Progress in parmacological mechanisms of terandrine / 中国药理学通报

ABSTRACT

Tetrandrine (Tet) is a bibenzylisoquinoline alkaloid isolated from Stephania tetrandra S Morr. Lots of studies demonstrated that Tet could ① act as a calcium antagonist via blocking plasma membrane voltage- or receptor-operating calcium channels, inhibiting extracellular calcium entry and intracellular calcium mobilization, so it could prevent hepatocytes, cardiomyocytes, pancreas cells and neurocytes from toxic or ischemia-reperfusion injuries. However, in HL-60 and leukamia T cells, Tet promoted calcium releasing from mitochondria or/and microsomes and induced these cells death. ② down-regulate T cell protein kinase C signal transduction pathway, inhibit T cell proliferation, interleukin-2 secretion and expression of the T cell activation antigen. It could also interrupted integrity of macrophages, reduced neutrophiles and macrophages respiratory-bursting and proinflammatory cytokines secretion through minimizing nuclear transcription factor kappa B DNA binding activity. ③ induce tumor cells apoptosis. ④ down-regulate P glucoprotein activity and reverse tumor cells multidrug resistance. ⑤ also inhibit platelet-derived growth factor induced hepaticstellate cells and human lung fibroblast proliferation, down-regulete type Ⅰ and type Ⅲ collagen secretion. In this article, we also reviewed the therapeutic effects of Tet on hepatic fibrosis, pulmonary fibrosis, portal hypertension, pulmonary hypertension, anti-inflammation and anti-tumors.