Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 15, No. 5, 2016, pp. 981-988
Bioline Code: pr16131
Full paper language: English
Document type: Research Article
Document available free of charge
Tropical Journal of Pharmaceutical Research, Vol. 15, No. 5, 2016, pp. 981-988
© Copyright 2016 - Tropical Journal of Pharmaceutical Research
Anti-apoptotic effects of phyllanthin against alcoholinduced liver cell death|
Sukketsiri, Wanida; Sawangjaroen, Kitja & Tanasawet, Supita
Purpose: To evaluate the anti-apoptotic effect of phyllanthin on alcohol-induced liver cell death in HepG2 cells alone and in co-culture with human monocytic (THP-1) differentiated macrophage cells.
Methods: Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The cells were pretreated with 1, 5 and 10 μM phyllanthin for 24 h followed by 1300 mM alcohol for HepG2 cells and 2000 mM alcohol for the co-cultured cells. Thereafter, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP) changes, apoptotic cell death and caspase-3/7 activities were assessed.
Results: Alcohol exposure significantly increased intracellular ROS generation (p < 0.001), decreased MMP changes (p < 0.001), increased the number of apoptotic and necrotic cells (p < 0.001) and also induced higher caspase-3/7 activity (p < 0.001) in the co-culture with THP-1 differentiated macrophage cells than in HepG2 cells alone. Pretreatment of HepG2 cells and co-cultured cells with phyllanthin for 24 h prior to alcohol exposure significantly decreased intracellular production of ROS (p < 0.001) and also increased the change in MMP (p < 0.001) as well as caused a decrease in the number of apoptotic and necrotic cells (p < 0.001), but inhibited caspase-3/7 activity (p < 0.001).
Conclusion: The results indicate that phyllanthin treatment may have a significant therapeutic effect on alcohol-related liver diseases.
Hepatoprotective; Human monocytic cells; Apoptosis; Mitochondrial membrane potential; Liver diseases; Reactive oxygen species; Co-culture
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