulcerative colitis (UC). This study examined whether Dibai Enema Liquid ...

Beijing University of Chinese Medicine

Benzodiazepine hypnotics' effects on glucose metabolism are seldom reported, and the association between long-term (≥4 weeks) benzodiazepine usage and prediabetes has not been studied. This study was aimed to investigate the association between benzodiazepine hypnotic usage for ≥ 3 months and the prevalence of prediabetes. We analyzed cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) during 2005 to 2008, selecting adult participants without diabetes who used benzodiazepine hypnotics for at least 3 months or did not take any hypnotics. Individuals taking other hypnotics, antipsychotics, glucocorticoids, or hypoglycemic drugs were excluded. We defined prediabetes as an hemoglobin A1C (HbA1C) 5.7-6.4%, as suggested by the American Diabetes Association. Prescribed drug information was self-reported and checked by official interviewers, and HbA1C data in NHANES was recognized by the National Glycohemoglobin Standardization Program. We calculated the propensity score according to the covariates and adjusted it using multivariate logistic regression. Lower thresholds of HbA1C ≥ 5.5% or ≥ 5.3% were also analyzed. Among 4694 eligible participants, 38 received benzodiazepine hypnotics; using these hypnotics for ≥ 3 months was not significantly associated with the prevalence of prediabetes, as well as HbA1C ≥ 5.5% or ≥ 5.3%. Adjusted for propensity score, the respective odds ratios for prediabetes, HbA1C ≥ 5.5%, and HbA1C ≥ 5.3% were 1.09 (95% confidence interval [CI] 0.19-6.32), 0.83 (95% CI 0.22-3.13), and 1.22 (95% CI 0.3-4.93). No significant association was found between benzodiazepine hypnotic usage ≥ 3 months and the prevalence of prediabetes.

Association of long-term benzodiazepine hypnotic use and prediabetes in US population: A cross-sectional analysis of national health and nutrition examination survey data.

: Depression is associated to gut microbiota imbalance. Our research examined the antidepressant potential of phlorizin (PHZ), a natural anti-inflammatory compound that influences gut microbiota, and explored its underlying mechanisms. : A corticosterone (CORT)-induced depression mouse model was used for evaluating the ameliorative influences of PHZ on depressive phenotypes and central neuroinflammation through behavioral tests and biochemical assays. 16S rRNA sequencing and metabolomics were used to evaluate gut microbiota composition and metabolite levels in serum and hippocampal tissue, respectively. Spearman correlation and broad-spectrum antibiotic cocktail (ABx) treatment experiments verified the effect of gut microbes in the PHZ-mediated modulation of key metabolites. A lipopolysaccharide (LPS)-induced BV2 microglial inflammation model was established to evaluate the role of metabolites in PHZ's antineuroinflammatory effects. : PHZ significantly alleviated depressive-like behaviors in CORT mice and suppressed hippocampal neuroinflammation by modulating microglial M1/M2 polarization. Furthermore, PHZ altered gut microbiota composition, influenced serum methionine (Met) metabolism, and significantly increased hippocampal L-methionine (L-Met) and S-adenosylmethionine (SAMe) levels. Cellular experiments confirmed that L-Met plays a critical role in PHZ-mediated antineuroinflammatory effects. Significant correlations were observed between Parabacteroides, Parasutterella, and Alistipes and serum Met levels. ABx treatment suppressed the increase in hippocampal L-Met levels, suggesting that PHZ regulates methionine metabolism via the microbiota. These findings indicate that PHZ alleviates depressive states in CORT mice by modulating the microbiota-gut-brain axis. : PHZ modulates the gut microbiota (namely , , and ) and increase L-Met and SAMe levels, thereby suppressing neuroinflammation and improving depressive phenotypes in mice.

Phlorizin Alleviates Depression-like Behaviors via Gut Microbiota Reprogramming-Induced Methionine to Inhibit Neuroinflammation in Mice Hippocampus.

Phlorizin (PHZ) is a glucoside of phloretin, belonging to the dihydrochalcone class within flavonoids; It is one of the active ingredients of the plant Cynomorium, and it has been shown that PHZ can regulate lipid metabolism disorders as well as having anti-aging properties. However, no studies have investigated whether PHZ ameliorates Aβ-induced toxicity in Alzheimer's disease (AD) by regulating fatty acid β-oxidation. This study aims to investigate the effects of PHZ on the regulation of fatty acid β-oxidation and resistance to Aβ-associated toxicity on the AD  and the mechanisms of action. Wild-type N2 and AD model CL4176  were used; lifespan, heat stress resistance, chronic paraquat stress, reactive oxygen species (ROS), behavioral performance, and lipofuscin accumulation assays were examined to evaluate the anti-aging effects; and non-esterified fatty acid (NEFA), triglyceride (TG) and lipidomic contents were quantified after PHZ treatment. The detection of genes related to fatty acid β-oxidation pathways was performed using qRT-PCR.  knockout mutant RB1716; and GFP-binding mutants PMD150 WBM170 were used to observe the effect of PHZ on NHR-49 pathways, and molecular docking studies were performed by combining PHZ with NHR-49 proteins. Results showed that PHZ improved worms' survival and delayed senescence, as demonstrated by enhanced performance in lifespan, heat stress, ROS, and paraquat assays and chronic paraquat assays; PHZ also reduced lipid accumulation in worms, affected the unsaturated fatty acid pathway, and significantly increased the expression of fatty acid metabolism-related genes , , and , and can be tightly coupled to NHR-49 targets. PHZ may play an anti-Aβ toxicity role by regulating lipid metabolism disorders through the NHR-49-related pathway and anti-aging in AD worms.

Phlorizin Ameliorates Amyloid-β Toxicity and Enhances Fatty Acid β-Oxidation in  via NHR-49-Dependent Pathway.

Central lipid metabolism disorders are crucial for the development of Alzheimer's disease (AD). Phlorizin (PHZ) improved lipid metabolism abnormalities in AD nematodes, but its mechanism of action in improving AD-related symptoms and whether it can alleviate AD cognitive impairment remain unclear. To elucidate the effects and mechanisms of PHZ on lipid metabolism disorders in an AD model, gavage administration of PHZ for 8 weeks improved cognitive dysfunction and lipid disorders in APPswe/PSEN1dE9 (APP/PS1) mice. Concurrently, in astrocytes induced by palmitic acid (PA)- mediated lipid metabolic disorder, PHZ treatment improved astrocytic lipid accumulation by upregulating the target peroxisome proliferator-activated receptor α (PPARα) and its downstream pathways, thereby promoting astrocytic fatty acid oxidation. We validated PHZ's strong in vitro binding affinity with PPARα. Co-culture systems of lipid-metabolically disordered astrocytes and neurons further demonstrated that PHZ significantly improved neuronal cell viability and reduced intracellular lipid accumulation, thereby decreasing the expression of enzymes associated with β-amyloid protein (Aβ) production. This study demonstrates that gavage administration of PHZ for 2 months improves cognitive deficits and pathological markers in AD mice. Furthermore, at the cellular level, PHZ may exert its effects by enhancing astrocytic lipid metabolism, thereby preventing neuronal lipotoxicity and mitigating AD progression.

Article	Year
Association of long-term benzodiazepine hypnotic use and prediabetes in US population: A cross-sectional analysis of national health and nutrition examination survey data. Medicine\| PubMed ID: 37960777	2023
Phlorizin Alleviates Depression-like Behaviors via Gut Microbiota Reprogramming-Induced Methionine to Inhibit Neuroinflammation in Mice Hippocampus. Pharmaceuticals (Basel, Switzerland)\| PubMed ID: 41011263	2025
Phlorizin Ameliorates Amyloid-β Toxicity and Enhances Fatty Acid β-Oxidation in via NHR-49-Dependent Pathway. International journal of molecular sciences\| PubMed ID: 41096572	2025
PPARα-Mediated Fatty Acid Catabolism in Astrocytes Was Involved in Improvement of Cognitive Dysfunction by Phlorizin in APP/PS1 Mice. Antioxidants (Basel, Switzerland)\| PubMed ID: 41300478	2025

Yan Fu

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