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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Calcitonin gene related peptide (CGRP) inhibits norepinephrine induced apoptosis in cultured rat cardiomyocytes not via PKA or PKC pathways.
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Calcitonin gene related peptide (CGRP) inhibits norepinephrine induced apoptosis in cultured rat cardiomyocytes not via PKA or PKC pathways.

机译：降钙素基因相关肽（CGRP）通过PKA或PKC途径抑制去甲肾上腺素诱导的大鼠心肌细胞凋亡。

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Evidence showed overrelease of norepinephrine can induce apoptosis in ventricle myocytes. Calcitonin gene related peptide and norepinephrine could be simultaneously up-regulated in early time of acute myocardial ischemia, suggesting a co-participation of calcitonin gene related peptide and norepinephrine in the pathology. In this study, we investigated a potential anti-apoptotic effect of calcitonin gene related peptide on myocardial apoptosis induced by norepinephrine and its link with the protein kinase A (PKA) or protein kinase C (PKC) pathway in cultured neonatal rat cardiomyocytes. Cultured cardiomyocytes were exposed to one of the treatments, separately: (1) 3 ml DMEM culture medium, (2) norepinephrine (10(-5)mol/l), (3) H89 (3 x 10(-5)mol/l), a specific PKA inhibitor, with norepinephrine (10(-5)mol/l), (4) calcitonin gene related peptide at a range of concentrations (10(-9)mol/l, 10(-8)mol/l and 10(-7)mol/l) with norepinephrine (10(-5)mol/l) and (5) calcitonin gene related peptide (10(-8)mol/l) with norepinephrine (10(-5)mol/l)+CGRP(8-7) (10(-7)mol/l), a specific antagonist of calcitonin gene related peptide receptor. Then, apoptosis rate and the activity of PKA and PKC were examined. The dose of norepinephrine induced a marked increase in apoptosis of the myocytes (31+/-2%), compared to the control (17+/-4%, p<0.05). The pro-apoptotic effect of norepinephrine was attenuated by H89 (3 x 10(-5)mol/l) or by calcitonin gene related peptide which could be completely reversed by CGRP(8-37). The activities of PKA and PKC were increased by norepinephrine but no difference in the activities of PKA and PKC was detected in the presence and absence of co-treatment with calcitonin gene related peptide (10(-8)mol/l). Calcitonin gene related peptide inhibits norepinephrine induced apoptosis in cultured cardiomyocytes, which is mediated by CGRP receptor but unlikely to be mediated by PKA or PKC pathway.
机译：有证据表明去甲肾上腺素的过度释放可以诱导心室肌细胞凋亡。降钙素基因相关肽和去甲肾上腺素可在急性心肌缺血的早期同时上调，提示降钙素基因相关肽和去甲肾上腺素共同参与病理。在这项研究中，我们调查了降钙素基因相关肽对去甲肾上腺素诱导的心肌细胞凋亡的潜在抗凋亡作用及其与培养的新生大鼠心肌细胞中蛋白激酶A（PKA）或蛋白激酶C（PKC）途径的联系。将培养的心肌细胞分别暴露于一种处理方法：（1）3 ml DMEM培养基，（2）去甲肾上腺素（10（-5）mol / l），（3）H89（3 x 10（-5）mol / l l），一种特定的PKA抑制剂，具有去甲肾上腺素（10（-5）mol / l），（4）降钙素基因相关肽，浓度范围为（10（-9）mol / l，10（-8）mol / l l和10（-7）mol / l）与去甲肾上腺素（10（-5）mol / l）和（5）降钙素基因相关肽（10（-8）mol / l）与去甲肾上腺素（10（-5）mol / l）+ CGRP（8-7）（10（-7）mol / l），降钙素基因相关肽受体的特异性拮抗剂。然后，检查细胞凋亡率以及PKA和PKC的活性。与对照组相比（17 +/- 4％，p <0.05），去甲肾上腺素的剂量诱导了心肌细胞凋亡的显着增加（31 +/- 2％）。去甲肾上腺素的促凋亡作用被H89（3 x 10（-5）mol / l）或降钙素基因相关肽减弱，而CGRP（8-37）可以完全逆转。去甲肾上腺素可增加PKA和PKC的活性，但是在存在和不存在与降钙素基因相关肽（10（-8）mol / l）共同治疗的情况下，PKA和PKC的活性均未发现差异。降钙素基因相关肽抑制去甲肾上腺素诱导的培养的心肌细胞凋亡，这是由CGRP受体介导的，但不太可能由PKA或PKC途径介导。

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