ArticleEvidence-based complementary and alternative medicine : eCAM2013
The impacts of along-channel acupuncture on the protein expressions of the chloride channel of the rats with myocardial ischemia.
Article in Evidence-based complementary and alternative medicine : eCAM, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Electroacupuncture improves myocardial ischemia injury via activation of adenosine receptors.Purinergic signalling · 2020Article
- Behavioral and Biochemical Effects of KXS on Postmyocardial Infarction Depression.Frontiers in pharmacology · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence suggests that chloride (CL(-)) channels are involved in myocardial ischemia. In this study, the impact of acupuncture on the protein expressions of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and CLC-2 CL(-) channel of the rats with myocardial ischemia were tested and its mechanism was explored. The rats for experiment were distributed randomly into 5 groups: blank control group, modeling control group, Neiguan (PC-6) treatment group, Lieque (LU-7) control group, and Non-acupoint control group. The rats of all groups, except the blank control group, had myocardial ischemia via multiple subcutaneous injection of isoproterenol (ISO). Electroacupuncture treatment was given to Neiguan (PC-6) treatment group, Lieque (LU-7) control group, and Non-acupoints control group, respectively, once a day for 7 days. The results show that acupuncture can alleviate the myocardial ischemia of cardiac tissue, decrease significantly the activities of serum SOD and MDA, and thereby influence the protein expressions of CFTR and CLC-2 in CL(-) channels. The results of the study implies that acupuncture suppresses the pathological changes of cardiac tissue of rats with myocardial ischemia and regulates the protein expression of CFTR and CLC-2 CL(-) channels, which may serve as one possible mechanism to reduce myocardial ischemia.
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