ABSTRACT
Fubai chrysanthemum is a kind of traditional Chinese medicine, which can be used as a common food, and is commonly used to improve and relieve visual fatigue. However, its pharmacodynamic material basis and action mechanisms in relieving visual fatigue have not been systematically studied. In this article, 11 absorbed ingredients from Fubai chrysanthemum were detected in rat plasma. Then, the target network pharmacology and KEGG pathway analysis were performed. It was found that Fubai chrysanthemum could inhibit various apoptotic cells and reduce oxidative damage of eyes by regulating the apoptosis pathway, thus alleviating visual fatigue. Further in vitro experiments showed that Fubai chrysanthemum could effectively protect against oxidation damage of adult retinal pigment epithelial cells (ARPE-19), retinal ganglion cells (RGC-5), and lens. The results of cell experiments showed that Fubai chrysanthemum could increase the cell activity, GSH content, and SOD content of ARPE-19 and RGC-5 after oxidative injury, while decreasing the IL-18 content. Similarly, in the study of lens transparency, we found that Fubai chrysanthemum could effectively alleviate the oxidative damage degree of the lens, and significantly increase the content of CAT, GSH, and SOD. The above results suggested that Fubai chrysanthemum could play an important role in alleviating visual fatigue through regulating cell apoptosis and antioxidative damage.
ABSTRACT
OBJECTIVE: To investigate the effect of low concentration of Wenyang Tonglin Decoction (WTD) on the binding conditions of R45 plasmid conjugative transfer under liquid phase conjugation and its mechanism. METHODS: Escherichia coli CP9 (R45) and Staphylococcus aureus RN450RF were cultured in medium containing WTD, and their minimum inhibitory concentration (MIC) values were obtained. Using promoter fusion technology, E. coli CP9 (R45) containing a promoter fusion was obtained. ß-Galactosidase activity of TrfAp and TrbBp was tested, and the mRNA expression of regulatory factors (TrbA, KorA, and KorB) was detected by real-time fluorescent quantitative polymerase chain reaction. RESULTS: The MIC of E. coli CP9 (R45) was 400 g/L and that of S. aureus RN450RF was 200 g/L. When the drug concentration in the culture medium was 200 g/L, the highest number of conjugants was (3.47 ±0.20) × 107 CFU/mL At 90 h of conjugation, the maximum number of conjugants was (1.15 ±0.06) × 108 CFU/mL When the initial bacterial concentration was 108 CFU/mL, the maximum number of conjugants was (3.47 ± 0.20) × 107 CFU/mL. When the drug concentration was 200 g/L, the ß-galactosidase activity of TrfAp and TrbBp significantly increased; the relative quantification of TrbA, KorA and KorB were significantly inhibited. CONCLUSION: Low concentration of WTD promoted the development of bacterial resistance by affecting promoters and inhibiting the expression of regulatory factors.
Subject(s)
Drugs, Chinese Herbal , Escherichia coli , Microbial Sensitivity Tests , Plasmids , Staphylococcus aureus , Drugs, Chinese Herbal/pharmacology , Staphylococcus aureus/drug effects , Staphylococcus aureus/genetics , Plasmids/genetics , Escherichia coli/drug effects , Escherichia coli/genetics , Conjugation, Genetic , Promoter Regions, Genetic/genetics , Drug Resistance, Bacterial/genetics , Drug Resistance, Bacterial/drug effects , beta-Galactosidase/metabolism , beta-Galactosidase/genetics , Dose-Response Relationship, Drug , RNA, Messenger/genetics , RNA, Messenger/metabolism , Gene Expression Regulation, Bacterial/drug effectsABSTRACT
SCOPE: Cerebral ischemia-reperfusion (IR) injury stands as a prominent global contributor to disability and mortality. Nervonic acid (NA), a bioactive elongated monounsaturated fatty acid, holds pivotal significance in human physiological well-being. This research aims to explore the prophylactic effects and fundamental mechanisms of NA in a rat model of cerebral IR injury. METHODS AND RESULTS: Through the induction of middle cerebral artery occlusion, this study establishes a rat model of cerebral IR injury and comprehensively assesses the pharmacodynamic impacts of NA pretreatment. This evaluation involves behavioral analyses, histopathological examinations, and quantification of serum markers. Detailed mechanisms of nervonic acid's prophylactic effects are revealed through fecal metabolomics and 16S rRNA sequencing analyses. Our findings robustly support nervonic acid's capacity to ameliorate neurological impairments in rats afflicted with cerebral IR injury. Beyond its neurological benefits, NA demonstrates its potential by rectifying metabolic perturbations across diverse pathways, particularly those pertinent to unsaturated fatty acid metabolism. Additionally, NA emerges as a modulator of gut microbiota composition, notably by selectively enhancing vital genera like Lactobacillus. CONCLUSION: These comprehensive findings highlight the potential of incorporating NA as a functional component in dietary interventions aimed at targeting cerebral IR injury.
Subject(s)
Dietary Supplements , Feces , Gastrointestinal Microbiome , Rats, Sprague-Dawley , Reperfusion Injury , Animals , Gastrointestinal Microbiome/drug effects , Male , Feces/microbiology , Feces/chemistry , Rats , Infarction, Middle Cerebral Artery , Brain Ischemia , Disease Models, AnimalABSTRACT
Genipin has been shown to exert anti-inflammatory effects, but its mechanism in protecting the ethanol-induced acute gastric injuries remains largely unclear. The present study aimed to investigate the effects of genipin on ethanol-induced acute gastric injuries in mice. After intragastrical administration of genipin for 7 consecutive days, acute gastric injuries were induced in the mice by ethanol treatment for 1 h. The expression levels of MDA, MPO, SOD, CAT, and NO in gastric tissues, and the levels of IL-6, TNF-α, MTL, SP, VIP and SS in serum samples were measured by ELISA. In addition, Western blotting was used to determine the expression levels of proteins involved in NLRP3 signaling pathway. The findings revealed that oral administration of genipin significantly ameliorated the pathological injury of gastric mucosa induced by ethanol, decreased the oxidative stress induced by ethanol and suppressed the expression levels of in-flammatory cytokines in gastric tissues and serum samples. In addition, it was observed that oral administration of genipin could remarkably inhibit the expression levels of related proteins in the NLRP3 signaling pathway. In conclusion, these results suggest that genipin may exhibit protective roles in ethanol-induced gastric mucosal injuries by activating antioxidant system and attenuating inflammatory reaction.