METHODS: Immunofluorescence staining was used to observe the structural features of PC12 cells after culturing in medium with nerve growth factor (NGF). After different doses and different durations of alcohol treatment, CCK-8 assay was performed to detect the viability of PC12 cells, flow cytometry assay was carried out to detect the apoptosis rate of PC12 cells, dual-luciferase reporter assay was used to definitude the regulatory relationship between miR-96-5p and Tp73, and western blot was used to detect the protein expression of TAp73.
RESULTS: The result of immunofluorescence staining demonstrated that PC12 cells abundantly expressed Map2, CCK-8 assay illustrated alcohol exposure significantly downregulated the cell viability of PC12 cells, Treatment with miR-96-5p inhibitor induced apoptosis and upregulated the expression of TAp73 in PC12 cells. Contrastingly, miR-96-5p mimic reversed the above effects and downregulation of TAp73 inhibited the apoptosis of PC12 cells.
CONCLUSION: The present study demonstrated that miR-96-5p participates in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73.
PURPOSE: The present study seeks to determine if TLP would prevent HFD-induced NAFLD in vivo and its underlying mechanisms from the perspectives of gut microbiota, metabolites, and hepatic inflammation.
METHODS: TLP was subjected to extraction and chemo-profiling, and in vivo evaluation in HFD-fed rats on hepatic lipid and inflammation, intestinal microbiota, short-chain fatty acids (SCFAs) and permeability, and body weight and fat content profiles.
RESULTS: The TLP was primarily constituted of gallic acid, corilagin and chebulagic acid. Orally administered HFD-fed rats with TLP were characterized by the growth of Ligilactobacillus and Akkermansia, and SCFAs (acetic/propionic/butyric acid) secretion which led to increased claudin-1 and zonula occludens-1 expression that reduced the mucosal permeability to migration of lipopolysaccharides (LPS) into blood and liver. Coupling with hepatic cholesterol and triglyceride lowering actions, the TLP mitigated both inflammatory (ALT, AST, IL-1β, IL-6 and TNF-α) and pro-inflammatory (TLR4, MYD88 and NF-κB P65) activities of liver, and sequel to histopathological development of NAFLD in a dose-dependent fashion.
CONCLUSION: TLP is promisingly an effective therapy to prevent NAFLD through modulating gut microbiota, mucosal permeability and SCFAs secretion with liver fat and inflammatory responses.
MATERIALS AND METHODS: Twenty-four rats were divided into three groups: normal saline, octenidine dihydrochloride and povidone-iodine. Wounds were made on the rats' backs, and A. baumannii germs were inoculated into the wounds. After 3 hours, the wound was irrigated with wound cleansing solution according to the group for 30 seconds. Each wound was taken swab culture before and after wound irrigation and tissue culture 5 hours after wound irrigation.
RESULTS: All specimens showed bacterial colony growth with a median value of 1.22 × 105 CFU before irrigation. Wound irrigation with normal saline did not reduce colony counts, while there was a 3-log reduction to 5-log reduction in the octenidine and povidone-iodine groups. Statistically, there was no significant difference in the mean number of colonies between the octenidine and povidone-iodine groups after irrigation (p = 0.535). However, 3 hours after irrigation, all specimens that experienced 3-log reduction showed regrowth to more than 1 × 105 CFU. In contrast, specimens subjected to 5-log reduction did not exhibit any regrowth.
CONCLUSION: The antiseptic effectiveness of octenidine dihydrochloride is equivalent to povidone-iodine in eradicating A. baumannii colonies in wounds in vivo.