The underlying hepatoprotective mechanism of PKC#963 in alcohol or carbon tetrachloride induced liver injury via inhibition of iNOS, COX‐2, and p‐STAT3 and enhancement of SOD and catalase

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Abstract
The aim of the present study is to explore the underlying hepatoprotective mechanism of PKC#963, consisting of Pinus koraiensis, Saururus chinensis, and Lycium barbarum in association with acute and chronic liver injury induced by alcohol or carbon tetrachloride (CCl4). Here, PKC#963 significantly suppressed aspartate aminotransferase (AST), alanine aminotransferase (ALT), phosphorylated signal transducer and activator of transcription 3 (p‐STAT3), inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX‐2) in CCl4‐treated HepG2 cells. Also, PKC#963 significantly suppressed reactive oxygen species (ROS) production in HepG2 cells. Consistently, PKC#963 suppressed the expression of AST, ALT, p‐STAT3, iNOS, COX‐2, interleukin 6 (IL‐6), tumor necrosis factor alpha (TNF‐α) and α‐smooth muscle actin (α‐SMA) and increased procaspase 3 in the liver tissues of CCl4 treated rats. In addition, PKC#963 enhanced alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH) for alcohol metabolism, superoxide dismutase (SOD), and catalase as antioxidant enzymes and also suppressed AST and ALT in alcohol‐treated rats. Furthermore, PKC#963 reduced hepatic steatosis and necrosis in CCl4‐treated rats by H&E (Hematoxylin and Eosin) staining. Taken together, these findings highlight evidence that PKC#963 has hepatoprotective potential via inhibition of iNOS, COX‐2, and p‐STAT3 and enhancement of SOD and catalase.
Funding Information
  • National Research Foundation of Korea (2020R1A2C1004816, 2021R1A2C2003277)

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