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目的观察缺氧复氧对大鼠小肠上皮细胞(intestinal epithelial cell,IEC)-6培养液中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及细胞内Ca~(2+)浓度和线粒体膜电位的影响,探讨复方中药-紫芪方对IEC-6肠上皮细胞缺氧复氧损伤的保护作用及机制。方法复制IEC-6细胞缺氧复氧损伤模型,采用紫外分光法测定缺氧复氧后及紫芪方血清治疗后细胞培养液中SOD活性及MDA含量；采用激光共聚焦显微镜测定细胞Ca~(2+)浓度和线粒体膜电位变化。结果细胞缺氧复氧损伤后,可导致细胞培养液中SOD活性显著降低、MDA含量显著升高、线粒体膜电位明显降低及细胞内Ca~(2+)浓度明显升高(P＜0．01)。紫芪方药物血清治疗后,可提高细胞培养液中SOD活性并降低其MDA含量,同时稳定了线粒体膜电位并降低细胞内Ca~(2+)浓度(P＜0．05)。结论缺氧复氧可导致IEC-6肠上皮细胞损伤；紫芪方血清对IEC-6小肠上皮细胞缺氧复氧损伤具有显著的保护作用。
Objective To observe the activity of superoxide dismutase (SOD), malondialdehyde (MDA) and intracellular Ca~(2+) concentration in rat intestinal epithelium (IEC)-6 medium after hypoxia/reoxygenation. And the effect of mitochondrial membrane potential on the protective effect and mechanism of compound Chinese herbal medicine-Xiqi Fang on anoxia-reoxygenation injury of IEC-6 intestinal epithelial cells. Methods The anoxia and reoxygenation injury model of IEC-6 cells was duplicated. The activity of SOD and the content of MDA in the cell culture medium were measured by UV spectrophotometry after hypoxia-reoxygenation and purpura treatment. The cells were determined by laser confocal microscopy. 2+) concentration and changes in mitochondrial membrane potential. Results After hypoxia/reoxygenation injury, SOD activity in the cell culture medium was significantly decreased, MDA content was significantly increased, mitochondrial membrane potential was significantly decreased, and intracellular Ca~(2+) concentration was significantly increased (P<0.01). ). After treatment with Ziqinfang drug serum, the activity of SOD and the content of MDA in the cell culture fluid were increased, and the mitochondrial membrane potential was stabilized and the intracellular Ca~(2+) concentration was decreased (P<0.05). Conclusion Hypoxia and reoxygenation can cause IEC-6 intestinal epithelial cell injury; Ziqinfang serum has a significant protective effect on anoxia and reoxygenation injury of IEC-6 intestinal epithelial cells.