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Background: Research indicates that, in myocardial tissue in acute myocardial ischemia calcitonin gene-related peptide (CGRP), norepinephrine (NE) levels are significantly higher, the adrenergic system and sensory nerves are involved in myocardial ischemic injury and protection, but its mechanism of action has not been elucidated. The desire to experiment from the cellular level describes its role, and its mechanism. Objective: To observe the calcitonin gene-related peptide (CGRP) to norepinephrine (NE)-induced apoptosis of neonatal rat cardiomyocytes, and its relationship with PKA and PKC signal transduction system. Research Contents and Methods: (1) culture and identification of myocardial cells. Sprague-Dawley (SD) rats were chosen 1-3d age established neonatal rat cardiomyocytes cultured in vitro model of myocardial cells were identified by immunocytochemical staining (SABC method). (2) CGRP NE-induced myocardial cell apoptosis NE PKA inhibitor H89 CGRP, CGRP receptor antagonist CGRP8-37 compatibility, the formation of the following combinations: control group (C group), NE (10-5M ) group, NH (NE 10-5M H893 × 10-5M) group and NC group (NE 10-5M CGRP 10-8M), NC8 (NE 10-5M CGRP 10-8M CGRP8-3710-7m), by TUNEL assay apoptosis of myocardial cells to calculate the rate of cardiac myocyte apoptosis. (3) CGRP NE-induced myocardial cells PKA pathway grouped with experiment 2, extract of cultured myocardial cells protein with a non-reflective kit to detect the activity of PKA (4) CGRP on NE-induced myocardial cells PKC signaling pathways divided into group C NE group, the NC group, the NC8 group (specifically, the same experiment 2), extraction cultured myocardial cell protein with a non-reflective kit (1) myocardial cells were successfully cultured to detect the activity of PKC experimental results shows that synchronization beating myocardial cells, immunohistochemical identification of success, more than 98% of the cells into cardiomyocytes. (2) a: Compared with the control group, NE group, NC8 rate of apoptosis was significantly higher; B: compared with the NE group, NH group, NC group apoptosis rate was significantly lower (P lt; 0.05) (3) a: Compared with the control group, NE group, NC group PKA activity increased, the NH group of PKA activity decreased (P lt; 0.05); b: NC group, NC8 NE group difference was not statistically significant (P gt; 0.05); c: the NC group NC8 group difference was statistically significant (P lt; 0.05). (4) a: Compared with control group, the NE group, NC group, NC8 PKC activity were significantly higher (P lt; 0.05); B: NE group, NC group, NC8 between PKC activity was no significant difference (P GT; 0.05). Conclusion 1.PKA signaling pathway may be involved in NE-induced cardiac myocyte apoptosis. 2.CGRP antagonistic NE-induced myocardial apoptosis. 3.CGRP than through regulation of PKA or PKC signaling pathway, inhibition of NE-induced cardiac myocyte apoptosis. Its mechanism of action is to be discussed.
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