| Manchurian dutchmanspipe stem can cause serious injuries of renal tubules, and renal failure in human. The harm to kidneys has been observed and many investigations have proceeded. There are experimental proof that Manchurian dutchmanspipe stem mainly causes interstitial fibrosis in renal tubules. The machanism is not very clear. Depierreux etal foud that the patients with aristolo-chic acid nephropathy (AAN) had dramatical lesion in small arteries, such as thickened walls and constricted cava. The lesion causes ischemia and interstitial fibrosis of the kidneys. Chen Yipu etal thout that aristolochic acid accumulated in epithelial cells of renal tubules, persistantly stimulating and poisoning the cells. The results were the activation, transdifferentiation and necrosis of the cells. Stimulated by all kinds of cytokines, the fibroblast cells in the interstitial synthesized and exreted many extracellular matrix ( ECM) , which caused interstitial fibrosis. At present, the therapy is in studies. The main contains of folium ginkgo are bitter intralipid, omniflavone. The bitter intralipid is a specif!tial antagonist of platelet activating factor ( PAF) receptor. Many animal experiments conformed that the antagonist of PAF could therapy the ischemic renal injuries by the alteration of renal hemodynamics. The flavone could obviously clean-hy-droxy free radicals. In vitro experiments conformed that flavone could inhibit the activity of angiotensin converting enzyme( ACE). In vivo experiments conformed flavone obviously inhibited endothelin (ET) after injected in rats'abdomy. The effects of expanding vessels was not inhibited by all kinds of antagonist of neuro-transmitters or hormome receptor. Moreover, folium ginkgo reduces the proliferating cell nuclear antigen (PCNA + ) in the renal tubules and renal interstitial and decrease the level of interstitial fibrosis. Hormone can inhibit the releation of inflammatory mediators, such as cytokines, adhesivemolecules, chemotactic factor, etal. Besides that, it can block the activation of inflammatory cells and reduce the inflammatory reaction. As the carrier of Prostaglandin E1 ( PGE, ) , PGE1 can alter the renal blood flow ( RBF) , inhibiting the proliferation of intrinsic cells in glomerulus and the accumulation of extracellular matrix. The purpose of this experiment is to find out the function of the folium ginkgo and Prostaglandin E1 ( PGE1) to the aristolochic acid nephropathy ( AAN) and the mechanism.Materials and Methods1. Materials1. 1 Animal ; 35 female Wistar rats whose body weight are from 200 to 250g are divided into four groups , the control group has 5 rats; each of non -therapy and therapy (1) (2)group has 10 rats. AAN groups and therapy groups (1) (2) contrast groups.1.2 Major reagent and physic: Manchurian Dutchman pipe Ginkgo leaf Prostaglandin E1TGF- CTGF FN test kits.1.3 Apparatus: light microscope image analyzer spectro-light meter cen-trifugation machine.2. Methods2. 1 Biochemical detectionSulfosalicylic acid-natrium sulfuricum turbidimetry is used to detect urine protein 24h; hemoglobin is detected by light-electricity chromatometry; BUN and Scr is detected with auto-biochemical-instrument.2.2 Pathology detectionwith cut paraffin sample into 3 m slide, which are stained with HE moth-od.2. 3 Immunohistochemical staining is performed by peroxidase-labeled stretavidin-biotin technique to detect TGF CTGF and FN on renal tissue .2.4 StatisticsQuantity data is appeared as X S, analyse the variance with F - test and T -test,linear regression is used to correlative analysis. Above all are performed with SPSS10.0 software,the difference is significant if p <0. 05.ResultAfter three months mean Hb level was found significantly lower in MD group than in FG group and PGE, group (p <0. 05) ; Mean urinary protein excretion level was found significantly higher in MD group than in FG group and PGE1 group , Mean BUN and Scr level was found significantly higher in MD group than in FG grop and PGE1 grop.
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