Influences of acupuncture on expressions of myocardial CFTR and ClC-2 in rats with acute myocardial ischemia
2014, 37 (4):
Objective To observe the influences of acupuncture on the protein expressions of myocardial CFTR and ClC-2 (regulatory proteins of chloride channel) in rats with acute myocardial ischemia (AMI), and discuss the mechanism of specificity of selecting acupoints along meridians. Methods SD rats (n=60) were randomly divided into blank group, model group, Neiguan (PC6) group, Lieque (LU7) group and non-acupoint group. Except of blank group, other groups were given multiple subcutaneous injection of isoproterenol for establishing AMI model. The Neiguan group, Lieque group and non-acupoint group were given electro-acupuncture in bilateral Neiguan, Lieque and middle point between Tianshu (ST25) and Shenque (CV8) once a day for 7 d. The changes of myocardial histology were observed by using microscope after HE staining. The content of creative kinase (CK-MB) was detected by using kit method, content of malonyldialdehyde (MDA) was detected by using EELISA, and protein expressions of CFTR and ClC-2 were detected by using Western blot method. Results The HE staining sections of myocardial tissue showed that fragmentation and disordered arrangement of myocardial fibers, sarcoplasm swelling, obvious inflammatory cell infiltration, and wide distribution of many brown granules in nucleus in model group, Lieque group and non-acupoint group, which were relieved in Neiguan group compared with model group. Compared with blank group, the protein expressions of CFTR and ClC-2 increased significantly (P<0.01), CK-MB content increased significantly (P<0.01) and MDA content increased in model group, Lieque group and non-acupoint group. Compared with model group, CK-MB content decreased (P<0.05), MDA content decreased (P<0.05) and expressions of CFTR and ClC-2 decreased significantly (P<0.01) in Neiguan group. Conclusion Acupuncture in Neiguan can effectively relieve the pathological changes induced by myocardial ischemia, and the mechanism may be related to regulating the protein expressions of CFTR and ClC-2.
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