Effect of electroacupuncture on ROCK1 and ROCK2 expression in rat peri-infarct cortex after focal cerebral infarction
10.3724/SP.J.1008.2014.00329
- Author:
Feng LI
1
Author Information
1. Laboratory of Traditional Chinese Medicine, Traditional Chinese Medicine College, Chongqing Medical University
- Publication Type:Journal Article
- Keywords:
Brain infarction;
Electroacupunture;
ROCK1;
ROCK2
- From:
Academic Journal of Second Military Medical University
2014;35(3):329-332
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of electroacupuncture (EA) intervention on the expression of Rho-associated kinase 1 (ROCK1) and Rho-associated kinase 2 (ROCK2) in rat peri-infarct cortex after middle cerebral artery occlusion (MCAO), so as to study the underlying mechanism by which EA improves cerebral ischemia. Methods Totally 40 male Sprague Dawley (SD) rats were equally randomized into four groups, control group, sham-operation group, model group and EA group. MACO in the model group and EA group was successfully established by an improved Longa procedure. EA was given 90 min after resuscitation for the EA group, once a day for 14 days. The modified neurological severity scores (mNSS) of rats in each group were determined on the 1st day, 3rd day, 7th day and the 14th day after operation. Immunohistochemistry and Western blotting analysis were used to detect the expression of ROCK1 and ROCK2 in the brain 14 d after operation. Results Neural dysfunction was not observed in the control group and sham-operation group. The values ofmNSS were significantly different between model group and EA group at 7 d, 14 d after operation (P<0. 05). Both immunohistochemical staining and Western blotting analysis indicated that the expression levels of ROCK1 and ROCK2 were up-regulated in model group, while those in EA group were significantly less than those in the model group (P<0. 05). Conclusion The expression of ROCK1 and ROCK2 is up-regulated in rat cortex after focal cerebral infarction, and the up-regulation can be prevented by EA intervention, which might be oneof the mechanisms by which EA promotes the recovery of neurological dysfunction after cerebral infarction.
