Objective:To investigate the effect of resveratrol (Res) on the fat synthesis in the liver cancer HepG2cells, and to elucidate its possible mechanism.Methods:The HepG2cells were cultured in vitro and divided into Res group (treated with 40μmol·L-1 DMSO-diluted Res for 24h) and control group (treated with the same concentration of DMSO for 24h) .The cell supernatant was collected, and the levels of triglyceride (TG) and total cholesterol (TC) in the cells in various groups were measured by ELISA.The mRNA and protein expression levels of lipase synthase acetyl-CoA carboxylase (ACC1) , fatty acid synthetase (FASN) and stearoyl-CoA desaturase (SCD1) in the cells in various groups were detected by qRT-PCR and Western blotting method.The levels of O-linked N-acetylglucosamine (O-GlcNAc) glycosylation in the cells in various groups were detected by Western blotting method.Results:Compared with control group, the levels of TG and TC in the cells in Res group were decreased, but the difference was not statistically significant (t1=1.886, P＞0.05;t2=2.457, P＞0.05) .Compared with control group, the levels of expressions of ACC1, FASN and SCD1mRNA and proteins in the cells in Res group were significantly decreased (P＜0.05or P＜0.01) ;the O-GlcNAc glycosylation level in the cells in Res group was significantly decreased (t=2.87, P＜0.05) .Conclusion:Res has the effect of inhibiting the fat synthesis in the liver cancer HepG2 cells.Its mechanism may be related to the reduction of cellular O-GlcNAc glycosylation level and the reduction of the expression of FASN.

Autoimmune diseases can present as different forms of sleep disorders, such as narcolepsy, insomnia, and sleep-related breathing disorders. These disorders can be life-threatening in severe cases. However, the lack of awareness of immune-related sleep disorders, along with the absence of uniform diagnostic and treatment standards, may lead to frequent missed diagnosis and misdiagnosis. This article will review the concepts, classification, pathogenesis, clinical features, diagnosis and treatment of immune-related sleep disorders, aimed at deepening the understanding of the diseases as well as facilitating early diagnosis and treatment.

ObjectiveTo explore the pharmacodynamic effect of the water extract of Citri Grandis exocarpium （WEC） on mice with alcohol-induced acute liver injury and provide data support for the development of this medicinal for anti-alcoholism and liver protection. MethodThe main components of WEC were determined by high performance liquid chromatography （HPLC）. Sixty Balb/c mice were randomized into 6 groups： control group （equal volume of 0.5% carboxymethyl cellulose sodium solution）， model group （equal volume of 0.5% carboxymethyl cellulose sodium solution）， low-， medium-， and high-dose WEC groups （0.5， 1.0， 2.0 g·kg^-1）， and Haiwang Jinzun tablet positive control group （2.0 g·kg^-1）. The administration lasted 14 days. One day before the end of the administration， mice were fasted for 12 h with free access to water. The mice， except the control group， were given 56° Chinese liquor （13 mL·kg^-1）. After 2 h， blood was taken from eyeballs and the liver was dissected and weighed. Automatic biochemical analyzer was employed to detect the expression of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， and alcohol dehydrogenase （ADH）. The pathological changes of liver tissues were observed based on hematoxylin-eosin （HE） staining， and apoptosis of hepatocytes based on TUNEL/DAB staining. The expression of proteins related to apoptosis was detected by Western blot. ResultAccording to the HPLC fingerprint， the main components of WEC were rhoifolin and naringin. Compared with the control group， the model group showed increase in liver/body weight ratio （P<0.01） and the expression of ALT and AST （P<0.05， P<0.01）， decrease in the expression of ADH （P<0.05）， blurred structure of hepatic lobules， pathological changes of liver tissue， loose cytoplasm with edema， severe steatosis， rise of the TUNEL-positive rate （P<0.01）， reduction in expression of Bcl-2 （P<0.01）， and increase in Bax and Caspase-3 （P<0.01）. Compared with the model group， medium-dose WEC lowered liver/body weight ratio （P<0.05）. All doses of WEC depressed the activity of ALT and AST （P<0.05， P<0.01）， up-regulated the expression of ADH （P<0.05）， significantly improved the pathological features of alcohol-induced cytoplasmic porosity， edema， and steatosis， down-regulated the TUNEL-positive rate （P<0.05， P<0.01）， enhanced the expression of Bcl-2 （P<0.05）， and decreased Bax and Caspase-3 （P<0.01）. ConclusionWEC regulates the expression of ALT， AST， and ADH and improves hepatic steatosis and hepatocyte apoptosis to fight against acute liver injury.