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目的:观察穿心莲内酯(andrographolide,AP)对异丙肾上腺素(isopropylarterenol,Iso)所致大鼠心肌肥厚的保护作用及其对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)、心钠素(atrial natriuretic peptide,ANP)、内皮素(endothelin,ET)和一氧化氮(nitric oxide,NO)的影响。方法:以Iso 1 mg.kg-1背部皮下注射(sc)连续10 d建立大鼠心肌肥厚模型。选模第2天给药组sc给予低、中、高剂量(0.1,0.3,1.0μmol.kg-1)的AP,溶剂组sc二甲基亚砜,正常组和模型组sc给予生理盐水,连续14 d,末次给药后禁食12 h,取血,分离血清及血浆,取心肌组织并制成10%匀浆。酶活性分析法检测血清及心肌组织乳酸脱氢酶(lactate dehydrogenase,LDH)活性;硝酸还原酶法检测血清NO含量;放射免疫法测定血浆AngⅡ,ANP和ET的含量。结果:与正常对照组相比,模型组大鼠血清LDH活性升高(1 425.4±304.7)U.mL-1,(P<0.01),心肌组织LDH活性降低(662.5±172.6)U.g-1,(P<0.05),血浆ET(62.45±12.27)ng.L-1(P<0.05),含量升高,ANP(241.82±127.71)ng.g-1,(P<0.05)和NO(37.21±2.62)μmol.L-1(P<0.01)含量降低。与模型组相比,AP处理后血清LDH活性降低(P<0.001),组织LDH活性升高(P<0.05),血浆AngⅡ及ET含量下降(P<0.05),而血浆ANP含量及血清NO含量升高(P<0.05)。结论:穿心莲内酯可能通过影响大鼠血管活性物质的平衡,抑制RAS系统及ET的合成,增加ANP及NO的合成,从而抑制心肌肥大及心力衰竭的进程,对心脏起保护作用。
OBJECTIVE: To observe the protective effect of andrographolide (AP) on myocardial hypertrophy induced by isopropylarterenol (Iso) and its effect on angiotensinⅡ (AngⅡ), atrial natriuretic peptide , ANP), endothelin (ET) and nitric oxide (NO) were measured. Methods: The rat model of myocardial hypertrophy was established by subcutaneous injection of Sc (Iso) 1 mg.kg-1 for 10 days. On day 2 of model selection, low, medium and high dose (0.1,0.3,1.0μmol.kg-1) APs were administered to the sc administration group, sc dimethyl sulfoxide control group was administered to the sc administration group, sc saline was given to the normal and model groups, For 14 days, the rats were fasted for 12 hours after the last administration, blood was taken and serum and plasma were separated. Cardiac tissue was taken and made into 10% homogenate. The activity of lactate dehydrogenase (LDH) in serum and myocardium was detected by enzyme activity assay, the content of NO was detected by nitrate reductase method, and the levels of AngⅡ, ANP and ET were measured by radioimmunoassay. Results: Compared with the normal control group, the serum LDH activity in model group was significantly higher than that in normal control group (1 425.4 ± 304.7 U.mL-1, P <0.01), LDH activity in myocardium was lower (662.5 ± 172.6) (P <0.05), plasma ET (62.45 ± 12.27) ng.L-1 (P <0.05) 2.62) μmol.L-1 (P <0.01). Compared with model group, serum LDH activity decreased (P <0.001), LDH activity increased (P <0.05), plasma AngⅡ and ET contents decreased (P <0.05), while plasma ANP content and serum NO content Increased (P <0.05). Conclusion: Andrographolide may protect heart by inhibiting the balance of vasoactive substances, inhibiting the synthesis of RAS system and ET, increasing the synthesis of ANP and NO, and thus inhibiting cardiac hypertrophy and heart failure.