Objective:To explore the influence of rhein on TLR4/NF-κB signaling pathway in IgA nephro-pathy rat models.Methods:All 75 SPF-grade healthy male SD rats were selected and randomized into 15 rats in the control group and 60 ones in the modeling group.The modeling group adopted combined immunisation of bovine serum albumin+lipopolysaccharide+castor oil+carbon tetrachloride to eastablish IgA nephropathy models,the control group was treated with equivalent amounts of 0.9% Nacl in the same manner for the same period of time.After successfully modelling,the rats were randomized into the model group,low and high doses groups of rhein,and telmisartan group with 14 ones in each group.0.5% sodium carboxymethylcellulose was given to the model group and the control group respectively;5 mg/mL and 10 mg/mL rhein suspensions were administered to low and high doses groups of rhein;and telmisartan group received 0.83 mg/mL telmisartan.The intragastric dose was 10 mL/kg for different groups,once each day,for eight weeks consecutively.To detect and compare the levels of 24 h UTP,SCr and BUN,mean optical density of IgA expression in renal tissue,Katafuchi score of renal histopathologic injury,as well as the expressions of TLR4,NF-κB p65,MCP-1 and TGF-β1 in renal tissue in different groups.Results:Compared with the model group,the levels of 24 h UTP,SCr and BUN,mean optical density of IgA expression in renal tissue,Katafuchi score of renal histopathologic injury,as well as the expressions of TLR4,NF-κB p65,MCP-1 and TGF-β1 in renal tissue were lower in low and high doses groups of rhein,and telmisartan group,and the difference had statistical meaning(P<0.05),and rhein intervention groups presented a certain dose-effect relationship.Conclusion:Rhein could apparently improve renal function in IgA nephropathy rats,reduce IgA deposition in renal tissue and relieve pathological injury,the higher the dose of the medicine was,the better the effects were,and its mechanism might be related to inhibiting the activity of TLR4/NF-κB signaling pathway.
IgA nephropathyrheinfibrosisTLR4/NF-κB signaling pathwayratzoopery