Coptidis Rhizoma: a comprehensive review of its traditional uses, botany, phytochemistry, pharmacology and toxicology

Wang, Jin; Wang, Lin; Lou, Guan-Hua; Zeng, Hai-Rong; Hu, Ju; Huang, Qin-Wan; Peng, Wei; Yang, Xiang-Bo

Berberine induces apoptosis in human colonic carcinoma cell line SW620; in the pancreatic cancer cell lines PANC-1 and MIA-PaCa2; and in breast cancer MCF-7 cells through the generation of ROS. Moreover, berberine had a greater apoptotic effect in PANC-1 cells than gemcitabine (Hsu et al. 2007; Xie et al. 2012; Park et al. 2015) . When compared with chemical drugs (meloxicam and rosiglitazone) and berberine, total alkaloids showed a greater apoptosis-inducing effect (Ke 2007) . Various apoptotic modulating signals are involved the induction of apoptosis by berberine. Berberine could markedly inhibit the expression of survivin in MGC-803gastric cancer cells, in SKOV3ovarian cancer cells Ma et al. 2015) ; and activated caspase-3, caspase-8, caspase-7 and caspase-9 in FaDu head and neck squamous cell carcinoma cells and malignant pleural mesothelioma (Yao 2014; Seo et al. 2015) . Berberine also regulated the activities of Bcl-2 and Bax in colon cancer cells (Chidambara et al. 2012), FoxO1 and FoxO3 in HepG2 cells (Shukla et al. 2014) , and p53 in MCF-7 and MDA-MB231breast cancer cells (Kim et al. 2012) . Additionally, cPLA-COX2 and JAK2/STAT3 signalling was inhibited in liver cancer cells and colon cancer cells HT-29 (Li O et al. 2013; Li C et al. 2014) . Berberine also promoted the Fas/FasL signalling pathway, and then triggered the activation of caspase-8 and caspase-9 precursors to induce apoptosis in human oral cancer cells . In HCT-116 colon cancer cells, berberine enhanced GRP78 activity by binding to and forming complexes with GRP78, which increased the ability of GRP78 to bind to VPS34. This suggested berberine could induce autophagic cancer cell death (La et al. 2017) . In vitro and in vivo experiments showed that coptisine inhibited the proliferation, growth and migration of HCC cells and colorectal cancer cells, and promoted their apoptosis. Other studies showed that coptisine activated microRNA miR-122 (Chai et al. 2018)