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目的:观察穿心莲内酯对去甲肾上腺素所致心肌肥厚大鼠的肌浆网Ca2+-Mg2+-ATPase活性的影响。方法:将40只雄性SD大鼠随机分为正常对照组(n=8)与心肌肥厚模型组(n=32),心肌肥厚组再分为4个亚组(n=8):模型组、穿心莲内酯高剂量组、穿心莲内酯低剂量组和二甲基亚砜(DSMO),采用腹腔注射去甲肾上腺素(NE)1.5mg·(kg·d)-1,2次/d,连续15d,建立大鼠心肌肥厚模型。次日麻醉后分别静脉输注生理盐水、不同剂量的穿心莲内酯及DSMO,输注30min后处死大鼠,测定心肌组织Ca2+-Mg2+-ATPase活性。结果:与正常组相比,模型组心肌肌浆网Ca2+-Mg2+-ATPase活性降低(P<0.01),与模型组相比,高剂量及低剂量穿心莲内酯治疗组心肌肌浆网Ca2+-Mg2+-ATPase活性显著升高(P<0.01),且呈现剂量依赖性效应。结论:穿心莲内酯可提高Ca2+-Mg2+-ATPase活性,从而抑制心脏纤维化,起到抗心肌肥厚作用。
AIM: To observe the effects of andrographolide on sarcoplasmic reticulum Ca2 + -Mg2 + -ATPase activity in normoxia-induced hypertrophic rats. Methods: Forty male SD rats were randomly divided into normal control group (n = 8) and cardiac hypertrophy model group (n = 32). Cardiac hypertrophy group was further divided into 4 subgroups (n = 8) High-dose andrographolide group, low-dose andrographolide group and dimethyl sulfoxide (DSMO) were injected intraperitoneally (NE 1.5 mg · kg -1) twice a day 15d, rat model of cardiac hypertrophy was established. After the next day of anesthesia, intravenous infusion of normal saline, different doses of andrographolide and DSMO were given respectively. Rats were sacrificed 30min after infusion, and the activity of Ca2 + -Mg2 + -ATPase in myocardium was measured. Results: Compared with the normal group, the activity of Ca2 + -Mg2 + -ATPase in the sarcoplasmic reticulum decreased (P <0.01) in the model group. Compared with the model group, Ca2 + -Mg2 + -ATPase activity was significantly increased (P <0.01), and showed a dose-dependent effect. Conclusion: Andrographolide can increase the activity of Ca2 + -Mg2 + -ATPase, thereby inhibiting cardiac fibrosis and playing a role in anti-hypertrophy.