Anti-glycative effects of asiatic acid in human keratinocyte cells

Background: Human skin keratinocyte (HaCaT) cells served to examine effects of asiatic acid (AA) at 1, 2, 4 and 8 μM against advanced glycative endproduct (AGE)-modified bovine serum albumin (BSA) induced glycative stress. Results: AGE-BSA treatment reduced cell viability; and increased reactive oxygen species, nitric oxide, protein carbonyl, interleukin (IL)-1beta and tumor necrosis factor-alpha levels in HaCaT cells. Yet AA pretreatments decreased these oxidative and inflammatory factors, dose-dependently lowering nitric oxide synthase activity and expression. AGE-BSA raised activity and expression of caspase-3 and caspase-8. AA pretreatments at 2-8 μM decreased activity and expression of these two caspases. AGE-BSA declined collagen I expression, but enhanced matrix metalloproteinase (MMP)-1, MMP-8 and MMP-9 protein expression. AA pretreatments at 2-8 μM maintained collagen I expression, and reduced three MMPs expression. AGE-BSA also up-regulated RAGE (receptor of AGE), p-p38 and p-JNK expression. AA pretreatments at 2-8 μM suppressed RAGE expression, and at 1-8 μM down-regulated p-p38 and p-JNK expression. Conclusion: Asiatic acid, via its anti-glycative activity, could protect skin. Thus, this compound could be developed as an external agent and applied for personalized medicine.