三七总皂苷预处理对大鼠小肠缺血再灌注损伤的保护作用

Pretreatment with Panax notoginseng saponins protects against small intestinal ischemia-reperfusion injury in rats

目的:探讨三七总皂苷对大鼠小肠缺血再灌注(ischemia-reperfusion,IR)损伤的保护机制.方法:用肠系膜上动脉夹闭-松夹方式复制SD大鼠IR模型.检测血浆脂多糖和D-乳酸含量;取血液、肝、脾、肠系膜淋巴结,做细菌培养;免疫组织化学检测小肠组织中的NF-B及TNF-表达;用脱氧核糖核酸末端转移酶介导的缺口末端标记技术检测小肠组织细胞凋亡.结果:PNS组肝、脾、肠系膜淋巴结及血液细菌培养阳性数显著低于模型组(P<0.05);三七总皂苷200mg/kg和400mg/kgPNS组血浆脂多糖浓度分别是461EU/L,320EU/L,与模型组(570EU/L)比较差异显著(P<0.05);PNS组的血浆D-乳酸浓度分别是0.37mmol/L,0.31mmol/L,与模型组(0.44mmol/L)比较差异显著(P<0.05);三七总皂苷也可降低NF-B和TNF-的表达,且细胞凋亡数密度低于模型组.结论:三七总皂苷通过降低NF-B和TNF-表达,减轻细胞因子对小肠的损伤,减少小肠黏膜细胞凋亡,发挥对小肠IR损伤的保护作用.

AIM：To explore the mechanism underlying the protective effect of Panax notoginseng saponins （PNS） against intestinal ischemia-reperfusion injury in rats.METHODS：A rat model of intestinal ischemiareperfusion injury was generated.Rats were divided into four groups：sham-operation group,model control group,low-（200 mg/kg） and high-dose （400 mg/kg） PNS groups.After pretreatment with PNS,plasma levels of D-lactate and lipopolysaccharide （LPS） were determined.Samples of the liver,spleen,mesenteric lymph nodes and blood were taken for culturing aerobic bacteria.The expression of NF-B and TNF-in the intestine was detected by immunohistochemistry.Cell apoptosis in the intestine was detected by terminal deoxynucleotidyl transferase-medi-ated dUTP nick end labeling （TUNEL） assay.RESULTS：The number of positive bacterial cultures in the liver,spleen,mesenteric lymph nodes and blood was significantly lower in the PNS group than in the model control group （all P 0.05）.Plasma levels of D-lactate and LPS were significantly lower in the PNS group （200 mg/kg,400 mg/kg） than in the model control group （LPS：461 EU/L,320 EU/L vs 570 EU/L;D-lactate：0.37 mmol/L,0.31 mmol/L vs 0.44 mmol/L,both P 0.05）.Treatment with PNS reduced the expression of NF-B and TNF-and the number of apoptotic cells in intestinal tissue （all P 0.05）.CONCLUSION：Pretreatment with PNS protects against intestinal ischemia-reperfusion injury in rats possibly by reducing mucosal cell apoptosis and down-regulating NF-B and TNF-expression in the small intestine.