Objective To investigate the effect of asiaticoside(ASI)on inflammatory response in diabetic nephropathy(DN)rats by regulating Janus kinase(JAK)/signal transducer and activator of transcription(STAT)signaling pathway.Methods Six SD rats were randomly selected as the control group(NC group),and the remaining rats were used to construct a DN rat model using streptozotocin(STZ).The successfully modeled rats were randomly divided into DN group,ASI group(45 mg/kg),JAK2/STAT3 signaling pathway activator Coumermycin A1(C-A1)group(100 µg/kg),and ASI+C-A1 group(45 mg/kg ASI+100 μg/kg C-A1).The NC group and DN group were given the same amount of physiological saline once a day for two consecutive weeks.At 12h after drug treatment,the levels of creatinine,albumin,and urea were measured by automated biochemical analyzer.The levels of serum interleukin-1 β(IL-1 β),interleukin-6(IL-6),tumor necrosis factor(TNF)-α,malondialdehyde(MDA),and superoxide dismutase(SOD)were detected by ELISA method.Pathological changes in renal tissue were detected by HE staining.The renal cell apoptosis was detected by TUNEL staining.The expression of JAK2/STAT3 pathway proteins was detected by Western blot.Results Compared with the NC group,the DN group exhibited symptoms such as glomerular atrophy,severe hyperplasia of glomerular thylakoids,separation of renal tubular epithelial,exposure of basement membrane,inflammatory cell infiltration,and interstitial edema.Compared with NC group,the levels of IL-1β,IL-6,TNF-α,MDA levels,creatinine,albumin,urea,cell apoptosis rate,p-JAK2/JAK2,p-STAT3/STAT3 protein in the DN group were significantly higher than those in NC group(P＜0.05),and the SOD level was significantly lower than that in NC group(P＜0.05).Compared with the DN group,the renal tissue lesions,inflammatory cell infiltration,IL-1β,IL-6,TNF-α,creatinine,albumin,urea,MDA,cell apoptosis rate,p-JAK2/JAK2,p-STAT3/STAT3 protein levels decreased in the ASI group,and the SOD level increased in the ASI group(P＜0.05).C-A1 attenuated the improvement effect of ASI on inflammatory damage in DN rats.Conclusion ASI may inhibit inflammatory response in DN rats by down-regulating the JAK2/STAT3 signaling pathway.
维普
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