中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
3期
366-370
,共5页
赵维%吴广礼%赵彬%何正佳%容俊芳
趙維%吳廣禮%趙彬%何正佳%容俊芳
조유%오엄례%조빈%하정가%용준방
山莨菪碱%肾%内质网%应激%热休克蛋白质类
山莨菪堿%腎%內質網%應激%熱休剋蛋白質類
산랑탕감%신%내질망%응격%열휴극단백질류
Anisodamine%Kidney%Endoplasmic reticulum%Stress%Heat-shock proteins
目的 评价山莨菪碱对大鼠急性肾损伤时内质网应激(ERS)的影响.方法 雄性SD大鼠42只,体重200 ～ 220 g,采用随机数字表法将其分为3组:对照组(C组,n=6),双侧后肢肌肉注射生理盐水10 ml/kg；急性肾损伤组(AKI组,n=18),双侧后肢肌肉注射50％ (v/v)甘油10 ml/kg；山莨菪碱组(AD组,n=18),腹腔注射山莨菪碱10 mg/kg,20 min后处理同AKI组.C组于肌肉注射生理盐水后即刻(T0),AKI组和AD组于甘油给药后1 h(T1)、6 h(T2)、24 h(T3)分别随机取6只大鼠,采集肾组织标本,HE染色后行肾小管损伤评分,采用免疫组化和Western blot法测定肾组织葡萄糖调节蛋白78(GRP78)和氧调节蛋白150(ORP150)表达.结果 与C组比较,AKI组和AD组各时点肾小管损伤评分升高,肾组织GRP78和ORP150表达上调(P＜0.01)；与AKI组比较,AD组各时点肾小管损伤评分降低,肾组织GRP78和ORP150表达下调(P＜0.05或0.01).结论 山莨菪碱可抑制肾小管上皮细胞ERS,可能减轻了ERS途径诱导的细胞凋亡,从而减轻了大鼠急性肾损伤.
目的 評價山莨菪堿對大鼠急性腎損傷時內質網應激(ERS)的影響.方法 雄性SD大鼠42隻,體重200 ～ 220 g,採用隨機數字錶法將其分為3組:對照組(C組,n=6),雙側後肢肌肉註射生理鹽水10 ml/kg；急性腎損傷組(AKI組,n=18),雙側後肢肌肉註射50％ (v/v)甘油10 ml/kg；山莨菪堿組(AD組,n=18),腹腔註射山莨菪堿10 mg/kg,20 min後處理同AKI組.C組于肌肉註射生理鹽水後即刻(T0),AKI組和AD組于甘油給藥後1 h(T1)、6 h(T2)、24 h(T3)分彆隨機取6隻大鼠,採集腎組織標本,HE染色後行腎小管損傷評分,採用免疫組化和Western blot法測定腎組織葡萄糖調節蛋白78(GRP78)和氧調節蛋白150(ORP150)錶達.結果 與C組比較,AKI組和AD組各時點腎小管損傷評分升高,腎組織GRP78和ORP150錶達上調(P＜0.01)；與AKI組比較,AD組各時點腎小管損傷評分降低,腎組織GRP78和ORP150錶達下調(P＜0.05或0.01).結論 山莨菪堿可抑製腎小管上皮細胞ERS,可能減輕瞭ERS途徑誘導的細胞凋亡,從而減輕瞭大鼠急性腎損傷.
목적 평개산랑탕감대대서급성신손상시내질망응격(ERS)적영향.방법 웅성SD대서42지,체중200 ～ 220 g,채용수궤수자표법장기분위3조:대조조(C조,n=6),쌍측후지기육주사생리염수10 ml/kg；급성신손상조(AKI조,n=18),쌍측후지기육주사50％ (v/v)감유10 ml/kg；산랑탕감조(AD조,n=18),복강주사산랑탕감10 mg/kg,20 min후처리동AKI조.C조우기육주사생리염수후즉각(T0),AKI조화AD조우감유급약후1 h(T1)、6 h(T2)、24 h(T3)분별수궤취6지대서,채집신조직표본,HE염색후행신소관손상평분,채용면역조화화Western blot법측정신조직포도당조절단백78(GRP78)화양조절단백150(ORP150)표체.결과 여C조비교,AKI조화AD조각시점신소관손상평분승고,신조직GRP78화ORP150표체상조(P＜0.01)；여AKI조비교,AD조각시점신소관손상평분강저,신조직GRP78화ORP150표체하조(P＜0.05혹0.01).결론 산랑탕감가억제신소관상피세포ERS,가능감경료ERS도경유도적세포조망,종이감경료대서급성신손상.
Objective To evaluate the effect of anisodamine on endoplasmic reticulum stress during acute kidney injury (AKI) in rats.Methods Forty-two nale Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 3 groups:control group (group C,n =6),AKI group (n =18) and anisodamine group (group AD,n =18).AKI was induced by intramuscular injection of 50％ (v/v) glycerol 10 ml/kg into bilateral hind limbs in groups AKI and AD.In addition,anisodamine 10 mg/kg was injected intraperitoneally 20 min before intramuscular injection of glycerol in group AD.In group C the rats received intramuscular injection of normal saline 10 ml/kg into bilateral hind limbs.Six rats were chosen immediately after injection of normal saline in group C or at 1,6 and 24 h after glycerol injection in groups AKI and AD and then anethetized with intraperitoneal pentobarbital.The animals were sacrificed and kidney specimens were obtained and cut into sections which were stained with hematoxylin and eosin for pathological examination.The pathological changes of the renal tubules were scored.The expression of glucose-regulated protein 78 (GRP78) and oxygen-regulated protein 150 (ORP150) in renal tissues was determined by immuno-histochemistry and Western blot.Results Compared with group C,the pathological scores were significantly increased and the expression of GRP78 and ORP150 was up-regulated at all time points in groups AKI and AD (P ＜ 0.01).Compared with group AKI,the pathological scores were significantly decreased and the expression of GRP78 and ORP150 was down-regulated at all time points in group AD (P ＜ 0.05 or 0.01).Conclusion Anisodamine can ameliorate AKI through inhibiting endoplasmic reticulum stress in renal tubular epithelial cells and decreasing endoplasmic reticulum stress-induced cell apoptosis in rats.
