Emine Mamal, Murat Basar, Hafize Uzun and Ismail Seckin
Background: Nitric oxide (NO), synthesis from L-arginine by Nitric oxide synthesizes (NOS) at kidney mesangial cells and involved in functional kidney defects such as acute kidney failure, inflammatory nephritis, diabetic nephropathy. CAPE (Caffeic acid phenethyl ester) is natural antioxidant which has anti-inflammatory, anti-tumor affects. In this study we investigated effects of NO on rat kidney and therapeutic and protective effects of CAPE. Methods: We used albino Wistar rats, weigh 150-200. Our experimental groups: 1) Control 2) L-arginine-given group 3) Preventative group (L-arginine and CAPE administered together) 4) Therapeutic group (after L-arginine administration; CAPE administered 7 days) (n=10/per group). Kidney tissues harvested and cortex region divided into two in order to perform western blot and immunohistochemistry. p38MAPK and active caspase-3 levels investigated with western blot and we performed p38MAPK immunohistochemistry. Differences between groups were calculated by means of one-way ANOVA and p<0.05 were considered to be statistically significant. Results: In L-arginine applied group p38MAPK level increased significantly, when compared to control and preventative group (p<0.001). On the other hand there were no statistical significance between control and preventative group (p<0.057). Additionally p38MAPK level increased in therapeutic group compared to control and preventative group (p<0.001). Moreover, in L-arginine-given group active caspase-3 level significantly increased compared to control and preventative group (p<0.05). However, active caspase-3 level in preventative group significantly decreased compared to therapeutic group (p<0.05). Conclusions: These results suggest that excess NO generation activates p38MAPK signaling pathway and triggers apoptosis in the kidney mesangial cells. Additionally, CAPE inhibits L-arginine’s effect and prevents mesangial cell apoptosis.
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