论文部分内容阅读
目的探讨实验性缺血后再灌注大鼠胃粘膜损伤与氧自由基脂质过氧化的关系及中药苍脂颗粒剂对胃粘膜损伤的细胞保护作用机制.方法大鼠腹腔动脉结扎,造成胃缺血20min后解除结扎,再灌注60min,取出胃粘膜,观察对照组、病理对照组及中药各组诸项指标变化.结果大鼠缺血再灌注后,胃粘膜LPO含量比对照组明显增加,SOD(1593±321→827±170NU/mg蛋白),NPSH(041±009→022±005mmol/mg蛋白),GSHPX(269±31→187±22U/mg蛋白)含量降低(P<001);术前口服苍脂颗粒剂组动物的胃粘膜LPO含量(121±61FU/mg蛋白)明显低于病理组(197±60FU/mg蛋白),SOD(827±170→1465±474NU/mg蛋白),NPSH(022±005→043±008mmol/mg蛋白),GSHPX(187±22→242±57U/mg蛋白)含量亦显著增加(P<005,P<001),而CAT和PGE2含量在实验各组的比较无统计学意义(P>005).结论氧自由基脂质过氧化参与胃缺血再灌注后的胃粘膜损伤过程,苍?
Objective To investigate the relationship between gastric mucosal lesion and oxygen free radical lipid peroxidation in experimental ischemia reperfusion rats and the protective mechanism of CGT on gastric mucosal injury. Methods The ligation of celiac artery in rats resulted in the ligation of gastric ischemia for 20min, the reperfusion for 60min and the gastric mucosa removed. The indexes of the control group, pathological control group and TCM groups were observed. Results The content of LPO in gastric mucosa increased significantly after ischemia-reperfusion in rats, and SOD (1593 ± 321 → 827 ± 170NU / mg protein) and NPSH (041 ± 009) → 022 ± 005 mmol / mg protein), GSHPX (269 ± 31 → 187 ± 22 U / mg protein) decreased (P <001) The content of LPO (121 ± 61FU / mg protein) in gastric mucosa was significantly lower than that in pathological group (197 ± 60FU / mg protein) and SOD (827 ± 170 → 1465 ± 474 NU / mg protein), NPSH (022 ± 005 → 043 ± 008 mmol / mg protein), GSHPX (187 ± 22 → 242 ± 5 7U / mg protein) also significantly increased (P <0 05, P <0 01), while CAT and PGE2 content in the real There was no significant difference between the groups (P> 005). Conclusion Oxygen-free radical lipid peroxidation participates in gastric mucosal lesion process after gastric ischemia-reperfusion.