Investigating the Antioxidant Effect of Deoxyschizandin in Doxorubicin-induced Hepatotoxicity: Role of PTEN Signaling Modulation

Abstract

Background: The hepatotoxicity of doxorubicin (DOX) is one of its main toxic side effects that cannot be ignored. As an important initiating factor for hepatocyte apoptosis and necrosis, oxidative stress is crucial in DOX-induced hepatotoxicity. Deoxyschizandin (Deo) is a highly effective antioxidant flavonoid that has potential therapeutic potential in liver diseases. Objectives: It is of great clinical significance to demonstrate that Deo can effectively treat DOX-related hepatotoxicity. Materials and methods: The hepatotoxicity animal model was established by DOX, and Deo was used for intervention to observe the therapeutic effect. At the cellular level, phosphatase and tensin homolog deleted on chromosome ten (PTEN) is used as a therapeutic target for Deo to explore its impact on oxidative stress in hepatocytes. Results: Liver function damage and oxidative stress successfully appear in animal bodies. Specific manifestations include biomarkers of liver function damage, abnormal biomarkers of oxidative stress, and excessive production of reactive oxygen species (ROS) in hepatocytes. PTEN signaling plays an important role in Deo’s inhibition of oxidative stress. Conclusion: Our studies indicate that Deo improved DOX-induced liver oxidative stress, whose mechanisms may be related to PTEN signaling.