Mechanism of capsaicin in the growth inhbition toyeast cells:
Of course, over time the capsaicin will dissipate on its own.
shows that administration of TOFA 1 h prior to treatment of HepG2 cells with 0.5 mM capsaicin for 12 h completely blocked the generation of ROS from approximately 260% back to 100% of the control. Deprivation of fatty acid alone following TOFA administration failed to increase ROS production. Thus, we suggest that accumulation of malonyl-CoA following FASN inhibition by capsaicin might be able to cause ROS generation, correlating with mitochondrial impairment and apoptosis induction in HepG2 cells.
T1 - The site of action of capsaicin on the guinea-pig isolated ileum
This study evaluated the selective impact of capsaicin on apoptotic induction mediated by FASN inhibition on HepG2 cells but not on normal human hepatocytes. We used normal human hepatocytes to represent control cells which have low FASN expression and enzymatic activities. The present finding is consistent with previous studies that showed that normal hepatocytes were characterized by a 5-fold lower FASN protein expression (data not shown), lower fatty acid, and triglyceride synthesis than HepG2 cells, as shown in . Previous studies have shown that FASN expression and its activity in normal cells are many times lower than that in cancer cells . Hepatocytes treated with 0.5 mM of capsaicin for 3 h had a comparable level of FASN protein expression and enzymatic activities to the control group. Furthermore, hepatocytes treated with 0.5 mM capsaicin for 6 h did not show any changes of mitochondrial integrity as shown in . These findings clearly suggest that capsaicin inducing FASN inhibition and enzymatic activities leading to induction apoptosis is selective in HepG2 cells but not in normal human hepatocytes. Thus, it affirms that FASN would be a potential target for anti-cancer therapy of capsaicin.