期刊文献+

左归丸对庆大霉素所致肾小管损伤大鼠c-Jun氨基末端激酶的影响 被引量:2

Effect of Zuogui Wan on the Expression of c-Jun N-terminal Kinase in Rats with Gentamicin-induced Renal Tubular Injury
原文传递
导出
摘要 目的:探讨左归丸对庆大霉素所致肾小管损伤大鼠c-Jun氨基末端激酶(JNK)的影响。方法:将40只雄性Wistar大鼠随机分为空白对照组(C组),模型组(M组),c-Jun氨基末端激酶特异性抑制剂(SP600125)组(S组),左归丸组(Z组),每组10只,对照组ip给予0.9%生理盐水2.5 mL.kg-1.d-1,模型组ip硫酸庆大霉素100 mg.kg-1.d-1,SP600125组左侧ip硫酸庆大霉素100 mg.kg-1.d-1,2 h后右侧ip SP600125 15 mg.kg-1.d-1,左归丸组ip硫酸庆大霉素100 mg.kg-1.d-1和ig左归丸水溶液10 g.kg-1.d-1,4组大鼠连续给药10 d。第11日测量各组大鼠尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG);HE染色观察各组大鼠肾脏病理状况;免疫组化技术检测各组大鼠肾脏JNK,c-Jun的表达;以Western blot方法检测各组大鼠肾脏c-Jun氨基末端激酶(JNK),c-Jun蛋白的表达。结果:尿NAG酶结果显示:与C组比较,M组尿NAG酶显著升高(P<0.01);与M组比较,S组和Z组尿NAG酶下降(P<0.05)。HE染色结果显示:C组肾小管、间质无特殊改变;M组肾小管上皮细胞出现空泡变性、管腔出现损伤,有大量的炎性细胞浸润;S组与Z组肾小管少量炎性细胞浸润,轻微肿胀变性。免疫组化结果显示:与C组比较,M组JNK,c-Jun在肾小管大量表达(P<0.01);与M组比较,S组和Z组JNK,c-Jun在肾小管表达较少(P<0.01)。免疫印迹杂交结果显示:M组JNK,c-Jun蛋白灰度值较对照组明显升高(P<0.01),S组与Z组较M组灰度值下降(P<0.01或P<0.05)。结论:左归丸对庆大霉素所致肾小管损伤大鼠的保护作用可能与抑制c-Jun氨基末端激酶的激活有关。 Objective: Effect of Zuogui Wan on the expression of c-Jun amino-terminal kinase(JNK) and c-Jun in rats with gentamicin-induced renal tubular injury. Method: Forty male Wistar rats were divided randomly into control group(C), model group(M), Sp600125 group(S) and Zuoguiwan group(Z). The C group was given ip injection of 0.9% saline 2.5 mL·kg-1·d-1, M group was given ip injection of gentamicin sulfate 100 mg·kg^-1·d^-1, S group was given ip injection of gentamicin sulfate 100 mg·kg^-1·d^-1 and ip injection of SP600125 15 mg·kg^-1·d^-1 Zuoguiwan group was given ip injection of gentamicin sulfate 100 mg·kg^-1·d^-1 and gavage Zuoguiwan aqueous solution 10 g·kg^-1·d^-1. Four groups of rats administered for 10 consecutive days. After the experiment measuring the NAG of rat. Hematoxylin-eosin to detect renal histopathology. Immunohistochemical techniques to detect JNK and c-Jun's expression of the rat kidney. Western blot techniques to detect JNK and c-Jun's expression of the rat kidney. Result: The results of biochemical index show: compared with the C group, the rats of M group NAG significantly increased, with a statistically significant difference (P〈0.01); compared with the M group, the biochemical parameters improved of S group and Z group, with a statistically significant difference (P〈0.05). The HE staining results show: the C group of renal tubule, renal interstitial no change; the M group of renal tubular epithelial cells swelling, vacuolar degeneration. The S group and Z group renal tubule epithelial cells slight swelling, degeneration. The immunohistochemical results show: compared with the C group, the rats of M group JNK, c-Jun abundantly expressed in the renal tubules, with a statistically significant difference (P〈0.01); compared with the M group, protein expression was not significant in the S group and Z group, with a statistically significant difference (P〈0.01). The results of western blot show: compared with the C group, the rats of M group JNK, c-Jun's gray values increased significantly, with a statistically significant difference (P〈0.01); compared with the M group, the gray values of S group and Z group decreased, with a statistically significant difference (P〈0.05, P〈0.01). Conclusion: The protective effect of Zuogui Wan relieved the gentamicin-induced renal tubular injury in rats, which mechanism may be involved in the inhibition of the c-Jun N-terminal kinase activation.
出处 《中国实验方剂学杂志》 CAS 北大核心 2013年第11期194-198,共5页 Chinese Journal of Experimental Traditional Medical Formulae
基金 国家临床重点专科建设项目(FW20113289)
  • 相关文献

参考文献10

二级参考文献37

  • 1夏安周,张召辉,邢淑华.银杏叶提取物对肾缺血-再灌注后细胞凋亡的影响[J].中国中西医结合急救杂志,2004,11(4):212-214. 被引量:14
  • 2安海燕,任可.补骨汤治疗肾性骨病的临床观察[J].中国中西医结合肾病杂志,2004,5(12):718-719. 被引量:13
  • 3Xu Z, Greene LA. Activation of the apoptotic JNK pathway through the Racl-binding scaffold protein POSH [ J ]. Methods Enzymol, 2006,406:479-489.
  • 4Kuan CY,Yang DD,Samanta Roy DR,et al. The JNK1 and JNK2 protein kinases are required for regional specific apoptosis during early brain development [ J ]. Neuron, 1999,22 (4) : 667-676.
  • 5Li DQ,Luo L,Chen Z,et al. JNK and ERK MAP kinases mediate induction of IL-1beta,TNF-alpha and IL-8 following hyperosmolar stress in human limbal epithelial cells[ J ]. Exp Eye Res ,2006,82 (4) :588-596.
  • 6Levkovitch-Verbin H, Harizman N, Dardik R, et al. Regulation of cell death and survival pathways in experimental glaucoma [ J ]. Exp Eye Res,2007,85(2):250-258.
  • 7Guma M, Rius J, Duong-Polk KX, et al. Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression[ J]. Proc Natl Acad Sci U S A,2009,106 (21) :8760-8765.
  • 8Roduit R,Schorderet DF. MAP kinase pathways in UV-induced apoptosis of retinal pigment epithelium ARPE19 cells[ J ]. Apoptosis, 2008,13 (3) :343-353.
  • 9Morishima Y, Gotoh Y, Zieg J, et al. Beta-amyloid induces neuronal apoptosis via a mechanism that involves the c-Jun N-terminal kinase pathway and the induction of Fas ligand [ J ]. J Neurosci, 2001,21 (19) :7551-7560.
  • 10Savage M J, Lin YG, Ciallella JR, et al. Activation of c-Jun N-terminal kinase and p38 in an Alzheimer's disease model is associated with amyloid deposition[J]. J Neurosci,2002,22(9) :3376-3385.

共引文献34

同被引文献21

引证文献2

二级引证文献23

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部