期刊文献+

淫羊藿苷改善重症急性胰腺炎模型大鼠肺损伤 被引量:2

Icariin ameliorates lung injury in severe acute pancreatitis of rat models
下载PDF
导出
摘要 目的探讨淫羊藿苷(ICA)通过抑制炎性反应减轻重症急性胰腺炎(SAP)模型大鼠肺损伤及机制。方法将大鼠随机分为假手术组(sham组)、模型组(SAP组,将5%牛黄胆酸钠按0.1 mL/kg通过微泵逆行泵入胆管)和实验组(ICA组,造模前2 h给予淫羊藿苷80 mg/kg干预)。每组6只大鼠,造模24 h后收集下腔静脉血、胰腺组织和肺组织。HE染色观察胰腺和肺脏病理损伤;ELISA测定血清淀粉酶活性、IL-6、IL-1β和TNF-α含量;免疫组织化学染色测定肺组织中炎性因子IL-6、IL-1β和TNF-α含量;Western blot测定肺组织中磷酸化JNK/JNK和磷酸化NF-κB/NF-κB比值。结果SAP组胰腺和肺脏的病理评分显著高于sham组(P<0.01),ICA组胰腺和肺脏的病理评分较SAP组明显降低(P<0.01);SAP组血清淀粉酶活性、血清IL-6、IL-1β和TNF-α含量以及肺组织中IL-6、IL-1β和TNF-α表达量较sham组明显升高(P<0.01),而ICA组血清淀粉酶活性、血清IL-6、IL-1β和TNF-α含量以及肺组织中IL-6、IL-1β和TNF-α表达量较SAP组明显降低(P<0.01);SAP组肺组织磷酸化JNK和磷酸化NF-κB水平较sham组显著升高(P<0.01),而ICA治疗可以显著降低肺组织中磷酸化JNK和磷酸化NF-κB水平(P<0.01)。结论ICA可能通过抑制JNK/NF-κB信号通路介导的急性炎性反应,从而改善SAP模型大鼠肺损伤。 Objective To evaluate the protective effect and inflammation inhibition mechanism of icariin(ICA)on lung injury in rat model with severe acute pancreatitis(SAP).Methods The rats were randomly divided into sham operation group(sham group),model group(SAP group,5%sodium taurocholate was retrograde pumped into bile duct according to 0.1 mL/kg through micropump)and experimental group(ICA group,icariin 80 mg/kg intervention was given 2 hours before modeling).There were 6 rats in each group.Twenty-four hours after the establishment of the model,the inferior vena cava blood,pancreatic tissue and lung tissue were collected.The pathological injury of pancreas and lung was observed by HE staining;The activity of amylase,serum IL-6,IL-1βand TNF-αwere measured by ELISA;The expression of inflammatory factors IL-6,IL-1βand TNF-αin lung tissue was determined by immunohistochemical staining;And the ratio of phosphorylated JNK/JNK to phosphorylated NF-κB/NF-κB in lung tissue was measured by Western blot.Results The pathological scores of pancreas and lung in SAP group were significantly higher than those in sham group;And the pathological scores of pancreas and lung in ICA group were significantly lower than those in SAP group.Serum amylase activity,serum IL-6,IL-1βand TNF-αcontent and the expression of IL-6,IL-1βand TNF-αin lung tissue in SAP group were significantly higher than those in sham group;While serum amylase activity,serum IL-6,IL-1βand TNF-αcontent and the expression of IL-6,IL-1βand TNF-αin lung tissue in ICA group were significantly lower than those in SAP group.The level of phosphorylated JNK and phosphorylated NF-κB in lung tissue of SAP group were significantly higher than those of sham group;While icariin might significantly reduce the level of phosphorylated JNK and phosphorylated NF-κB in lung tissue.Conclusions ICA ameliorates lung injury in SAP rat model by inhibiting acute inflammation response,which is potentially mediated by JNK/NF-κB signal pathway.
作者 谷文浩 郭飞霞 徐宇鹏 陆馨雨 胡青青 GU Wen-hao;GUO Fei-xia;XU Yu-peng;LU Xin-yu;HU Qing-qing(Zhejiang University of Traditional Chinese Medicine,Hangzhou 310000;Department of Internal Medicine,Wenzhou Lucheng District People’s Hospital,Wenzhou 325000;Laboratory of Translational Medicine,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China;the First Clinical Medical College,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China;Department of Pediatrics,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China)
出处 《基础医学与临床》 2022年第9期1400-1405,共6页 Basic and Clinical Medicine
基金 温州市科技局科技计划(Y2020231)。
关键词 淫羊藿苷 炎性反应 c-Jun氨基末端激酶(JNK) NF-κB 重症急性胰腺炎 肺损伤 icariin inflammation c-Jun N-terminal kinase(JNK) NF-κB severe acute pancreatitis lung injury
  • 相关文献

参考文献2

二级参考文献12

  • 1张明钧,王志蓉,王兴鹏,袁耀宗,徐家裕.急性出血坏死性胰腺炎大鼠模型的改良[J].上海第二医科大学学报,1995,15(3):244-245. 被引量:15
  • 2Zaqer RA, Johnson AC, Lund S, et al. Acute renal fail- ure: determinants and characteristics of the injury-induced hyperinflammatory response [ J ]. Am J Physiol Renal Phys- iol, 2006, 291: F546-556.
  • 3Meng LQ, Tang JW, Wang Y, et al. Astragaloside IV syn- ergizes with ferulic acid to inhibit renal tubulointerstitial fi- brosis in rats with obstructive nephropathy [ J ]. Br J Phar- macol, 2011, 162: 1805-1818.
  • 4Kanellis J, Ma FY, Kandane-Rathnayake R, et al. JNK signalling in human and experimental renal ischaemia/ reperfusion injury [ J ]. Nephrol Dial Transplant, 2010, 25 : 2898-2905.
  • 5Hou X, Shen YH, Li C, et al. PPARalpha agonist fenofi- brate protects the kidney from hypertensive injury in sponta- neously hypertensive rats via inhibition of oxidative stress and MAPK activity [ J ]. Biochem Biophys Res Commun, 2010, 394: 653-659.
  • 6Ohashi N, Urushihara M, Satou R, et al. Glomerular an- giotensinogen is induced in mesangial cells in diabetic rats via reactive oxygenspecies-ERK/JNK pathways [ J ]. Hy-pertens Res, 2010, 33: 1174-1181.
  • 7Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign:international guidelines for management of severe sepsis and septic shock [J]. Intensive Care Med, 2013, 39 165-228.
  • 8Zarjou A, Agarwal A. Sepsis and acute kidney injury [ J ]. J Am Soc Nephrol, 2011, 22: 999-1006.
  • 9Ma FY, Liu J, Nikolic-Patreson DJ. The role of stress acti- vated protein kinase signaling inrenal pathophysiology [ J ]. Braz J Med Biol Res, 2009, 42: 29-37.
  • 10Kim OS, Kim YS, Jang DS, et al. Cytoprotection against hydrogen peroxide-induced cell death in cultured mouse me- sangial cells by erigeroflavanone, a novel compound from the flowers of Erigeron annuus [ J]. Chem Biol Interact, 2009, 180 : 414-420.

共引文献29

同被引文献40

引证文献2

二级引证文献2

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