Andrographolide Inhibits Proliferation Of Human Lung Cancer Cells And The Related Mechanisms

This study is to determine effect of Andrographolide (AD) on the growth of the non-small cell lung cancer cell line H3255. Expression of vascular endothelial growth factor (VEGF), transforming growth factor beta 1 (TGF-beta 1), and the activity of protein kinase C (PKC) were also detected. The H3255 cells were treated with 1.0, 2.5, or 5.0 mu M AD for 24 h. MTT assay was performed to examine cell viability. Levels of VEGF and TGF-beta 1 were detected by ELISA. The ATPase activity and PKC activity were tested. AD treatments decreased cell viability via a concentration-dependent manner, leading to decreases in the Na+-K+-ATPase activities (P < 0.05). AD also increased levels of the DNA fragmentation and releasing of lactate dehydrogenase. AD also reduced VEGF and TGF-beta 1 levels, and inhibited protein kinase C activities in H3255 cells (P < 0.05). AD inhibits proliferation of lung cancer cells via a concentration-dependent manner by a mechanism related to reducing levels of VEGF and TGF-beta 1. Thus, AD might be a potent anti-lung cancer agent.