Hepatoprotective properties of kombucha tea against TBHP-induced oxidative stress via suppression of mitochondria dependent apoptosis
Authors:
Semantee Bhattacharya, Ratan Gachhui, Parames C Sil
Abstract:
Kombucha, a fermented tea (KT), is claimed to possess many beneficial properties. Recent studies have suggested that KT prevents paracetamol and carbon tetrachloride-induced hepatotoxicity. We investigated the beneficial role of KT was against tertiary butyl hydroperoxide (TBHP) induced cytotoxicity and cell death in murine hepatocytes. TBHP is a well known reactive oxygen species (ROS) inducer, and it induces oxidative stress in organ pathophysiology. In our experiments, TBHP caused a reduction in cell viability, enhanced the membrane leakage, and disturbed the intra-cellular antioxidant machinery while simultaneous treatment of the cells with KT and this ROS inducer maintained membrane integrity and prevented the alterations in the cellular antioxidant status. These findings led us to explore the detailed molecular mechanisms involved in the protective effect of KT. TBHP introduced apoptosis as the primary phenomena of cell death, as evidenced by flow cytometric analyses. In addition, ROS generation, changes in the mitochondrial membrane potential, cytochrome c release, activation of caspases (3 and 9), and Apaf-1 were detected confirming involvement of mitochondrial pathway in this pathophysiology. Simultaneous treatment of KT with TBHP, on the other hand, protected the cells against oxidative injury and maintained their normal physiology. In conclusion, KT was found to modulate the oxidative stress-induced apoptosis in murine hepatocytes, probably due to its antioxidant activity and functioning via mitochondria dependent pathways and could be beneficial against liver diseases, where oxidative stress is known to play a crucial role.
Keywords: tertiary butyl hydroperoxide, reactive oxygen species, murine hepatocytes, cyto-toxicity and apoptosis, kombucha tea, antioxidant and cytoprotection
Country: India
Citation: Pathophysiology. Jun;18(3):221-34
Study Mailing Address:
Department of Life Sciences & Biotechnology, Jadavpur
University, 188 Raja S C Mullick Road, Kolkata 700032, India.
Date Updated: March 9, 2020