| Background：Ischemic heart disease is one of most common cardiovasculardisease, myocardial ischemia can lead to a series ofpathophysiological processes, ultimately resulting in heartfunction disorders. Numerous animal experiments and clinicalobservations found that, although myocardial ischemia regainedthe blood supply, it also increased the damage caused bymyocardial ischemia, and then appeared arrhythmias, enlargedinfarct size, and persistence myocardial systolic dysfunctionand so on. Thus, to revealing the mechanism of ischemiareperfusion injury(IRI) may become a further treatment ofischemic heart disease research targets.Cardiac gap junction (GJ) is an important basic structure forcommunication between the myocardial cells, mainly to achieveelectrical coupling and chemical exchange of informationbetween cells. The connexin43(Cx43) play a major role in heartdevelopment and heart disease. Reported that the myocardial ischemia/reperfusion injury can lead to Cx43remodeling,including structure changed and dysfunction, but the thischanges and IRI causing the intracellular calcium overload, alot of oxygen free radicals, and acidosis. In recent years, thestudy of myocardial protection by ischemic preconditioningmethod to regulate the expression of Cx43was shown to beeffective in reducing ischemia reperfusion injury.Wenxin Granule (WXG) has been known as an ion channel inhibitionof myocardial cells, using to treat a variety of arrhythmias.Earlier studies shown that WXG can protect the myocardial cellsby reducing the oxygen free radicals, and inhibiting the lipidperoxidation.Objectives：The aim of the study was to observe the protect effects of WenxinGranule on myocardial ischemia reperfusion injury, and investigatethe potential mechanisms of WXG in upregulating the expressionof Connexin43.Methods：Sixty male Wistar rats were randomly divided into sham group(N=15), control group (N=15), low dosage group with2.43g WXGper kg of body weight (N=15), high dosage group with9.72g WXGper kg of body weight (N=15). WXG was administrated by gastric perfusion. Besides sham group, left descending anteriorcoronary artery in other groups were subjected to30min ofregional ischemia and60min of reperfusion. The tissuespecimen was evaluated by HE staining and immunohistochemistry.Measured the plasma creatine kinase(CK), lactatedehydrogenase(LDH), and the myocardial Ca2+-ATPase, superoxidedismutase(SOD) and malondialdehyde (MDA).Results：In control group, the activities of myocardial enzymesdecreased markedly (P<0.01). HE staining indicated that severedamage in myocardial tissue. Immunohistochemistry was revealedthat the expression of Cx43was evidently decreased (P<0.01)and the distribution was disturbed. And myocardial Ca2+-ATPasewere decreased (P<0.05), the concentration of MDA increaseobviously (P<0.01) and activity of SOD degrade (P<0.05).In WXG groups the myocardial enzymes was significantlylower(P<0.01)；the damage of myocardial tissue was milder, ascompared with the control group. Immunohistochemistry showedin normal distribution and content of Cx43(P<0.05). Andmyocardial Ca2+-ATPase and SOD were increased (P<0.05), theconcentration of MDA reduced (P<0.05). Conclusion：1.Wenxin granule can reduce the extent of myocardialischemia-reperfusion injury by upregulating the expression ofConnexin43.2.The mechanism of Wenxin Granule upregulates the expressionof Cx43was related to the reduction of calcium overload andthe oxygen free radicals. |
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