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益肾胶囊对糖尿病肾病肾组织SOCS3及Col-Ⅰ、Ⅳ表达的影响 被引量:7

The Effect of Yishen Capsule on SOCS - 3、Collagen Type Ⅰand Ⅳ in Diabetic Nephropathy Rats
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摘要 目的:观察益肾胶囊对糖尿病肾病大鼠肾组织SOCS-3、Ⅰ、Ⅳ型胶原表达的影响,探讨益肾胶囊延缓糖尿病肾病肾纤维化的机制。方法:36只健康雄性Wistar大鼠,通过尾静脉单次注射链脲佐菌素(60 mg/kg),制造糖尿病大鼠模型,后随机分为DN模型组、益肾胶囊组、氯沙坦钾组,各12只,益肾胶囊组每只灌胃益肾胶囊(625 mg.kg-1.d-1),氯沙坦组每只灌胃氯沙坦钾片(30 mg.kg-1.d-1),另取12只健康大鼠作为正常对照组。正常对照组及模型组每日给予等量蒸馏水。12周后测定各组大鼠体重、24 h尿蛋白定量、血肌酐、尿素氮;采用HE、Masson和PAS染色观察肾组织病理变化,采用免疫组化法检测肾组织中SOCS-3、Ⅰ、Ⅳ型胶原表达水平。结果:实验12周末,与正常组比较,模型组大鼠病理改变较明显,24 h尿蛋白定量、血肌酐、尿素氮明显上升(P<0.05),肾组织中SOCS-3、Ⅰ、Ⅳ型胶原表达明显上调。与模型组比较,治疗组大鼠病理改变减轻,24 h尿蛋白定量、血肌酐、尿素氮水平明显降低(P<0.05);肾组织中SOCS-3表达显著上调,Ⅰ、Ⅳ型胶原表达显著抑制(P<0.05)。结论:益肾胶囊可能通过上调SOCS-3表达,抑制Ⅰ、Ⅳ型胶原的表达,从而减轻了DN大鼠肾小球硬化和肾小管间质纤维化的程度,延缓糖尿病肾病的进展。 Objective:To observe the effect of Yishen capsule on SOCS -3 ,Collagen type Ⅰ and Ⅳ in Diabetic nephropathy rats and to investigate the mechanism of Yishen Capsule to delay diabetic nephropathy fibrosis. Methods: The rat models of diabetic nephropathy were established by intraperitoneal injection of STZ ( Streptozotocin 60 mg/kg). Then the rats were randomly divided into three groups: DN group(only distilled water by gavage), Y group (Yishen capsule 625 mg.kg-1. d-1 by gavage), L group (Losar- tan 30 mg . kg-1. d-1 by gavage) . The additional set of healthy rats were given no STZ were used as control group (N group). Each group consisted of 12 rats. By 12 weeks, the body weight, 24 h urinary albumin excretion, serum creatinine (Scr) and blood u- rea nitrogen (BUN) level were measured in each rat. Then, renal tissue samples were observed under optical microscope. Expression of SOCS - 3 ,Collagen type Ⅰ , Ⅳ in ream tissue samples were detected by immunohistochemistry. Results: Compared with N group, DN group had significant elevated 24 h urinary albumin, Scr and BUN ( P 〈 0.05 ), the pathological changes in the renal tissue sam- ples in DN group were also obvious. Compared with DN group, the treated groups had significant lower 24h urinary albumin, Scr and BUN (P 〈 0.05 ). The pathological changes in the renal tissue samples were much relieved in the treated group. The expression level of SOCS3 in treated group was significant higher than that in DN group, but the expression level of Collagen type Ⅰ , Ⅳ were lower than that in DN group ( P 〈 0.05 ). Conclusion: Yishen capsule may through the up - regulation of SOCS3 expression to inhibit the ex- pression of Collagen type Ⅰ , Ⅳ, thus reduce the DN rat glomerular sclerosis and renal tubule interstitial fibrosis degree, then delay the progress of diabetic nephropathy.
出处 《中国中西医结合肾病杂志》 2013年第7期573-575,共3页 Chinese Journal of Integrated Traditional and Western Nephrology
基金 国际科技合作项目(No.2011081066) 国家自然基金资助项目(No.81173364)
关键词 益肾胶囊糠尿病肾病SOCS-3 Ⅰ、Ⅳ型胶原 WORDS Yishen capsule DN SOCS -3 Collagen type Ⅰ Collagen typeⅣ
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参考文献7

  • 1National Kidney Foundation. Kidney Disease Outcome Quality Initiative K/DOQI clinical practice guidelines for chronic kidney disease, evaluation classification, and stratification. Am J Kidney Disease,2002,39 (2 Supple 2) : S241 - S246.
  • 2Huang JS, Guh J Y, Chen HC, et al. Role of receptor for ad- vanced glycationend -product (RACEI and the JAK/STAT - signaling pathway in AGE- induced collagenproductioninNRK - 49Fcells. J Ceil Biolehem,2001,81 ( 1 ) :102 - 113.
  • 3Nicholson SE, Souza D, Fabri LJ, et al. Suppressor of cytokine signaling- 3 Preferentially binds to the SHP- 2 -binding site on the shared cytokine receptor subunit gpl30. Proc Natl Acad Sci USA,2000,97(6) :6493 -6498.
  • 4靳远萌,陈楠.JAK/STAT通路在肾间质纤维化中的进展[J].肾脏病与透析肾移植杂志,2012,21(3):255-259. 被引量:17
  • 5Zhang Y, Wang C. Suppressor of cytokine signaling21 reduces high glocose2 induced TGF2 beta and fibronectin synthesis in human messangial cells J. FEBS Lett,2008,582(23 -24) :3484 - 3488.
  • 6李娟,方敬爱.益肾胶囊对糖尿病肾病大鼠肾组织SOCS3、TGF-β_1、MCP-1表达的影响[J].中国中西医结合肾病杂志,2011,12(4):291-294. 被引量:21
  • 7黄海长,李惊子,王海燕.结缔组织生长因子诱导肾成纤维细胞转为成肌纤维细胞[J].科学通报,2002,47(1):37-40. 被引量:66

二级参考文献48

  • 1Tuttle KR.Linking metabolism and immunology:Diabetic nephropathy is an inflammatory disease.J Am Soc Nephrol,2005,16(6):1537-1538.
  • 2Mora C,Navarro JF.Inflammation and diabetic nephropathy.Curr Diab Rep,2006,6(6):463-468.
  • 3Marrero MB,Banes-Berceli AK,Sten DM,et al.Role of the JAK/STAT signaling pathway in diabetic nephropathy.Am J Physiol Renal Physiol,2006,290(4):F762-F768.
  • 4Wang X,Shaw S,Amiri F,et al.Inhibition of the JAK/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronection synthesis in mesangial cells.Diabetes,2002,51(12):3505-3509.
  • 5Rai JL,Himge I,Dneamn H,et al.Recommendations for the management of special populations:renal disease in diabetes.Am J Hyper tens,2003,16(11):46-49.
  • 6Yoshimura A,Ohkubo T,Kiguchi T,et al.A novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to tyrosinephosphorylated interleukin 3 and erythropoietin receptors.EMBO J,1995,14(12):2816-2826.
  • 7Naka T,Narazaki M,Hirata M,et al.Structure and function of a new STAT-induced STAT inhibitor.Nature,1997,387(6636):924-929.
  • 8Starr R,Wilson TA,Viney EM,et al.A family of cytokine-inducible inhibitors of signalling.Nature,1997,387 (6636):917-921.
  • 9James A.Are SOCS suppressors,regulators,and degraders J Leukocyte Bio,2004,75(5):743-748.
  • 10Russell SM,Johnson JA,Noguchi M,et al.Interaction of IL-2R beta and gamma c chains with Jak1 and Jak3:implications for XSCID and XCID.Science,1994,266(5187):1042-1045.

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