三七总皂甙对肺缺血再灌注损伤时氧化应激及TXA_2/PGI_2失衡的影响

Influence of Panax notoginsenosides on the change of oxidative stress and the relation- ship between Thromboxance A2 and Prostacyclin induced by lung ischemia-reperfusion injury

目的:探讨氧自由基(OFR)和血栓素A2(TXA2)、前列环素(PGI2)在肺缺血再灌注损伤(IRI)中的作用以及三七总皂甙对其影响。方法:复制在体兔肺IRI模型。30只日本大耳兔,随机均分为三组:假手术组(S组)、缺血再灌注组(IR组)和缺血再灌注+三七总皂甙注射液组(PSN组)。检测血清超氧化物歧化酶(SOD)活性、黄嘌呤氧化酶(XO)活性和丙二醛(MDA)浓度,测定肺组织TXB2、6-keto-PGF1 α含量与比值的变化。结果:IR组血清XO、MDA均显著高于S组,SOD明显低于S组(均P<0．05和P<0．01)。 IR组肺组织TXB2显著高于S组(P<0．01),6-keto-PGF1α差异无明显;PNS组与IR组相比TXB2均下降非常明显(P<0．01),TXB2/6-keto-PGF1α降低很显著(P<0．01),与IR组相比差异有显著性(P<0．05和 P<0．01)。结论:三七总皂甙能降低氧自由基水平,抑制血小板释放TXA2,调控TXA2/PGI2的平衡,通过遏制无复流现象,减轻肺IRI。

Objective： To explore the role of oxygen free redicals（OFR）, TXA2 and PGI2 in lung ischemia and reperfusion injury （IRI） and effect of Panax notoginsenosides injection on them. Methods： Rabbit lung model of ischemia reperfusion injury was constituted in vivo. Thirty rabbits were divided into three groups randomly： sham-operatlon group（group S）, ischemia reperfusion group（group IR） and ischemia reperfusion plus panax notoginsenosides injection（group PNS）. Malondialdehyde （MDA）,superoxide dismutase （SOD） and xanthine oxidase （XO） in serum were measured, and TXB2 and 6-keto-PGF1 α levels in lung tissue were separately measured with radioimmunoassay. Results： in IR group, XO and MDA increased and SOD decreased in serum, while the same changes happened in PI group but less severely. TXB2 levels in lung increased significantly （P〈0.01） while 6-keto-PGF1α shad not any remarkable change during lung ischemia-reperfusion compared with the S group. For the SI group protected with panax notoginsenosldes, as compared with IR group, TXB2 levels decreased very significantly （P〈0.01）, TXB2/6-keto-PGF1 α decreased very remarkably （P〈 0.01）. Conclusion： 0FR is an important factor during IRI, panax notoginsenosides may attenuate lung ischemia- reperfusion injury through dropping 0FR level and antagonizing oxidative stress, and inhibit platelet to release TXA2, regulate TXA2/ PGI2 balance and restrain no-fellow phenomenon, so that it has the protective effects on postischemia reperfusion lung. Prostacyclin;