OBJECTIVE： To observe the effect of pathological lesion of renal tissue in rats with spontaneous hypertension （SHR）， and study its mechanisms based on nuclear factor κB （NF-κB） signaling pathway. METHODS： 21 SHR were randomly divided into model group and ICA low-dose， high-dose groups （20， 40 mg/kg， denoted by ICA-L， ICA-H groups）； other 7 homologous Kyoto rats （WKY） were regarded as control group. All rats were intragastrically administrated， twice a day， for 11 weeks， rats in control group and model group received equal volume of double distilled water， ig. Pathological changes in renal tissue in each group were observed； Western blot method was used to detect protein expressions of p-NF-κB-p65， IκB and TNF-α in renal tissue. RESULTS： Compared with control group， model group showed disorder renal structure， narrow and irregular glomerular cysts； the protein expression of IκB was significantly down-regulated， protein expressions of p-NF-κB-p65 and TNF-α were significantly up-regulated （P＜0.01）. Compared with model group， the above-mentioned changes of rats showed improvement in ICA-L， ICA-H groups； the protein expression of IκB was significantly up-regulated in ICA-L， ICA-H groups （P＜0.05 or P＜0.01）； the protein expressions of p-NF-κB-p65 and TNF-α were significantly down-regulated （P＜0.01） in ICA-H groups； p-NF-κB-p65 protein expression was significantly down-regulated in ICA-L group （P＜0.05）； while there was no significant difference in TNF-α protein expression in ICA-L group （P＞0.05）. CONCLUSIONS： ICA plays a role in improving renal pathological lesion in SHR， and the mechanism may be related to inhibiting NF-κB signaling pathway.