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Anti-glycative effects of asiatic acid in human keratinocyte cells.

Wang ZH - Biomedicine (Taipei) (2014)

Bottom Line: Yet AA pretreatments decreased these oxidative and inflammatory factors, dose-dependently lowering nitric oxide synthase activity and expression.AA pretreatments at 2-8 μM decreased activity and expression of these two caspases.AA pretreatments at 2-8 μM maintained collagen I expression, and reduced three MMPs expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Effects of AA on activity of (a) GPX and NOS, and protein expression (b) GPX and iNOS in HaCaT cells pretreated by AA at 1, 2, 4 or 8 μM for 36 hr, followed by exposure to 100 μg/ml AGE-BSA for 24 hr. Cells containing neither AA n orAGE-BSA (AGE) as control. Data mean±SD (n=10). a-fMeans among bars without common letter differ, P<0.05.
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Fig3: Effects of AA on activity of (a) GPX and NOS, and protein expression (b) GPX and iNOS in HaCaT cells pretreated by AA at 1, 2, 4 or 8 μM for 36 hr, followed by exposure to 100 μg/ml AGE-BSA for 24 hr. Cells containing neither AA n orAGE-BSA (AGE) as control. Data mean±SD (n=10). a-fMeans among bars without common letter differ, P<0.05.

Mentions: Treatments of 8 μM AA alone in HaCaT cells (without AGE-BSA exposure) did not affect any measurement when compared to controls (P>0.05). Figure 2 plots AGE-BSA exposure reducing 50% viability; AA pretreatments dose-dependently enhanced viability (P<0.05). AGE-BSA exposure lowered GSH content 52%, raising ROS, NO and protein carbonyl levels 8.4, 8.5, and 18.3 fold, respectively (Table 1, P<0.05). Pretreatment with AA retained 21-85% GSH content, lowering ROS, NO, and protein carbonyl 18-72%, 17-76%, and 15-70%, respectively; dose-dependent manner was evident in decreasing ROS, NO and protein carbonyl levels (P<0.05). AGE-BSA lowered GPX activity 54% and protein expression 61%, yet enhanced NOS activity 5.2 fold and iNOS expression 5.5 fold (Figure 3). AA pretreatments dose-dependently retained GPX activity and expression (P<0.05). AA at 8 μM meant GPX activity and protein expression similar to that of controls (P>0.05). Pretreatments also decreased NOS activity 13-55% and iNOS expression 19-68% (P<0.05). AGE-BSA increased IL-1beta 6.4 fold, IL-67.3 fold, and TNF-alpha release6.1 fold in HaCaT cells (Table 2, P<0.05). AA pretreatments at 2-8 μM lowered IL-1beta, IL-6, and TNF-alpha formation (P<0.05).


Anti-glycative effects of asiatic acid in human keratinocyte cells.

Wang ZH - Biomedicine (Taipei) (2014)

Effects of AA on activity of (a) GPX and NOS, and protein expression (b) GPX and iNOS in HaCaT cells pretreated by AA at 1, 2, 4 or 8 μM for 36 hr, followed by exposure to 100 μg/ml AGE-BSA for 24 hr. Cells containing neither AA n orAGE-BSA (AGE) as control. Data mean±SD (n=10). a-fMeans among bars without common letter differ, P<0.05.
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Related In: Results  -  Collection

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Fig3: Effects of AA on activity of (a) GPX and NOS, and protein expression (b) GPX and iNOS in HaCaT cells pretreated by AA at 1, 2, 4 or 8 μM for 36 hr, followed by exposure to 100 μg/ml AGE-BSA for 24 hr. Cells containing neither AA n orAGE-BSA (AGE) as control. Data mean±SD (n=10). a-fMeans among bars without common letter differ, P<0.05.
Mentions: Treatments of 8 μM AA alone in HaCaT cells (without AGE-BSA exposure) did not affect any measurement when compared to controls (P>0.05). Figure 2 plots AGE-BSA exposure reducing 50% viability; AA pretreatments dose-dependently enhanced viability (P<0.05). AGE-BSA exposure lowered GSH content 52%, raising ROS, NO and protein carbonyl levels 8.4, 8.5, and 18.3 fold, respectively (Table 1, P<0.05). Pretreatment with AA retained 21-85% GSH content, lowering ROS, NO, and protein carbonyl 18-72%, 17-76%, and 15-70%, respectively; dose-dependent manner was evident in decreasing ROS, NO and protein carbonyl levels (P<0.05). AGE-BSA lowered GPX activity 54% and protein expression 61%, yet enhanced NOS activity 5.2 fold and iNOS expression 5.5 fold (Figure 3). AA pretreatments dose-dependently retained GPX activity and expression (P<0.05). AA at 8 μM meant GPX activity and protein expression similar to that of controls (P>0.05). Pretreatments also decreased NOS activity 13-55% and iNOS expression 19-68% (P<0.05). AGE-BSA increased IL-1beta 6.4 fold, IL-67.3 fold, and TNF-alpha release6.1 fold in HaCaT cells (Table 2, P<0.05). AA pretreatments at 2-8 μM lowered IL-1beta, IL-6, and TNF-alpha formation (P<0.05).

Bottom Line: Yet AA pretreatments decreased these oxidative and inflammatory factors, dose-dependently lowering nitric oxide synthase activity and expression.AA pretreatments at 2-8 μM decreased activity and expression of these two caspases.AA pretreatments at 2-8 μM maintained collagen I expression, and reduced three MMPs expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus