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目的用组织浴槽血管环技术研究细胞外信号调节激酶1/2(extracellular regulated protein kinases1/2,ERK1/2)通路和血管内皮细胞在15-KETE诱导缺氧大鼠肺动脉收缩中的作用。方法 16只体质量为(220±20)g清洁级Wistar大鼠随机分为2组(n=8),正常对照组置于正常环境中饲养(FiO2=21%),缺氧组置于缺氧的培养箱中饲养(FiO2=10%),连续饲养9 d后处死,游离直径约为0.5—1.0 mm肺内肺动脉(PA)。剪成3 mm长的动脉环,在组织浴槽内进行张力研究。比较在15-KETE给药前后肺动脉环张力变化;机械法去除动脉环内皮,比较内皮完整和去内皮后,15-KETE对缺氧性肺动脉环的收缩作用;用ERK1/2上游激酶抑制剂U0126孵育肺动脉环,比较U0126孵育前后15-KETE对缺氧性肺动脉环的收缩作用;机械法去除动脉环内皮,再比较U0126孵育前后15-KETE对缺氧性肺动脉环的收缩作用。结果 1)15-KETE对缺氧大鼠肺动脉环有收缩作用,呈浓度一效应关系,与正常对照组比较差异显著(P<0.05);2)内皮完整和内皮去除的肺动脉环,15-KETE对其缩血管作用均受到抑制,但差异显著(P<0.05);3)内皮完整肺动脉环,在U0126孵育前后,15-KETE的缩血管作用均受到抑制,但差异显著(P<0.05);4)内皮去除的肺动脉环,U0126孵育前后,15-KETE的缩血管作用也受到抑制,差异显著(P<0.05)。结论 15-KETE可浓度依赖性地收缩缺氧大鼠肺动脉环;15-KETE引起缺氧肺动脉收缩可能与ERK1/2信号转导通路和血管内皮细胞有关,并且位于平滑肌的ERK1/2通路也参与15-KETE诱导缺氧大鼠肺动脉环的收缩。
Objective To investigate the role of extracellular regulated protein kinase 2 (ERK1 / 2) pathway and vascular endothelial cells in the contraction of pulmonary arteries induced by 15-KETE in hypoxic rats using tissue bath vascular ring technique. Methods Sixteen Wistar rats of (220 ± 20) g clean grade were randomly divided into two groups (n = 8). The normal control group was housed in normal environment (FiO2 = 21% Oxygen incubator (FiO2 = 10%). After continuous feeding for 9 days, they were sacrificed and their free pulmonary artery (PA) diameter was about 0.5-1.0 mm. Cut into 3 mm long arterial rings and study the tension in the tissue bath. Kinetic method was used to remove the endothelium of the arterial rings, and 15-KETE was used to compare the contractile effects of 15-KETE on the hypoxic pulmonary rings. The ERK1 / 2 upstream kinase inhibitor U0126 The pulmonary artery rings were incubated, and the contractile effect of 15-KETE before and after U0126 incubation on the hypoxic pulmonary rings was compared. The endothelium of the arterial rings was removed mechanically, and the contractile effect of 15-KETE on hypoxic pulmonary rings was compared before and after U0126 incubation. Results 1) 15-KETE had a synergistic effect on the pulmonary artery rings in hypoxic rats, showing a concentration-effect relationship with the normal control group (P <0.05). 2) Endothelium-intact and endothelium- (P <0.05); 3) Endothelium intact pulmonary artery rings inhibited the vasoconstriction of 15-KETE before and after U0126 incubation, but the difference was significant (P <0.05); 4) Endothelium removal of pulmonary artery rings, U0126 before and after incubation, 15-KETE vasoconstriction was also inhibited, the difference was significant (P <0.05). Conclusions 15-KETE can attenuate the pulmonary artery rings of hypoxia rats in a concentration-dependent manner. The contraction of hypoxic pulmonary arteries induced by 15-KETE may be related to the ERK1 / 2 signal transduction pathway and vascular endothelial cells, and the ERK1 / 2 pathway in smooth muscle is also involved 15-KETE induces contraction of pulmonary artery rings in hypoxic rats.