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

In pressure-overload-induced cardiac hypertrophy, berberine inhibited the mTOR, p38, and ERK1/2 MAPK signaling pathways to enhance autophagy, consequently attenuating left ventricular remodeling and cardiomyocyte apoptosis (Li MH et al. 2014 ). However, excessive autophagy activity can also cause cell death, termed 'autophagic cell death', also known as type-II programed cell death ). It has been reported that berberine could reduce excessive autophagy by suppressing autophagy-related proteins, such as LC3-II, SIRT1, BNIP3 and Beclin-1, thus protecting H9c2 cells from hypoxia/reoxygenization (HR)-induced cell death (Huang et al. 2015) . In non-ischemic areas of diabetic animal hearts, berberine increased myocardial glucose uptake, glycolysis, and fatty acid oxidation ). The observation that berberine could act as an M2 muscarinic agonist, which reduced the spontaneous contraction rate of cardiomyocytes in culture might contribute to our understanding of berberine's complex actions on the heart (Salehi and Filtz 2011) .