不同剂量抗心衰颗粒对心衰大鼠治疗效果及原癌基因家族c-fos、c-myc表达影响

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目的:探讨抗心衰颗粒对SD大鼠心衰模型心功能及c-fos、c-myc影响,从而探讨其作用机制及合理剂量。方法:60只同源SD大鼠随机分为6组,冠状动脉结扎法建立心衰大鼠模型,另以假手术法作为对照,分别以抗心衰颗粒高、中、低剂量和卡托普利(阳性组)灌胃,模型组和对照组以等量生理盐水灌胃,8周后比较大鼠心功能及c-fos、c-myc表达。结果:与模型组相比,阳性组各指标出现明显改善(P<0.05),部分指标接近对照组(P>0.05),说明卡托普利对心衰大鼠具有较好治疗效果;抗心衰颗粒高、中剂量组各指标与阳性组接近(P>0.05),明显优于模型组(P<0.05),而低剂量组各指标虽然与模型组差异具有统计学意义(P<0.05),但在LVEF、LVEDd、LVMI仍与阳性组和高、中剂量组存在统计学差异(P<0.05);模型组c-fos、c-myc均高于对照组(P<0.05),阳性组、高剂量组和中剂量组c-fos、c-myc均高于对照组(P<0.05)且低于模型组(P<0.05),但低剂量组c-fos、c-myc高于对照组(P<0.05),与模型组差异无统计学意义(P>0.05)。结论:抗心衰大鼠在高、中剂量时可以改善心功能,其机制复杂,可能与其抑制心衰大鼠心肌c-fos和c-myc表达、拮抗心肌重构有关。 Objective: To investigate the effect of anti-heart-failure granules on cardiac function and c-fos, c-myc in SD rat model of heart failure and to explore its mechanism of action and reasonable dosage. Methods: Sixty homologous SD rats were randomly divided into 6 groups. Coronary artery ligation was used to establish a rat model of heart failure. Sham-operated rats were used as the control. High, medium and low doses of anti-heart failure granules, The rats in the model group and the control group were intragastrically administrated with equal volume of saline, and the cardiac function and the expression of c-fos and c-myc in rats were compared 8 weeks later. Results: Compared with the model group, each index of the positive group was significantly improved (P <0.05), and some of the indicators were close to the control group (P> 0.05), indicating that captopril has a good therapeutic effect on heart failure rats; (P <0.05), which was significantly better than that of the model group (P <0.05), while the indexes of low dose group and the model group were statistically significant (P <0.05) , But the levels of c-fos and c-myc in model group were higher than those in control group (P <0.05), but there was no significant difference between LVEF, LVEDd and LVMI in positive group and high and medium dose group , C-fos and c-myc in high dose group and middle dose group were significantly higher than those in control group (P <0.05) and lower than those in model group (P <0.05) Group (P <0.05), but no significant difference with model group (P> 0.05). CONCLUSION: The anti-heart failure rats can improve cardiac function at high and medium doses. The mechanism is complex, which may be related to inhibiting the expression of c-fos and c-myc and antagonizing myocardial remodeling in heart failure rats.
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