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目的探讨淫羊藿素脂质体对大鼠肝脏缺血再灌注(I/R)损伤的作用及其机制。方法建立大鼠70%肝脏I/R损伤模型。将120只雄性大鼠随机分成淫羊藿素脂质体+I/R损伤(ICT+I/R)组、空白脂质体+I/R损伤(LIP+I/R)组、单纯I/R损伤组和假手术(Sham)组,每组再随机分成2h和6h两个亚组。Sham组仅游离肝门,其余各组均行70%肝脏缺血60min。血流阻断前10min,ICT+I/R组、LIP+I/R组分别经门静脉注射淫羊藿素脂质体(1.5mg/kg)、空白脂质体(与淫羊藿素脂质体等体积),I/R组和Sham组不行任何预处理。经2、6h血流再灌注后,采集各组血液及肝脏组织标本,检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平以及肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、一氧化氮合酶(NOS)、诱导型一氧化氮合酶(iNOS)、内皮型一氧化氮合酶(eNOS)以及髓过氧化物酶(MPO)含量。采用H-E染色法观察肝脏组织形态,TUNEL染色法观察肝细胞凋亡情况并测定凋亡指数(AI)。结果再灌注2h,ICT+I/R组的ALT、MDA、MPO、AI较LIP+I/R组和I/R组下降,差异有统计学意义(P<0.01);再灌注6h,与LIP+I/R组和I/R组相比,ICT+I/R组的ALT、AST、MDA、AI下降,同时SOD、NO、NOS、eNOS升高,差异有统计学意义(P<0.05,P<0.01)。结论淫羊藿素脂质体能够通过增加SOD含量、减少MDA的生成,促进eNOS表达的升高、增加NO的含量以及抑制MPO的聚集、减少肝细胞凋亡等多途径发挥抗大鼠肝脏I/R损伤的保护作用。
Objective To investigate the effect of icariin liposomes on hepatic ischemia-reperfusion (I / R) injury in rats and its mechanism. Methods Establishment of 70% hepatic I / R injury model in rats. A total of 120 male rats were randomly divided into 3 groups: Icaritin + I / R injury group (ICT + I / R), blank liposome + I / R injury group R injury group and sham operation group. Each group was divided into two subgroups: 2h and 6h. Sham group only free hepatic portal, the rest of the group were 70% hepatic ischemia 60min. In the ICT + I / R group and the LIP + I / R group, the icariin liposomes (1.5 mg / kg) and the liposomes Volume), I / R group and Sham group without any pretreatment. After 2,6h perfusion, blood and liver tissue samples of each group were collected to detect serum ALT, AST and superoxide dismutase (SOD) MDA, NO, NOS, iNOS, eNOS, and myeloperoxidase (MPO) content. The morphology of liver tissue was observed by H-E staining. The apoptosis of hepatocytes was observed by TUNEL staining and the apoptosis index (AI) was measured. Results Compared with LIP + I / R group and I / R group, the ALT, MDA, MPO and AI in ICT + I / R group decreased significantly at 2h after reperfusion (P <0.01) Compared with the I / R group, the levels of ALT, AST, MDA, AI in the ICT + I / R group decreased and SOD, NO, NOS and eNOS increased at the same time P <0.01). Conclusion Icaritin liposome can exert anti-rat liver I activity by increasing the content of SOD, decreasing the production of MDA, increasing the expression of eNOS, increasing the content of NO, inhibiting the accumulation of MPO and reducing the apoptosis of hepatocytes / R injury protection.