Cryptotanshinone

Cryptotanshinone9(CT), the major tanshinone isolated from Salvia miltiorrhiza Bunge, can suppress Bcl-2 expression and augment Fas sensitivity in DU145 cells, and JNK and p38 MAPK act upstream of Bcl-2 expression in Fas-treated DU145 cells; CT significantly blocks activation of these kinases and sensitizes several tumor cells to a broad range of anti-cancer agents; suggests that CT has therapeutic potential in the treatment of human prostate cancer.^[1]

Cryptotanshinone has an inhibitory effect on MMP-9 production and migration of human aortic smooth muscle cells treated with TNF-alpha in a dose-dependent manner, suggests that CT has anti-atherosclerosis and anti-neointimal formation activity.^[2]

Cryptotanshinone enhances TNF-α-induced apoptosis in chronic myeloid leukemia KBM-5 cells, in comparison with the treatment with either drug alone, the treatment with cryptotanshinone further suppressed TNF-α-mediated expression of c-FLIP.^[3]

Cryptotanshinone as an AR inhibitor to suppress androgen/AR-mediated cell growth and PSA expression by blocking AR dimerization and the AR-coregulator complex formation; and CT effectively inhibits CWR22Rv1 cell growth and expressions of AR target genes in the xenograft animal model; the previously un-described mechanisms of CT may explain how CT inhibits the growth of prostate cancer (PCa)cells and help us to establish new therapeutic concepts for the treatment of PCa.^[4]

Cryptotanshinone induces ER stress-mediated apoptosis in HepG2 and MCF7 cells , also evidences sensitizing effects to a broad range of anti-cancer agents including Fas/Apo-1, TNF-α, cisplatin, etoposide or 5-FU through inducing ER stress, highlighting the therapeutic potential in the treatment of human hepatoma and breast cancer.^[5]

Cryptotanshinone protects primary cortical neurons from -induced neurotoxicity through the activation of /pathway, such neuroprotective effects may be of interest in AD and other .^[6]

Cryptotanshinone can inhibits cyclooxygenase-2 enzyme activity.^[7]

[1] Park I J, Kim M J, Park O J, et al. Cancer Lett, 2010, 298(1):88-98.

[2] Suh S J, Jin U H, Choi H J, et al. Biochem Pharmacol 2007, 72(12):1680-9.

[3] Kim J H, Jeong S J, Kwon T R, et al. Apoptosis, 2011, 16(7):696-707.

[4] Xu D, Lin T H, Li S, et al. Cancer Lett, 2012, 316(1):11-22.

[5] Park I J, Kim M J, Park O J, et al. Apoptosis An Int J on Programmed Cell Death, 2012, 17(3):248-57.

[6] Zhang F, Zheng W, Pi R, et al. Exp Brain Res, 2008, 193(1):109-18.

[7] Jin D Z, Yin L L, Ji X Q, et al. Eur J Pharmacol, 2006, 549(1–3):166-72.

[8] Xiao-Li L I, Xiao-Rong L I, Wang L J, et al. Chinese Trad Patent Med, 2008, 30(1):77-80.