Quercetin Protects Hepatocytes against CCl4-Induced Apoptosis via SIRT1 Regulation

Abstract: Quercetin (Que) is a flavonoid compound found ubiquitously in nature with a variety of biological activities, including anti-apoptosis, anti-oxidant, free-radical scavenging, anti-inflammatory and anti-tumor effects. Carbon tetrachloride (CCl4), a commonly used toxic laboratory reagent which causes liver lesion and liver fibrosis, has been extensively applied in liver-related studies. The complex mechanisms of CCl4-induced hepatotoxicity involve apoptosis, oxidative stress, and inflammation. This study aimed to clarify the possible protective effects of Que against CCl4-induced hepatotoxicity using a murine hepatocyte cell culture model. Our results indicate that Que significantly decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Additionally, Que increased cell viability, glutathione (GSH), and superoxide dismutase (SOD) levels. Overall, Que significantly abrogated CCl4-induced cell apoptosis by upregulating the expression of Bcl-2 and decreasing the levels of Bax and cleaved caspase-3. Furthermore, Que obviously reversed the inhibition of Sirtuin 1 (SIRT1) expression. Our results provide the first evidence that Que protected against CCl4-induced apoptosis in hepatocytes by regulating the SIRT1 pathway. © 2021, Pleiades Publishing, Ltd.