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目的:观察β-七叶皂苷钠对大鼠视网膜缺血-再灌注损伤后诱导型一氧化氮合酶(i NOS)及Caspase-2表达的影响,探讨其对缺血-再灌注视网膜保护作用可能的机制。方法:SD大鼠随机分为正常对照组、缺血-再灌注模型组、β-七叶皂苷钠组。通过前房灌注法建立视网膜缺血-再灌注损伤模型。分别于术后12、24 h行免疫组化、实时荧光定量RT-PCR检测i NOS的表达,免疫组化检测Caspase-2的表达。结果:免疫组化、RT-PCR均显示与相同时间点模型组比较,β-七叶皂苷钠组i NOS表达显著降低(P<0.01),免疫组化显示与相同时间点模型组比较,β-七叶皂苷钠组Caspase-2表达显著降低(P<0.01)。结论:β-七叶皂苷钠可能通过抑制i NOS的表达,减少视网膜神经细胞的凋亡,对视网膜缺血-再灌注损伤发挥保护作用。
Objective: To observe the effect of β-aescinate on the expression of inducible nitric oxide synthase (iNOS) and Caspase-2 after retinal ischemia-reperfusion injury in rats and its protective effect on retinal ischemia-reperfusion injury Possible mechanism. Methods: SD rats were randomly divided into normal control group, ischemia-reperfusion model group and β-aescinate sodium group. Retinal ischemia-reperfusion injury model was established by anterior chamber perfusion. Immunohistochemistry was performed at 12 and 24 hours after operation. The expression of iNOS was detected by real-time fluorescence quantitative RT-PCR and the expression of Caspase-2 was detected by immunohistochemistry. Results: Immunohistochemistry and RT-PCR showed that the expression of iNOS was significantly decreased in the β-aesculin sodium group (P <0.01) compared with the model group at the same time point. Immunohistochemistry showed that β Caspase - 2 expression in sodium aescinate group was significantly decreased (P <0.01). CONCLUSION: Sodium β-aescinate may play a protective role on retinal ischemia-reperfusion injury by inhibiting the expression of iNOS and decreasing the apoptosis of retinal neurons.