An autophagic mechanism study on effect of electroacupuncture at different times pretreating myocardial ischemia-reperfusion injury.
10.13703/j.0255-2930.2018.10.015
- Author:
Wanying CHEN
1
;
Zehao ZHONG
1
;
Hua BAI
1
;
Hongru ZHANG
1
;
Shengfeng LU
2
,
3
;
Yihuang GU
1
Author Information
1. the Second Clinical Medical College, Nanjing University of CM, Nanjing 210023, Jiangsu Province, China.
2. the Second Clinical Medical College, Nanjing University of CM, Nanjing 210023, Jiangsu Province, China
3. Key Laboratory of Acupuncture and Medicine of Ministry of Education, Nanjing University of CM, Nanjing 210023, Jiangsu Province.
- Publication Type:Journal Article
- Keywords:
Beclin-1;
ULK1;
autophagy;
electroacupuncture preconditioning;
myocardial ischemia-reperfusion injury
- MeSH:
Acupuncture Points;
Animals;
Autophagy;
Electroacupuncture;
Male;
Myocardial Ischemia;
Rats;
Rats, Sprague-Dawley
- From:
Chinese Acupuncture & Moxibustion
2018;38(10):1087-1092
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the difference of protective effect of electroacupuncture (EA) at different times pretreating myocardial ischemia-reperfusion injury (MIRI) and the protein expressions of ULK1 and Beclin-1 in myocardial tissue, so as to explore the relation of the difference and autophagic mechanism.
METHODS:Sixty-three male SD rats were randomized into 7 groups, a sham group, a model group, an EA pretreating for 1 d (EA-1d) group, an EA pretreating for 2 d (EA-2d) group, an EA pretreating for 3 d (EA-3d) group, an EA pretreating for 4 d (EA-4d) group, an EA pretreating for 5 d (EA-5d) group, 9 rats in each group. All the rats in the pretreating groups were treated with EA 1-5 days before MIRI surgery. EA (2 Hz/100 Hz, 2 mA) was used at bilateral "Neiguan (PC 6)" for 20 min. All the rats except for those in the sham group was underwent left thoracotomy and ligation of the left anterior descending (LAD) coronary artery for 30 minutes followed by 4 hours of reperfusion to establish the MIRI model. The same operation was performed in the sham group except for the ligation of the LAD. Throughout the experiment, electrocardiogram was continuously monitored. The myocardial infarct sizes were assessed by Evans blue and triphenyltetrazolium chloride (TTC) staining. The serum concentrations of cardiac troponinⅠ(cTnⅠ) was detected by ELISA. The expressions of ULK1 and Beclin-1 in the heart tissues were analyze by Western blot.
RESULTS:Compared with the sham group, the concentrations of cTnⅠ and the protein expressions of ULK1 and Beclin-1 increased in the model group (all <0.05). Compared with the model group, the infarct sizes decreased in the EA-1d, EA-2d, EA-3d, EA-4d and EA-5d groups (all <0.05), with less risk sizes in the EA-3d, EA-4d and EA-5d groups (all <0.05). The levels of cTnⅠin the EA-4d and EA-5d groups decreased ( both <0.05); the expressions of ULK1 protein decreased in the EA-1d, EA-2d, EA-3d, EA-4d and EA-5d groups (all <0.05); the expressions of Beclin-1 protein decreased in the EA-2d, EA-3d, EA-4d and EA-5d groups (all <0.05). The infarct sizes in the EA-4d and EA-5d groups were lower than that in the EA-1d group (both 0.05). The cTnⅠconcentration in the EA-4d group was less than that in the EA-1d group (<0.05).
CONCLUSION:Pretreatment with EA for 1-5 days can improve the infarct size in MIRI, with better effect of the pretreatment for 4-5 days. The cardioprotective effect may be related to the inhibition of autophagy. But the difference of the protective effects is not related to the protein expressions of ULK1 and Beclin-1.
