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比索洛尔对β1肾上腺素受体自身抗体阳性心力衰竭大鼠Bcl-2/Bax的影响 被引量:2

The effects of bisoprolol on Bcl-2/Bax in heart failure rats with positive cardiac β_1-AR autoantibodies
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摘要 目的探讨比索洛尔在降低β1肾上腺素受体(β1-AR)自身抗体阳性率和抗体滴度的同时,是否可以抑制细胞凋亡。方法将90只SD大鼠中80只采用缩窄腹主动脉方法,建立心力衰竭的大鼠模型,15只死亡,入组65只,将大鼠随机分为治疗组(40只)和非治疗组(25只)。治疗组接受比索洛尔4周治疗后,应用ELISA技术检测两组大鼠血清β1-AR自身抗体阳性率和滴度。应用免疫组织化学测两组大鼠血清β1-AR自身抗体阳性的Bax/Bcl-2。结果治疗组较治疗前β1-AR自身抗体阳性率降低27.5%(P<0.05);非治疗组无统计学差异(P>0.05);治疗组较治疗前β1-AR自身抗体滴度降低(P<0.01);非治疗组β1-AR自身抗体阳性滴度无显著差异(P>0.05);治疗组中Bcl-2的表达在β1-AR自身抗体阳性大鼠比阴性大鼠、非治疗组β1-AR阳性大鼠明显增高(P<0.01);Bax的表达比非治疗组阳性大鼠降低(P<0.01);且比同组阴性略有降低。结论比索洛尔治疗降低心力衰竭大鼠β1-AR自身抗体阳性率及抗体滴度,升高了β1-AR自身抗体阳性心力衰竭大鼠Bcl-2/Bax的比值。 Objective To explore whether bisoprolol can inhibit cardiomyocyte apoptosis simultaneously with reduction of the positive rate and antibody titer of β1-AR autoantiboclies. Methods Eighty of 90 male SD rats underwent constriction of the abdominal aorta to establish heart failure model. Sixty five of them were randomly divided into treatment group and without treatment group. ELISA was used to measure β1-AR sutoantibody positive rate and average titer. Immuno histochemistry was used to measure Bcl-2/Bax. Results After bisoprolol treatment, β1-AR autoantibocly positive rate( P 〈0.05) was reduced by 27.5% as compared with before treatment, while there was no change in without treatment group( P 〉0.05). Titer of β1-AR autoantiboclies in the treatment group decreased significantly ( P 〈0.01);while there was no significant change in without treatment group( P 〉0.05). Expression of Bcl-2 in treatment group with positive cardiac β1-AR autoantibodies was significantly increased as compared with that in β1-AR antibody negative and without treatment rats( P 〈0.01). Expression of Bax in treatment group with posi rive cardiac β1- AR autoantiboclies was depressed significantly as compared with that in without treatment group ( P 〈0.01), and slightly decreased as compared with that in negative group. Conclusions After bisoprolol treatment,β1-AR autoantiboclies positive rate and average titer are decreased,and Bcl-2/Bax ratio in heart failure rats with positive cardiac β1-AR autoantibodies is increased.
出处 《中华老年心脑血管病杂志》 CAS 北大核心 2008年第4期297-299,共3页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词 心力衰竭 充血性 比索洛尔 受体 肾上腺素能β1 自身抗体 heart failure, congestive bisoprolol receptors, aclrenergic, beta-1 autoantiboclies
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  • 1Luciano DL,Barbara R,Valerio G, et al. Skeletal muscle myofibrillar protein oxidation in heart fallure and the protective effect of carvedilol. J Mol Cell Cardiol, 2005,38 : 803-807.
  • 2Barrell GK. Immunological influences on reproductive neuroendocrinology. Soc Reprod Fertil Supp, 2007,64 :109-122.
  • 3Brooks C, Dong Z. Regulation of mitochondrial morphological dynamics during apoptosis by bcl-2 family proteins: a key in bak? Cell Cycle,2007,6:3043-3047.
  • 4Tan C, Dlugosz PJ,Peng J, et al. Auto activation of the apoptosis protein Bax increases mitochondrial membrane permeability and is inhibited by Bcl-2. J Biol Chem,2006,281 : 14764-14775.

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