CAJ | 학술논문

目的：探讨白芍总苷( TGP)对糖尿病肾脏组织中内质网应激( ERS )的影响。方法50只大鼠随机分为对照组、模型组和TGP给药组[50、100、200 mg/(kg·d)灌胃]。用链脲佐菌素( STZ)诱导大鼠制备糖尿病模型,8周后留取适量肾组织用免疫组织化学法检测葡萄糖调节蛋白78(GRP78)、磷酸化的蛋白激酶样内质网激酶(p-PERK)及磷酸化的真核细胞翻译起始因子2α( p-eIF2α)蛋白的表达。结果各TGP给药组大鼠尿白蛋白排泄率( UAER)较模型组明显减少(P<0．01),模型组大鼠UAER水平明显高于对照组(P<0．01)。与对照组相比,模型组大鼠p-PERK在肾小管-间质中的表达以及GRP78、p-eIF2α在肾小球、肾小管-间质中的表达均显著增加( P<0．01)。与模型组相比, TGP各给药组大鼠GRP78、p-PERK在肾小管-间质中的表达以及p-eIF2α在肾小球、肾小管-间质中的表达明显降低(P<0．01)。结论糖尿病大鼠肾脏中ERS反应明显,TGP对糖尿病肾病大鼠的肾脏保护可能与抑制ERS反应有关。
목적：탐토백작총감( TGP)대당뇨병신장조직중내질망응격( ERS )적영향。방법50지대서수궤분위대조조、모형조화TGP급약조[50、100、200 mg/(kg·d)관위]。용련뇨좌균소( STZ)유도대서제비당뇨병모형,8주후류취괄량신조직용면역조직화학법검측포도당조절단백78(GRP78)、린산화적단백격매양내질망격매(p-PERK)급린산화적진핵세포번역기시인자2α( p-eIF2α)단백적표체。결과각TGP급약조대서뇨백단백배설솔( UAER)교모형조명현감소(P<0．01),모형조대서UAER수평명현고우대조조(P<0．01)。여대조조상비,모형조대서p-PERK재신소관-간질중적표체이급GRP78、p-eIF2α재신소구、신소관-간질중적표체균현저증가( P<0．01)。여모형조상비, TGP각급약조대서GRP78、p-PERK재신소관-간질중적표체이급p-eIF2α재신소구、신소관-간질중적표체명현강저(P<0．01)。결론당뇨병대서신장중ERS반응명현,TGP대당뇨병신병대서적신장보호가능여억제ERS반응유관。
Objective To study the effect of total glucosides of paeony ( TGP) on endoplasmic reticulum stress in the kidney from experimental diabetic rats. Methods Rats were randomly divided into three groups:control group, model group and TGP treated groups. Diabetes rat model was induced with streptozotocin. In TGP group, TGP 50, 100,200 mg/(kg·d) were orally administered once a day for 8 weeks. The expressions of GRP78,p-PERK and p-eIF2α were determined by immunostaining in the kidney. Results The urinary albumin excretion rate( UAER) in model group was significantly higher than that in TGP treatment group. Analysis of the immunostaining showed the expression of GRP78,p-PERK and p-eIF2α was significantly increased compared with control rats in the kidney. TGP treatment with 50,100 and 200 mg/(kg·d) could markedly reduce GRP78 and p-PERK expression in the tu-bulointerstitium,p-eIF2αexpression in the glomeruli and tubulointerstitium. Conclusion The TGP protection of re-nal tissue in diabetic rats may be associated with inhibition of endoplasmic reticulum stress.