Effect of Electroacupuncture Preconditioning on Myocardial Ischemia and Expression of TLR 4, MyD 88 and NF-κB mRNAs in "Neiguan" (PC 6) Area in Rats with Myocardial Ischemia-reperfusion Injury
10.13702/j.1000-0607.170308
- Author:
Yi ZHU
1
Author Information
1. Department of Acupuncture-moxibustion, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Cutaneous TLR 4/MyD 88/NF-κB signaling;
Electroacupuncture;
Myocardial ischemia-reperfusion injury;
PC 6 area
- From:
Acupuncture Research
2018;43(5):302-306
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: To observe the effect of electroacupuncture (EA) preconditioning on acute myocardial ischemia (MI) and expression of Toll-like receptor 4 (TLR 4), myeloid differentiation factor 88 (MyD 88) and nuclear factor-κB (NF-κB) mRNAs in the "Neiguan" (PC 6) area of rats with MI-reperfusion injury (MIRI), so as to explore its mechanisms underlying improvement of MIRI. METHODS: Forty-eight male Wistar rats were randomly divided into control, control ＋ EA, sham operation, model, EA and sham EA groups (n＝8). The MIRI model was established by occlusion of the descending anterior branch of the left coronary artery for 30 min, followed by reperfusion. Before modeling, EA preconditioning was respectively applied to PC 6 or sham PC 6 for 30 min, once daily for 5 days. Electrocardiogram (ECG) of the standard limb-lead Ⅱ was recorded before and after the modeling, and 0.25 h after reperfusion. The expression levels of TLR 4, MyD 88 and NF-κB genes in the PC 6 tissue were detected by Real-time PCR. RESULTS: Compared with the control group, the height of ECG J-point was significantly increased in the model group (P<0.01), suggesting an acute MI, and the height of J-point was significantly lower in the EA group than in the model and sham EA groups (P<0.01). In comparison with the control group, the expression levels of TLR 4, MyD 88 and NF-κB mRNAs were markedly up-regulated in the area of PC 6 in the model group (P<0.01). Compared with the model group, the increased expression levels of TLR 4, MyD 88 and NF-κB mRNAs in the EA preconditioning group were significantly inhibited (P<0.05). No significant differences were found among the control, control＋EA and sham operation groups and between the model and sham EA groups in the expression levels of TLR 4, MyD 88 and NF-κB mRNAs (P>0.05)．. CONCLUSION: EA preconditioning can improve myocardial ischemia and reduce the expression of TLR 4, MyD 88 and NF-κB mRNAs in PC 6 area of MIRI rats, suggesting an involvement of the regional cutaneous TLR 4/MyD 88/NF-κB signaling suppression in the initiation-transfer-amplification of EA stimulating signal inputs for relieving MIRI.
