TLR2 促进大鼠肾缺血再灌注损伤中的炎症反应和氧化应激.

Objective: To explore the effects of renal ischemia-reperfusion injury (RIRI) on the TLR2 signaling pathway and the role of TLR2 in RIRI. Methods: Twenty-one Wistar rats were randomly divided into sham operation group (Sham), renal ischemia reperfusion model group (I/R) and T2.5 treatment group (T2.5). After 24 hours of ischemia-reperfusion, heart blood and left kidney tissue were collected. Pathological analysis of renal tissue was observed, and serum creatinine (Cr) and blood urea nitrogen (BUN) were detected by kit. Inflammation and oxidative stress of renal tissue were detected by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Results: Compared with the sham group, the renal tissue of the model group showed obvious damage, and the renal structure of the T2.5 group performed well, the difference was statistically significant (P<0.05). Compared with the sham group, the Serum Cr and BUN levels significantly increased in the I/R group, while T2.5 inhibited that increase of serum Cr and BUN and reduced renal damage of I/R rats (P<0.05). Compared with the sham group, the relative expression of TLR2 and TLR4 significantly increased in the renal tissue of the I/R group, while T2.5 regulated TLR signaling pathway by inhibiting that increase of TLR2, TLR4 in injured renal tissue (P<0.05). Compared with the sham group, the expression of NF-kB and its phosphorylation both significantly increased in the I/R group (P<0.05). T2.5 significantly down-regulated the phosphorylation of NF-kB in I/R rats (P<0.05), while had no significant effect on NF-kB expression (P>0.05). Compared with the sham group, the concentrations of pro-inflammatory factors IL-6, IL-1β and TNF-α significantly increased in the renal tissue of I/R group(P<0.05). T2.5 can promote the inflammation of I/R rats by down-regulating IL-6 and IL-β levels (P<0.05), while had no significant effect on TNF-α level (P>0.05). Compared with the sham group, the SOD activity significantly de- Creased in the I/R group, T2.5 significantly reversed this decreasing by up regulating SOD activity(P<0.05). MDA activity in the I/R group was significantly increased than sham group (P<0.05), while T2.5 had no significant effect on MDA activity in I/R rats (P>0.05). Conclusion: TLR2 promotes inflammatory response and oxidative stress in ischemia-re perfusion injury by activating TLR signaling pathway, up-regulating the phosphorylation of NF-kB, further regulating the release of pro-inflammatory factor and activity of antioxidant enzymes. [ABSTRACT FROM AUTHOR]