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AIM To review the progress in pharmacological mechanisms of terandrine (Tet) and its therapeutic use indigestive diseases.METHODS We reviewed almost all the papers related to Tet from various magazines published in Englishand Chinese in recent years.RESULTS It has been demonstrated that Tet had multiple bioactivities: ① Tet could act as a Ca2+antagonist via blocking cellular plasma membrane voltage- or receptor-operating Ca2+ channels, inhibiting extracellular Ca2+ entry into the cell and intracellular Ca2+ mobilization to the cytosol, so as to preventhepatocytes, cardiomyocytes, pancreas cells and neurocytes from toxic or ischemia-reperfusion injuries.However, in HL-60 and leukemic T cells, Tet promoted Ca2+ releasing from mitochondria and microsomes,increased the concentration of intracellular Ca2 + , and induced cell death; ② Tet inhibited phobol 12-myristat13-acetate (PMA) plus ionomycin-induced T cell proliferation, interleukin-2 secretion and expression of theT cell activation antigen, CD71. It could also interrupt the integrity of macrophages, and reduced respiratoryburst of neutrophils and macrophages and proinflammatory cytokines secretion through minimizing nucleartranscriptional factor kappa B DNA binding activity; ③ Tet could induce tumor cell apoptosis, and down-regulate P-glucoprotein activity; and ④ Tet has the therapeutic effects on hepatic fibrogenesis, portalhypertension, immunomodulation, etc.CONCLUSION Tet can act as a Ca2 + channel blocker, inhibit proinflammatory factors releasing, modulateimmunoreaction, and induce tumor cell apoptosis. It can be used to prevent hepatocyte injury induced bytoxins and virus, inhibit hepatic fibrogenesis, reduce portal venous pressure, and can be used as an anti-tumor drug as well.