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| Effect of electro-acupuncture at Renzhong(DU26) on the expression of ACE-AngⅡ/ACE2-Ang (1-7) axis related factors in rats with cerebral infarction |
| Hits 531 Download times 309 Received:December 06, 2021 |
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| DOI
10.11656/j.issn.1672-1519.2022.06.14 |
| Key Words
cerebral infarction;ACE-Ang Ⅱ/ACE2-Ang (1-7) axis;electro-acupuncture;vasomotor;Renzhong (DU26) |
| Author Name | Affiliation | E-mail | | ZHANG Ye | Institute of Acupuncture and Moxibustion, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China
National Clinical Research Center for Traditional Chinese Medicine Acupuncture and Moxibustion, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China | | | LI Jing | Institute of Acupuncture and Moxibustion, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China
National Clinical Research Center for Traditional Chinese Medicine Acupuncture and Moxibustion, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China | 1725155193@qq.com |
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| Abstract
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| Objective The purpose of this study is to observe the change of ACE-AngⅡ/ACE2-Ang(1-7) axis pathway in rats with cerebral infarction and the effect of electro-acupuncture(EA) intervention. The mechanism of acupuncture in the treatment of cerebral infarction was discussed from the point of vasodilation.Methods The 126 rats were randomly divided into blank control, model group and EA group. The model group and EA group were divided into 10 time groups according to postoperative 1, 3, 6, 9, 12, 18, 24 h, 3, 7 and 12 d. After modeling, the EA group was acupunctured at Renzhong (DU26) acupoint every day. The neurological deficit, cerebral infarction area, cerebral blood flow (CBF) and immuno-histochemistry were detected.Results 1) After acupuncture, the NSS score of MCAO model rats decreased gradually with the prolongation of ischemia time, and the scores of each time phase were significantly higher than those in the blank control(P < 0.01);the scores of the EA group were lower than those in the model group, and the differences were significant between the at 3, 7 and 12 d (P < 0.01). 2) TTC staining results showed that compared with the blank control(P < 0.05, P < 0.01), and the EA group in each phase was significantly less than the model group in the same time phase(P < 0.05, P < 0.01). 3) Immuno-histochemical results: the expression of ACE in the model group was up-regulated to 18 hours and down-regulated, which was significantly higher than that in the blank control from 1 h~7 d(P < 0.01);the expression of ace in the EA group was lower than that in the model group except 6 h, with significant differences at 9 h 18 h and 24 h(P < 0.05, P < 0.01). The expression of AngⅡ in model group was up-regulated to 24 h after operation, and significantly higher than blank control (P < 0.05, P < 0.01) at 3~9 h and 18 h~7 d, and the difference was significant in 3 h, 6 h and 18 h~3 d(P < 0.05, P < 0.01). AT1 expression in model group was up-regulated to 24 h after operation, and there was significant difference in 1 h and 9 h~24 h (P < 0.05, P < 0.01). The expression of AT1 in EA group was lower than that in model group after 9 h, and the difference was significant in 12, 18, 24 h (P < 0.05). The expression of ACE2 in EA group was up-regulated from 3 h to 18 h after operation, and was higher than that in the blank control at 1 h~12 d, and there was significant difference in 1 h, 9 h~3 d(P < 0.05), and the difference was significant in the EA group at 24 h~3 d(P < 0.05). The expression of Ang (1-7) in model group was up-regulated from 9 h to 12 h after operation, except for 1 h, 6 h phase, which was significantly higher than that in the blank control(P < 0.05, P < 0.01). The EA group was up-regulated from 3~24 h later, and was higher than that in the model group from 24 h~7 d, and the difference was significant(P < 0.05). The expression of MAS in model group was up-regulated from 12 h to 3 d, and the phase of MAS in the model group was higher than that in the blank control at 3, 6 h and 12 h~12 d, and the difference was significant (P < 0.05, P < 0.01);the expression of the EA group was higher than that in the model group after 9 h, among which the difference was significant(P < 0.05).Conclusion EA intervention can significantly improve the neurological symptoms of MCAO rats, reduce the volume of cerebral ischemia, improve CBF perfusion, down regulate the expression of ACE, Ang Ⅱ and ATL, up regulate the expression of ANG(1-7), ACE2 and MAS, and improve the prognosis of cerebral infarction. |
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