Chrysophanol

Description :

Anti-Inflammatory activity of chrysophanol through the suppression of NF-kappaB/caspase-1 activation in vitro and in vivo.[Pubmed: 20877234 ]Chrysophanol induces necrosis through the production of ROS and alteration of ATP levels in J5 human liver cancer cells.[Pubmed: 20169580 ]Mol Nutr Food Res. 2010 Jul;54(7):967-76. Anthraquinone compounds have been shown to induce apoptosis in different cancer cell types. Effects of Chrysophanol, an anthraquinone compound, on cancer cell death have not been well studied. METHODS AND RESULTS: The goal of this study was to examine if Chrysophanol had cytotoxic effects and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell death was induced by Chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption. Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect cells against Chrysophanol-induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (DeltaPsi(m)) were also determined to assess the effects of Chrysophanol. However, reductions in adenosine triphosphate levels and increases in lactate dehydrogenase activity indicated that Chrysophanol stimulated necrotic cell death. CONCLUSIONS: In summary, human liver cancer cells treated with Chrysophanol exhibited a cellular pattern associated with necrosis and not apoptosis. Molecules. 2010 Sep 16;15(9):6436-51. Chrysophanol is a member of the anthraquinone family and has multiple pharmacological effects, but the exact mechanism of the anti-inflammatory effects of Chrysophanol has yet to be thoroughly elucidated. In this study, we attempted to determine the effects of Chrysophanol on dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced inflammatory responses in mouse peritoneal macrophages. The findings of this study demonstrated that Chrysophanol effectively attenuated overall clinical scores as well as various pathological markers of colitis. Additionally, Chrysophanol inhibited the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and the expression of cyclooxygenase (COX)-2 levels induced by LPS. We showed that this anti-inflammatory effect of Chrysophanol is through suppression of the activation of NF-kappaB and caspase-1 in LPS-stimulated macrophages. These results provide novel insights into the pharmacological actions of Chrysophanol as a potential molecule for use in the treatment of inflammatory diseases.