CAJ | 학술논문

目的为了建立缺氧和内毒素致肾小管损伤模型,观察Caspase-3在肾组织的表达,以探讨其肾小管的损伤机制.方法以SD大鼠为实验动物,予麻醉及机械通气,同时予阴茎静脉注射伤寒杆菌脂多糖,吸入氧浓度从21%降至5%的氧,通气至180rain结束.取肾组织作HE染色病理切片检查及用Caspase-3免疫组化S-P法染色观察模型肾组织的病理改变及肾组织中Caspase-3的表达.结果 (1)病理组织学所见:大部分肾小球充血,内皮及系膜细胞轻度肿胀,肾近曲小管上皮明显肿胀,呈浊样改变;大部分远曲小管镜下未见明显改变,部分上皮细胞肿胀,浊样变性在;整个肾间质呈充血现象.无炎性细胞浸润,(2)免疫组化结果:Caspase-3染色位于胞浆,大部分远曲小管上皮呈Caspase-3阳性反应,以外髓远曲小管为明显;近曲小管偶见Caspase-3阳性细胞,肾小球Caspase-3染色阴性.结论 (1)缺氧及内毒素可致肾小管损伤,且以近曲小管为著,远曲小管及内髓部损伤相对较轻,(2)Caspase-3在远曲小管明显表达,提示在缺氧及内毒素致肾小管损伤中,同时存在细胞变性坏死及细胞凋亡,近曲小管以细胞变性坏死为著,而远曲小管细胞凋亡明显.
목적 위료건립결양화내독소치신소관손상모형,관찰Caspase-3재신조직적표체,이탐토기신소관적손상궤제.방법 이SD대서위실험동물,여마취급궤계통기,동시여음경정맥주사상한간균지다당,흡입양농도종21%강지5%적양,통기지180rain결속.취신조직작HE염색병리절편검사급용Caspase-3면역조화S-P법염색관찰모형신조직적병리개변급신조직중Caspase-3적표체.결과 (1)병리조직학소견:대부분신소구충혈,내피급계막세포경도종창,신근곡소관상피명현종창,정탁양개변;대부분원곡소관경하미견명현개변,부분상피세포종창,탁양변성재;정개신간질정충혈현상.무염성세포침윤,(2)면역조화결과:Caspase-3염색위우포장,대부분원곡소관상피정Caspase-3양성반응,이외수원곡소관위명현;근곡소관우견Caspase-3양성세포,신소구Caspase-3염색음성.결론 (1)결양급내독소가치신소관손상,차이근곡소관위저,원곡소관급내수부손상상대교경,(2)Caspase-3재원곡소관명현표체,제시재결양급내독소치신소관손상중,동시존재세포변성배사급세포조망,근곡소관이세포변성배사위저,이원곡소관세포조망명현.
Objectives To observe the expression of caspase-3 in the kidney of a rat model of renal tubular damage induced by endotoxin and hypoxia and explore the mechanism of renal tubular damage. Methods Ten rats were anesthetized with artificial ventilation and received 2 mg/kg lipopolysaccharide (LPS) injection through the penile vein. The FiO_2 was reduced 90 min later from 21% to 5%, and the ventilation was withdrawn after another 90 min. Immediately after ventilation withdrawal, the kidney of the rats were obtained for immunocytochemistry and HE staining. Results HE staining showed obvious hyperemia in most of the glomeruli, mild swelling of the endothelial and mesangial cells, severe swelling and turbidity in the proximal tubular epithelial cells without obvious changes in most of the distal proximal tubules. A small portion of the interstitial epithelial cells showed swelling and turbidity, and the entire renal interstitium appeared hyperemic but without inflammatory cell infiltration. Immunocytochemistry detected the presence of caspase-3 in the cytoplasm, and most of the distal renal tubule cells were positive for caspase-3, while only occasional cells showed caspase-3 positivity in the proximal tubular epithelial cells. Most of the proximal tubular epithelial and glomerulus cells were negative for caspase-3. Conclusions Endotoxin and hyoxia can induce renal damage, particularly in the proximal renal tubule cells, and the distal tubular epithelial cells sustain relatively light damage. Caspase-3 is strongly expressed in the distal renal tubular cells, suggesting that in renal tubular damage induced by endotoxin and hypoxia, cell degeneration, necrosis and apoptosis coexist in the tubular epithelial cells; degeneration and necrosis occur primarily in the proximal tubular epithelial cells, while apoptosis is obvious in the distal renal cells.