二氢丹参酮

Dihydroisotanshinone I can inhibit the migration of both androgen-dependent and androgen-independent prostate cancer cells. Dihydroisotanshinone diminishes the ability of prostate cancer cells to recruit macrophages and reduces the secretion of chemokine (C-C motif) ligand 2 (CCL2) from both macrophages and prostate cancer cells in a dose-dependent manner. It inhibits the protein expression of p-STAT3 and decreases the translocation of STAT3 into nuclear chromatin. It also suppresses the expression of tumor epithelial-mesenchymal transition genes, including RhoA and SNAI1. Pretreating the cells with dihydroisotanshinone I at concentrations ranging from 2.5 μM to 20 μM for 24 hours cause dose-dependent protection against hepatotoxicity induced by menadione. Adding dihydroisotanshinone I to freshly isolated hepatocytes at concentrations between 50 nM to 200 nM inhibit NADH-induced superoxide production dose-dependently.