| Objective:Chronic ischemic renal disease is one of the most important reasons leading to end-stage renal disease , but its pathogenesis is still a lack in depth .Studies have shown that the renin - angiotensin system activation, renal tubular interstitial infiltration of inflammatory cells, renal intrinsic cells transdifferentiation to myofibroblasts, may have effects on the progress of chronic ischemic nephropathy .PNS was mainly active ingredient extracted from traditional herb Panax notoginseng ,which had many biological effects including the strong role of inhibiting mesenchymal cells and improving renal microcirculation ,and may play an important role in the clinical treatment of renal disease. The main purpose of this study was to explore the mechanism of chronic ischemic renal injury, and to observe the PNS'effects on the prevention and treatment of chronic ischemic nephropathy and these may provide some theoretical basis the application of PNS for clinical prevention and treatment of chronic kidney disease.Methods: All forty-eight male healty SD rats were randomly divided into sham-operation group, model group, and PNS group, every group has sixteen rats. The bilateral renal arteries were partly ligated to establish rat model with bilateral renal artery stenosis, Rats of PNS group we start to give the PNS 50mg.kg-1.d-1 by intra-abdominal injection after operation, the other groups′rats are given sterile water for injection 50mg.kg-1.d-1. On the 14th day, 28th, 45th and 60th day, we detected serum ICAM-1 by ELISA ,measuring plasma AngⅡby radioimmunoassay,observing pathological changes in rat kidneys using HE,/Masson staining and observed the change of expression of tubulointerstitialα-smooth muscle actin ,parallelly semi-quantitative analysis.Results: At the same time point, levels of serum ICAM-1 and plasma AngⅡlevels of model group group were significantly higher compared with sham-operated group (P <0.01), and the serum ICAM-1 and plasma AngⅡgradually increased with the extension of ischemic time in model group (P <0.05); A large number of Shrinkage and expansion of tubular ,renal tubular epithelial cell necrosis, renal interstitial widened, inflammatory cell infiltration and renal interstitial fibrosis were observed by HE and Masson staining. Immunohistochemistry results showed that,α-SMA expressed in part of the damaged renal tubular epithelial cells in model group 14 days later, a small amount ofα-SMA also expressed in renal interstitia after 28 days, and the amount of expression in tubular - interstitial cells gradually increased with the extension of ischemic time;Yet we found no significant changes in renal pathology and noα-SMA expression in sham operation group at any time point.,The serum ICAM-1 and plasma AngⅡlevels decreased significantly compared with model group after treatment of PNS. (P <0.05), and the renal pathological changes and expression ofα-SMA in renal tubular - interstitial cells were similar to the model group, however the extent of renal pathological changes and the amout ofα-SMA expression were lighter than the model group at the same point.Conclusions:In the cases of chronic renal ischemia, the expression ofα-SMA (Myo-FB the transdifferentiation from renal intrinsic cells expressα-SMA ), renin - angiotensin system activation and the increasing expression of ICMA-1 may speed up the process chronic ischemic renal injury . PNS could inhibit the related links, and postpone the development of renal interstitial fibrosis and protect the kidney. |
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