UNASSIGNED: We injected the antigen peptide segment of the β1AR into the postpartum Wistar rats to make the immune models and their cardiac function was detected by echocardiography. Also, the concentration of β1AR antibodies and apoptosis rate of left ventricular myocytes was tested by SA-ELISA, TUNEL, HE staining, qRT-PCR and western blot methods. Finally, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and its related proteins were examined by qRT-PCR and western blot methods.
UNASSIGNED: We found that the level of β1AR antibodies in the serum was significantly increased and the postpartum rats exhibited symptoms of PPCM after autoimmunity. Moreover, the expression of peroxisome PGC-1α, which was a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF), was decreased in autoimmune perinatal rats. In addition, the expression of the apoptosis factor caspase 3 as well as the apoptosis rate of left ventricular myocytes was significantly increased.
UNASSIGNED: The results suggested that the symptoms of PPCM that appeared in autoimmune perinatal rats may be due to the increase of β1AR antibodies, which inhibited the pathway associated with peroxisome PGC-1α.
■我们将β1AR的抗原肽段注射到产后Wistar大鼠中进行免疫模型,并通过超声心动图检测其心功能。此外,用SA-ELISA法检测β1AR抗体浓度和左心室细胞凋亡率,TUNEL,HE染色,qRT-PCR和蛋白质印迹方法。最后,通过qRT-PCR和Westernblot方法检测过氧化物酶体增殖物激活受体γ共激活因子-1α(PGC-1α)及其相关蛋白的表达。
■我们发现血清中β1AR抗体水平显着升高,产后大鼠在自身免疫后表现出PPCM症状。此外,过氧化物酶体PGC-1α的表达,它是线粒体代谢的主要调节因子,及其下游转录物血管内皮生长因子(VEGF),在自身免疫性围产期大鼠中降低。此外,凋亡因子caspase3的表达以及左心室心肌细胞的凋亡率明显升高。
■结果表明,自身免疫性围产期大鼠出现的PPCM症状可能是由于β1AR抗体的增加,抑制与过氧化物酶体PGC-1α相关的途径。