The mechanism of electroacupuncture therapy after cerebral ischemic injury
10.3760/cma.j.issn.0254-1424.2015.04.002
- VernacularTitle:电针治疗大鼠急性缺血性脑损伤的作用机制
- Author:
Yukai WANG
;
Li REN
;
Mingna HUANG
;
Chi LONG
;
Haiying HUANG
- Publication Type:Journal Article
- Keywords:
Cerebral Ischemia;
Electroacupuncture therapy;
Mechanisms
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2015;37(4):247-251
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the operation of Nav1.6 voltage-gated sodium channels in rats with acute cerebral injury after electroacupuncture therapy and investigate the mechanism.Methods Male Sprague-Dawley rats were randomly divided into an ischemia control group (IC,n =48),an electroacupuncture group (ET,n =48),a nimodipine therapy group (NT,n =48) and a sham operation group (SO,n =24),and were treated accordingly.A model of acute cerebral ischemia was induced by occlusion of the right middle cerebral artery using the suture method.The expression of Nav1.6,the concentration of Ca2+ and infarct volume were observed at 6 h,1 d,2 d and 3 d after ischemia with the real-time quantitative fluorescence PCR,immunofluorescence and 2,3,5-triphenyl tetrazolium chloride methods,respectively.Results The Joshua score for neural function was zero in the sham operation group,and increased gradually in the three other groups 6 h and1 and 2 d after ischemia.The average Joshua score 3 d after ischemia was significantly lower than 1 d earlier in each group.In the ET group the expression of Nav1.6 was significantly upregulated at first,followed by a significant decrease.The concentration of Ca2+ behaved similarly.However,no significant changes were observed in the infarction volume percentage.At 3 d after ischemia the expression of Nav 1.6,the Joshua grades,the Ca2+ concentrations and the infarction volume percentage were all significantly lower in the ET group compared with the IC,NT and SO groups.Conclusion Electroacupuncture therapy after acute cerebral ischemia can inhibit the expression of Navl.6,reduced Na + inflow and calcium overload,and mitigate acute cerebral ischemic injury,at least in rats.The protective effect may be attributed to inhibiting the expression of Nav 1.6.
