Caspase-3在缺氧和内毒素致肾小管损伤的肾组织表达

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.

Abstract：

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 The FiO_2 was reduced 90 min later from 21% to 5%, and the ventilation was withdrawn after another 90 min.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.

Expression of caspase-3 in rat kidney with renal tubular damage induced by lipopolysaccharide and hypoxia

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.