| Objective:A short high-intensity intermittent exercise can induce endogenous myocardial protection, reduce myocardial injury, this process are called exercise preconditioning(EP). The research and clinical trials of protection induced by EP have been extensively developed, but more focused on the delta and epsilon PKC, and the role of alpha PKC in EP protective effect is still unclear. Using alpha PKC inhibitors chelerythrine chloride(CHE) to observing the change of alpha PKC activation and translocation during the early and late stage of EP myocardial protection, proving whether alpha PKC in mediated EP myocardial protection or not, provides reference and theoretical basis for EP studies and clinical trials.Methods:SD rats randomly divided into8groups:control (C) group, exhaustive exercise (EE) group, early exercise preconditioning (EEP) group, late exercise preconditioning (LEP) group, early exercise preconditioning plus exhaustive exercise (EEP+EE) group, late exercise preconditioning plus exhaustive exercise (LEP+EE) group, chelerythrine chloride plus early exercise preconditioning plus exhaustive exercise (CHE+EEP+EE) group, chelerythrine chloride plus late exercise preconditioning plus exhaustive exercise (CHE+LEP+EE) group. EE group for an exhaustive exercise, EEP and LEP group conducted a brief high-intensity intermittent preconditioning exercise, EEP+EE and LEP+EE group respectively conducted an exhaustive exercise after preconditioning exercise immediately and24h later, CHE+EEP+EE and CHE+LEP+EE group conducted the same exercise with EEP+EE and LEP+EE group, but intraperitoneal injections of CHE10min before preconditioning exercise. Detecting rats serum cardiac troponin I (cTnI) to assess myocardial damage, hematoxylin basic fuchsin picric acid(HBFP) staining for observing myocardial ischemia anoxic condition, Western Blot detection for alpha PKC protein expression quantity changes, immunohistochemical for alpha PKC protein expression position changes. Results:1)Compared with group C, group EE significantly increase in cTnI levels, HBFP staining positive area and IOD values, alpha PKC protein expression and translocation, translocate to cell membrane and intercalated disc;2) Compared with group EE, group EEP+EE and LEP+EE were reduced significantly in cTnI levels, alpha PKC protein expression and translocation, but HBFP staining positive area and IOD values in group EEP+EE was significantly reduced,group LEP+EE was significant increased;3)Compared with group EEP+EE, cTnI levels of group CHE+EEP+EE was significantly elevated, HBFP staining positive area and IOD values decreased but no significant, alpha PKC protein expression and translocation were significantly reduce; Compared with group LEP+EE, group CHE+LEP+EE was significantly reduced in of cTnI levels,but significant increase in HBFP staining positive area and IOD values, alpha PKC protein expression and translocation had no significant change.Conclusion:Exhaustion exercise can increase the alpha PKC protein expression and cause myocardial cell damage. Exercise preconditioning was a healthy way to induce myocardial protection, with reduce alpha PKC protein expression and translocation appropriately. CHE can inhibit alpha PKC activity during early EP, but had no significant effect in late EP.Alpha PKC mediated early EP myocardial protection, but the role of alpha PKC in late EP myocardial protection needs further research. |