Baicalin attenuates aflatoxin B1-induced hepatotoxicity via suppressing c-Jun-N-terminal kinase-mediated cell apoptosis

Aflatoxin B₁ (AFB₁) is classified as a Class I carcinogen and common pollutant in human and animal food products. Prolonged exposure to AFB₁ can induce hepatocyte Apoptosis and lead to hepatotoxicity. Therefore, preventing AFB₁-induced hepatotoxicity remains a critical issue and is of great significance. Baicalin, a polyphenolic compound derived from Scutellaria baicalensis Georgi, has a variety of pharmacodynamic activities, such as antiapoptotic and Anticancer activities. This study systematically investigated the alleviating effect of baicalin on AFB₁-induced hepatotoxicity from the perspective of Apoptosis and explored the possible molecular mechanism. In the normal human liver cell line L02, baicalin treatment significantly inhibited AFB₁-induced c-Jun-N-terminal Kinase (JNK) activation and cell Apoptosis. In addition, the in vitro mechanism study demonstrated that baicalin alleviates AFB₁-induced hepatocyte Apoptosis through suppressing the translocation of phosphorylated JNK to the nucleus and decreasing the phosphorylated c-Jun/c-Jun ratio and the Bax/Bcl2 ratio. Molecular docking and drug affinity responsive target stability assays demonstrated that baicalin has the potential to target JNK. This study provides a basis for the therapeutic effect of baicalin on hepatocyte Apoptosis caused by AFB₁, indicating that the development of baicalin and JNK pathway inhibitors has broad application prospects in the prevention of hepatotoxicity, especially hepatocyte Apoptosis.

Aflatoxin B1; Apoptosis; Baicalin; Hepatotoxicity; c-Jun-N-terminal Kinase.