Protective effects of maslinic acid on high fat diet-induced liver injury in mice.

AIMS: Due to the prevalence of high-fat diets and lack of exercise, diseases related to nutrient metabolism such as nonalcoholic fatty liver disease (NAFLD) have become one of the reasons causes endangering human liver health. Maslinic acid (MA) is a pentacyclic triterpenoid acid that is abundant in fruits such as hawthorn and jujube. In this study, we investigated the effect of MA on NAFLD to inform the development of dietary supplements for the treatment and prevention of NAFLD. MATERIALS AND METHODS: The NAFLD model was established by feeding mice a high-fat diet (HFD). HEPG2 cells were treated with oleic acid and used as a cell culture model. Testing kits, haematoxylin and eosin staining, oil red O staining, western blotting, and immunofluorescence were performed with in vivo and in vitro experiments. KEY FINDINGS: The current study revealed that MA significantly reduced liver weight, body weight and serum lipid levels, and protected against liver steatosis and injury induced by a HFD. MA increased the expression of Beclin1, ATG1, and Bcl-2 mRNA and protein while decreasing the expression of TNF-α and IL-1ß, caspase-3 and Bax mRNA and protein. Beclin1, and ATG1 were obviously increased, and the mRNA and protein expression of TNF-α and IL-1ß were obviously reduced, the mRNA and protein expression of Caspase-3 and Bax were obviously reduced, and the mRNA and protein expression of Bax were obviously increased by MA. SIGNIFICANCE: MA reduces the content of fat in the liver cells of NAFLD mice through lipophagy activitiy and reduces inflammation and apoptosis injury.

Astragaloside IV inhibits cell proliferation in vulvar squamous cell carcinoma through the TGF-ß/Smad signaling pathway.

OBJECTIVE: To explore the inhibition of the proliferation of vulvar squamous cell carcinoma (VSCC) by astragaloside IV. METHODS: MTT examined the cell proliferation of VSCC. Flow cytometry analyzed cell cycle and apoptosis. Western blot assay detected the expression of some relevant proteins. RESULTS: AS-IV reduced the proliferation of SW962 cells in a concentration- and time-dependent manner, induced cell-cycle arresting in G0/G1 phase, as demonstrated by the up-regulation of P53 and P21 expression, and the down-regulation of cyclin D1 expression. AS-IV enhanced the expression of Bax and cleaved-caspase 3, and suppressed Bcl-2 and Bcl-xl expression, which resulted in apoptosis increased. Furthermore, the expression of Beclin-1 and LC3-B was upregulated and that of P62 was downregulated, which suggested that AS-IV could increase the incidence of autophagy in SW962 cells. After inhibiting autophagy by 3-methyladenine (3-MA), cell apoptosis decreased upon AS-IV treatment. Similarly, TGF-ß1 stimulated SW962 cells, cell proliferation enhanced, and the expression of TGF-ßRII and Smad4 was decreased. Furthermore, the expression of proteins that promote apoptosis and autophagy decreased. After AS-IV treatment, the expression levels of the above proteins exhibited the opposite effect. CONCLUSION: AS-IV inhibits cell proliferation and induces apoptosis and autophagy through the TGF-ß/Smad signaling pathway in VSCC.