| Background: Ischemic-reperfusion injury (IRI) is a severe complication in kidney transplantation, shock and bypass operation of coronary artery, et al. Recent studies showed that several cytokines causing leukocyte congregation and acute stage reaction have important effects on IRI. Some medicines for preventing or curing IRI are related to cytokines. Kidney is the organ which is easy to occur IRI. Almost all renal cells have the ability to produce cytokines, and meanwhile, they are also the targets of the cytokines. Some cytokines are used as the marker for renal acute inflammation. Tumor necrosis factor-a (TNF-a) is produced at sites of local inflammation, TNF-a can make macrophage release interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8) et al. The later cytokines can active macrophage again and induce more IL-1, IL-6, IL-8, TNF-a release. Hence, the interaction of all kinds of cytokines forms the net effect. Anisodamine (654-2), a kind of component extracted from Chinese herbal medicine, has the functions of vessel dilatation, microcirculation improvement, oxyradical resistance et al. It is often used in the therapy on shock and other serious illness. Recent years, researchers indicate that 654-2 has some therapy effects by modulating inflammatory mediators.Objective: To study the changes of TNF-a, IL-8 and IL-6 in kidney and plasma during renal IRI in rats and the effect of 654-2 intervention.Methods: Renal IRI models were made in rats(the right kidney was resected, and the left renal artery was closured by a clip for 1 hour and then was loosened to reperfusion). The concentration of TNF-a, IL-8 and IL-6 were detected by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Using biochemical analyzer, concentration of serum urea nitrogen (SUN) and creatinine (Scr) were detected. The renal coefficient (RC) was calculated: kidney weight/rat body weight.Results: In ischemic group and the group of reperfusion for 1 hour (R1h), concentration of TNF-a and IL-8 increased significantly in kidney (P＜0. 01 or P＜0. 05), with the ongoing of reperfusion, both decreased near to the level of sham operation control group; while the change of IL-8 in serum was converse, it reduced notably in ischemic group and Rlh (P＜0. 01), then raised near to the level of control group after reperfusion for 4 hours (R4h). Concentration of serum TNF-a was no obvious changes in each group. IL-6 in ischemic group was lower than that in control group (P＜0. 01), but in group Rlh, it increased to the level of control group. Concentration of renal IL-6 in group R4h and reperfusion for 24 hours (R24h) were lower than that in group Rlh and control group (P＜0. 05). The changes of IL-6 in kidney and blood were direct correlation in straight line in different periods (r=0. 857, P＜0. 01). With 654-2 preconditioning, the concentration of IL-6 in group R4h and R24h were higher than that in no preconditioning group; meanwhile SUN, Scr as well as RC in group R4h+654-2 were notably higher than that in group R4h; but in group R24h+654-2, Scr was remarkably lower and SUN was no difference compared with no preconditioning group. After 654-2 preconditioning, IL-8 and TNF-a were no significant changes in serum and kidney.Conclusion: This results suggest that TNF-a, IL-8 and IL-6 maybe have important effects on early renal IRI in rats. 654-2 preconditioning could increase the concentration of IL-6 but had no obvious effects on IL-8 and TNF-a. 654-2 preconditioning plays a disadvantage role in early stage of renal IRI. It is interesting that if the earlier damage was correlated with the up regulation of IL-6. With the ongoing of reperfusion, 654-2 begins to exert its cure effect. The dual effects of 654-2 need to be deeply explored. |
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