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目的探讨共济失调毛细血管扩张突变-蛋白激酶B(ATM-PKB/Akt)在梗死灶周围心肌中的改变及苯肾上腺素对其的干预效应。方法32只雄性SD大鼠分为心肌梗死组、假手术组、心肌梗死苯肾上腺素组、假手术苯肾上腺素组,每组8只。按Litwin方法建立心肌梗死及假手术模型。多谱勒超声仪测定心脏左室后壁厚度(LVPWd)、左室舒张末期内径(LVDd)和短轴缩短率(FS)、射血分数(EF);干预12周后Western blot检测梗死灶周围心肌中磷酸化共济失调毛细血管扩张突变蛋白(p-ATM)底物,免疫组化检测磷酸化蛋白激酶B(p-PKB/Akt)蛋白表达。结果干预后12周,与假手术组比较,心肌梗死组LVPWd增厚,LVDd显著变大,FS、EF显著降低(P<0.05)。与假手术苯肾上腺素组比较,心肌梗死苯肾上腺素组LVPWd、LVDd、FS、EF均无显著差异(P>0.05)。Western blot显示心肌梗死组与假手术组p-ATM底物蛋白表达无显著差异(P>0.05);与心肌梗死苯肾上腺素组(0.99±0.07)比较,心肌梗死组和假手术组p-ATM底物蛋白表达显著下调(P<0.05);与假手术苯肾上腺素组(0.65±0.04)比较,心肌梗死苯肾上腺素组p-ATM底物蛋白表达显著增高(P<0.05)。免疫组化显示心肌梗死组与假手术组p-Akt阳性细胞数无显著差异(P>0.05);与心肌梗死苯肾上腺素组(98.80±3.17)比较,心肌梗死组(74.38±3.06)和假手术组(74.50±3.99)阳性细胞数显著下调;与假手术苯肾上腺素组(75.88±2.77)比较,心肌梗死苯肾上腺素组阳性细胞数显著增高(P<0.05)。结论梗死灶周围心肌中ATM-Akt蛋白表达及活性无显著改变,但苯肾上腺素能显著增强ATM-Akt蛋白表达及活性。
OBJECTIVE: To investigate the alteration of ATM-PKB / Akt in myocardium around infarct and the effect of phenylephrine on it. Methods Thirty-two male Sprague Dawley rats were divided into myocardial infarction group, sham operation group, phenylephrine group and sham-operated phenylephrine group, with 8 rats in each group. Litwin method to establish myocardial infarction and sham model. Left ventricular posterior wall thickness (LVPWd), left ventricular end diastolic diameter (LVDd), short axis shortening (FS) and ejection fraction (EF) were measured by Doppler sonography. Cardiac phosphorylation of ataxia telangiectasia mutated protein (p-ATM) substrate, immunohistochemical detection of phosphorylated protein kinase B (p-PKB / Akt) protein expression. Results Compared with the sham-operation group, LVPWd increased, LVDd increased significantly, FS and EF decreased significantly (P <0.05) at 12 weeks after intervention. There was no significant difference in LVPWd, LVDd, FS and EF between the phenylephrine group and the sham-operated phenylephrine group (P> 0.05). The protein expression of p-ATM in myocardial infarction group and sham operation group was not significantly different (P> 0.05) by Western blot. Compared with phenylephrine group (0.99 ± 0.07) in myocardial infarction group, p-ATM (P <0.05). The protein expression of p-ATM in phenylephrine group was significantly higher than that in sham-operated group (0.65 ± 0.04) (P <0.05). Immunohistochemistry showed that there was no significant difference in the number of p-Akt positive cells between myocardial infarction group and sham operation group (P> 0.05). Compared with the phenylephrine group (98.80 ± 3.17), myocardial infarction group (74.38 ± 3.06) The number of positive cells in the operation group (74.50 ± 3.99) was significantly down-regulated. Compared with the sham group (75.88 ± 2.77), the number of phenylephrine positive cells in the myocardial infarction group was significantly increased (P <0.05). Conclusion ATM-Akt protein expression and activity in myocardium around the infarct area have no significant changes, but phenylephrine can significantly enhance the expression of ATM-Akt protein and activity.