Sivalokanathan Sarveswaran, Vijayababu Marati Radhakrishnan, Balasubramanian Maruthaiveeran Periyasamy
Department of Pharmacology and Environmental Toxicology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600 113, Tamil Nadu, India.
World J Gastroenterol. 2006 Feb 21;12(7):1018-24. doi: 10.3748/wjg.v12.i7.1018.
To investigate the effects of Terminalia arjuna (T. arjuna) extract on human hepatoma cell line (HepG2) and its possible role in induction of apoptosis.
Human hepatoma cells were treated with different concentrations of ethanolic extract of T. arjuna and its cytotoxicity effect was measured by trypan blue exclusion method and lactate dehydrogenase leakage assay. Apoptosis was analyzed by light and fluorescence microscopic methods, and DNA fragmentation. The mechanism of apoptosis was studied with expression of p53 and caspase-3 proteins. Glutathione (GSH) content was also measured in HepG2 cells after T. arjuna treatment.
T. arjuna inhibited the proliferation of HepG2 cells in a concentration-dependent manner. Apoptotic morphology was observed in HepG2 cells treated with T. arjuna at the concentrations of 60 and 100 mg/L. DNA fragmentation, accumulation of p53 and cleavage of procaspase-3 protein were observed in HepG2 cells after the treatment with T. arjuna. The depletion of GSH was observed in HepG2 cells treated with T. arjuna.
T. arjuna induced cytotoxicity in HepG2 cells in vitro. Apoptosis of HepG2 cells may be due to the DNA damage and expression of apoptotic proteins. Depletion of GSH may be involved in the induction of apoptosis of HepG2 cells.
研究阿朱那诃子(Terminalia arjuna)提取物对人肝癌细胞系(HepG2)的影响及其在诱导细胞凋亡中可能发挥的作用。
用不同浓度的阿朱那诃子乙醇提取物处理人肝癌细胞,通过台盼蓝排斥法和乳酸脱氢酶泄漏试验测定其细胞毒性作用。采用光学显微镜和荧光显微镜方法以及DNA片段化分析细胞凋亡情况。通过检测p53和半胱天冬酶 - 3蛋白的表达来研究细胞凋亡的机制。在阿朱那诃子处理后的HepG2细胞中还测定了谷胱甘肽(GSH)含量。
阿朱那诃子以浓度依赖性方式抑制HepG2细胞的增殖。在浓度为60和100 mg/L的阿朱那诃子处理的HepG2细胞中观察到凋亡形态。用阿朱那诃子处理后的HepG2细胞中观察到DNA片段化、p53积累和前半胱天冬酶 - 3蛋白的裂解。在阿朱那诃子处理的HepG2细胞中观察到GSH的消耗。
阿朱那诃子在体外对HepG2细胞具有细胞毒性作用。HepG2细胞的凋亡可能是由于DNA损伤和凋亡蛋白的表达。GSH的消耗可能参与了HepG2细胞凋亡的诱导。