Abstract
Coptidis Rhizoma is the dried rhizome from the Coptis chinensis Franch. that has been shown to have a number of beneficial pharmacological properties including antioxidant, anti-inflammatory, and anti-cancer effects. However, the anti-cancer effects of Coptidis Rhizoma on hepatocellular carcinoma (HCC) remain unclear. In this study, we investigated the anti-cancer properties of Coptidis Rhizoma ethanol extract (CR) in HCC Hep3B cells and in a xenograft mouse model. Our results showed that the CR significantly inhibited cell growth and induced apoptosis in Hep3B cells through increased expression of Bcl-2 associated x-protein (Bax) and cleavage of poly-ADP ribose polymerase (PARP), reduced expression of Bcl-2, and activated caspases. CR also increased the generation of intracellular reactive oxygen species (ROS), which caused a loss of mitochondrial membrane potential (MMP, ΔΨm) and activation of the mitochondria-mediated intrinsic apoptosis pathway. Moreover, N-acetylcysteine (NAC), a ROS inhibitor, markedly blocked the effects of CR on apoptotic pathways. CR also induced the expression of light chain 3 (LC3)-I/II, a key autophagy regulator, whereas CR-mediated autophagy was significantly suppressed by NAC. In addition, pre-treatment with NAC perfectly attenuated the inhibition of cell invasion and migration of CR-stimulated Hep3B cells. Furthermore, oral administration of CR suppressed Hep3B tumor growth in xenograft mice without toxicity, alterations to body weight, or changes in hematological and biochemical profiles. Taken together, our findings suggest that CR has anti-tumor effects that result from ROS generation, and may be a potential pharmacological intervention for HCC.
Highlights
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and the second leading cause of cancer death [1,2]
To investigate the effect of Coptidis Rhizoma ethanol extract (CR) on Hep3B cell proliferation, the cells were exposed to various concentrations of CR for 24 h and cell viability was measured by a 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay
These results suggest that CR induced apoptosis through the caspase-dependent pathway in Hep3B cells
Summary
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and the second leading cause of cancer death [1,2]. Strategies for the treatment of HCC vary between the early and advanced stages [3]. Despite the variety of therapies available during each stage, HCC patients have a high recurrence rate and most endure serious side effects during treatment [4,5]. Numerous studies have reported that traditional medicines represent potential anti-cancer treatments, and have low toxicity and fewer side effects than current therapies [6,7]. Liu et al [6] noted that alkaloids extracted from certain traditional medicines can treat a variety of cancers including liver cancer, through apoptosis and autophagy induction as well as by inhibiting cell proliferation, migration, and invasion
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