希望Ⅱ号对被动吸烟小鼠心脏的保护作用

摘要

目的 观察希望Ⅱ号对被动吸烟小鼠心脏的保护作用,并探究其作用机制.方法 将72只雄性昆明种小鼠随机分为6组,分别为对照组,模型组,阳性药组,希望Ⅱ号低、中、高剂量组.对照组暴露于实验室空气中,模型组每日暴露于香烟烟雾3 h,持续45 d,至第16天开始给药,第45天处死小鼠,分离心脏.检测心脏丙二醛(malondialdehyde, MDA)含量,总超氧化物歧化酶(total superoxide dismutase, T-SOD)、铜锌超氧化物歧化酶(copper-zinc superoxide dismutase, Cu-ZnSOD)、髓过氧化物酶(myeloperoxidase, MPO)活性.进行心脏组织形态学观察,计算心脏胶原纤维面积比,采用免疫组织化学法检测心脏转化生长因子β1(transforming growth factor beta 1, TGF-β1)表达水平.结果 与对照组比较,模型组Cu-ZnSOD、T-SOD活性显著降低(P<0.05),MPO活性和MDA含量显著升高(P<0.05),心肌纤维比显著增加(P<0.05),心脏TGF-β1表达水平显著升高(P<0.05).与模型组比较,希望Ⅱ号低、中、高剂量组Cu-ZnSOD、T-SOD活性显著升高(P<0.05),MPO活性、MDA含量、心肌纤维比、心脏TGF-β1表达水平显著降低(P<0.05).结论 希望Ⅱ号对被动吸烟小鼠心脏的保护作用与调节心脏氧化应激反应有关.%Objective To investigate the cardioprotective effect of Xiwang Ⅱ in mice exposed to passive smoking and its mechanism of action.Methods A total of 72 male Kunming mice were randomly divided into control group, model group, positive drug group, and low-, middle-, and high-dose Xiwang Ⅱ groups.The mice in the control group were exposed to laboratory air, and those in the model group were exposed to cigarette smoke for 45 consecutive days (3 hours a day).The drugs were administered since day 16 of exposure and the mice were sacrificed on day 45 to collect heart tissue.The level of malondialdehyde (MDA) in the heart was measured, as well as the activities of cardiac total superoxide dismutase (T-SOD),copper-zinc superoxide dismutase (Cu-ZnSOD), and myeloperoxidase (MPO).The histomorphological features of the heart were observed and the collagen fiber area in the heart was calculated.Immunohistochemistry was used to measure the expression of transforming growth factor-β1 (TGF-β1) in the heart.Results Compared withthe control group, the model group had significant reductions in the activity of Cu-ZnSOD and T-SOD (P<0.05) and significant increases in MPO activity, MDA level, cardiac muscle fibers, and TGF-β1 expression (all P<0.05).Compared with the model group, the low-, middle-, and high-dose Xiwang Ⅱ groups had significant increases in the activities of Cu-ZnSOD and T-SOD (P<0.05) and significant reductions in MPO activity, MDA level, cardiac muscle fibers, and TGF-β1 expression (all P<0.05).Conclusion Xiwang Ⅱ exerts its cardioprotective effect on mice exposed to passive smoking by regulating oxidative stress response in the heart.