过氧化物酶增殖体激活受体β对急性肺损伤大鼠肺组织细胞凋亡的作用机制及影响

Mechanism and effect of peroxisome proliferators-activated receptor-β on acute lung injury in rats with lung tissue apoptosis

目的探讨过氧化物酶增殖体激活受体β(PPARβ)在急性肺损伤(ALI)发生发展中对肺组织细胞凋亡可能的作用机制,以期从新的视角揭示ALI的发病机理,并为ALI的防治提供新的理论基础。方法参照Cainazzo et al.方法复制失血性休克大鼠ALI模型,测定动脉血氧分压(PaO2)、肺泡灌洗液(BALF)及肺组织细胞凋亡率、计算肺组织湿/干重(W/D)值、病理形态学检查。采用PPARβ的激动剂对大鼠ALI模型进行干预,观察其对失血性休克ALI大鼠的BALF细胞和肺组织细胞凋亡的影响。结果应用PPARβ的激动剂后大鼠的PaO2较对照组显著升高(P<0.05),BALF及肺组织细胞凋亡率、W/D值、肺组织病理学积分均较对照组显著降低(P<0.05)。结论 PPARβ的激动剂对ALI肺组织有一定程度的保护作用,其作用机制是通过抑制炎症反应,减少炎性介质分泌,促进炎症细胞凋亡及减少肺组织细胞凋亡实现的。

Objective To explore the mechanism and effect of peroxisome proliferators-activated receptor-β（ PPAR-β） on acute lung injury （ ALI） in rats with lung tissue apoptosis. Methods The arterial blood oxygen par-tial pressure （PaO2） and BALF were detected, the rate of lung tissue apoptosis and lung wet/dry weight （W/D） were calculated. Their pathological morphology was checked. It used PPAR-β activator to intervene on ALI in rat model. ALI uncontrolled hemorrhagic shock and BALF cell apoptosis of lung tissue were observed. Results The lev-el of PaO2 was obviously higher in the study group than in the control group （P＆lt;0. 05）, and the decrease of BALF, lung tissue apoptosis rate, W/D value and lung tissue pathology score was more pronounced in the study group than in the control group （P〈0. 05）. Conclusion PPAR-βagonists has a certain degree of protection for ALI lung tissue, which mechanism of action is by inhibiting the inflammatory reaction and reducing the secretion of inflammatory medi-ators.