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目的:观察染料木素(Gen)对异丙肾上腺素(Iso)所致心肌肥厚大鼠的抗氧化及抑制炎症反应作用。方法:采用背部sc给予Iso 1 mg.kg-1.d-1,连续10 d,建立大鼠心肌肥厚模型。造模第2天,正常对照组及模型组于背部sc给予NS2 mL.kg-1.d-1,溶剂对照组给予等体积7%DMSO,Gen组给予等体积的Gen 0.03,0.1,0.3μmol.kg-1,连续14 d。末次给药后禁食12 h,称体重,麻醉,取静脉血,分离血清,取心脏,称左心室质量,计算左心室质量参数;检测血清超氧化物歧化酶(superoxide dismutase,SOD)、髓过氧化物酶(myeloperoxidase,MPO)活性及丙二醛(malondialdehyde,MDA)含量;放射免疫学方法检测心肌组织白细胞介素2(interleukin-2,IL-2)含量。结果:与正常对照组相比,模型组大鼠左心室质量参数明显升高(2.48±0.11)mg.kg-1,P<0.001,血清SOD活性明显降低(128.19±11.20)U.mL-1,P<0.05,血清MDA含量增高(15.81±1.96)mmol.mL-1,P<0.05,血清MPO活性提高(12.22±2.34)U.mL-1,P<0.05,心肌组织IL-2含量增高(11.41±1.08)pg.mgprot-1,P<0.05。染料木素低、中、高剂量明显提高血清SOD活性(160.47±16.01,164.36±9.39,172.03±8.42)U.mL-1,P<0.01,降低血清MDA含量(11.96±2.17,11.72±0.73,10.93±0.52)mmol.mL-1,P<0.05,降低血清MPO活性(9.84±2.03,8.91±2.03,7.51±1.97)U.mL-1,P<0.01,降低心肌组织IL-2含量(9.70±1.81,5.95±3.39,6.33±1.19)pg.mg prot-1,P<0.05。结论:染料木素可通过提高抗氧化能力及抗炎症反应抑制Iso诱导的大鼠心肌肥厚。
OBJECTIVE: To observe the effect of genistein on the anti-oxidative and anti-inflammatory responses of rats with myocardial hypertrophy induced by isoproterenol (Iso). Methods: The rat model of myocardial hypertrophy was established by sc sc administration of Iso 1 mg.kg-1.d-1 for 10 days. On the second day after model establishment, normal control group and model group were given NS2 mL.kg-1.d-1 sc on the back, and the solvent control group was given an equal volume of 7% DMSO. The Gen group was given equal volume of Gen 0.03,0.1,0.3 μmol kg-1 for 14 days. After the last administration, rats were fasted for 12 hours, and then weighed, anesthetized, venous blood was taken, serum was separated, the left ventricular mass was taken, and the left ventricular mass was calculated. The serum superoxide dismutase (SOD) The activity of myeloperoxidase (MPO) and the content of malondialdehyde (MDA) were determined. The content of interleukin-2 (IL-2) in myocardium was detected by radioimmunoassay. Results: Compared with the normal control group, the left ventricular mass index of the model group was significantly increased (2.48 ± 0.11) mg.kg-1, P <0.001, and the serum SOD activity was significantly decreased (128.19 ± 11.20) U.mL-1 (P <0.05). The level of MDA in serum increased (15.81 ± 1.96) mmol.mL-1, P <0.05, the level of MPO increased (12.22 ± 2.34) U.mL- (11.41 ± 1.08) pg.mgprot-1, P <0.05. Low, medium and high doses of genistein significantly increased serum SOD activity (160.47 ± 16.01,164.36 ± 9.39,172.03 ± 8.42) U.mL-1, P <0.01, decreased serum MDA content (11.96 ± 2.17, 11.72 ± 0.73, 10.93 ± 0.52) mmol.mL-1, P <0.05, lower serum MPO activity (9.84 ± 2.03,8.91 ± 2.03,7.51 ± 1.97) U.mL-1, P <0.01, reduce myocardial IL-2 content ± 1.81, 5.95 ± 3.39, 6.33 ± 1.19) pg.mg prot-1, P <0.05. Conclusion: Genistein can inhibit the myocardial hypertrophy induced by Iso in rats by enhancing the anti-oxidative and anti-inflammatory responses.