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目的:利用基因芯片研究抗纤灵治疗肾小管间质纤维化的机理。方法:将18只SPF级SD大鼠中12只行unilateral ureteral occlusion(UUO)模型,随机分为模型组(UUOG)和抗纤灵组(KXLG),另外6只为假手术组。UUO和假手术组给予生理盐水灌胃;抗纤灵组给予抗纤灵灌胃。所有大鼠均在14天处死留取左肾组织。运用定制芯片检测基因变化结果。结果:与假手术组比较。UUO组TGF-β1、smad2、smad3基因显著上调,和假手术组比较上调超过1.5倍,P<0.01,Smad7基因显著下调,和假手术组比较下调超过1.5倍,P<0.01。而抗纤灵组TGF-β1、smad2、smad3基因显著下调,和UUO组比较下调超过1.5倍,P<0.01,Smad7基因显著上调,和UUO组比较上调超过1.5倍,P<0.01。结论:发现抗纤灵能显著降低组织内TGF-β1、Smad2、Smad3基因水平,免疫组化结果也表明抗纤灵能明显降低TGF-β1/Smads介导的基因转录活性。结果提示抗纤灵能抑制性调节TGF-β1/Smads信号通路,抑制肾纤维化的发生。
Objective: To study the mechanism of anti-fibrosis treatment of tubulointerstitial fibrosis by gene chip. Methods: Twenty-eight SPF SD rats were randomly divided into model group (UUOG) and KXLG (untreated ureteral occlusion) model. Twelve of them were sham-operated group. UUO and sham operation group were given saline; Kangxianling group was given Kangxiao Ling gavage. All rats were sacrificed at 14 days left renal tissue. Using custom chips to detect gene changes. Results: Compared with the sham operation group. The expression of TGF-β1, smad2 and smad3 in UUO group was significantly upregulated compared with that in sham-operated group (P <0.01). The Smad7 gene was down-regulated more than 1.5-fold and P <0.01 compared with sham operation group. Compared with UUO group, TGF-β1, smad2 and smad3 genes were significantly down-regulated in anti-fibronectin group, and down-regulated more than 1.5 times, P <0.01. Smad7 gene was significantly up-regulated compared with UUO group. Conclusion: Kangxianling can significantly reduce the level of TGF-β1, Smad2 and Smad3 in the tissue, and the results of immunohistochemistry also showed that Kangxianling can significantly reduce the gene transcription activity mediated by TGF-β1 / Smads. The results suggest that anti-fibronectin can inhibit TGF-β1 / Smads signaling pathway and inhibit the occurrence of renal fibrosis.