Abstract | OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention on the neurological function and the expression change of Slit-Robo GTPase-activating protein-1 (srGAP 1) and cell division-cycle 42 (Cdc 42) in the cortex of rats with cerebral ischemic injury (CIRI) , so as to explore the mechanism of EA in the management of cerebral infarction. METHODS: A total of 48 male Sprague Dawley (SD) rats were randomly and equally divided into control, model, non- acupoint EA and EA groups (n = 12/group). The CIRI model was established based on the modified Zea Longa method. EA intervention was applied for 30 min, once a day for 14 days. Modified neurologic severity scores (mNSS) were assessed on day 1,3,7 and 14 after mode- ling. Immunofluorescence assay was used to detect the immunoactivity and distribution of srGAP 1 and Cdc 42 in the cortical ischemic region. Western blot was employed to detect the expression of srGAP 1 and Cdc 42 in the affected cortex. RESULTS: The mNSS displayed that the neurological score in the EA group was significantly lower than that in the model group and non- acupoint EA group at the 7th d and 14th d (P<0. 01). Immunofluorescence results showed that cerebral srGAP 1 and Cdc 42 were ex- pressed mainly in the cytoplasm. The fluorescence intensity of srGAP 1 of the EA group was significantly lower than that of the model group and non- acupoint EA group(P<0. 01). Meanwhile the fluorescence intensity of Cdc 42 of the EA group was markedly higher than that in the model group and non- acupoint EA group(P<0. 01). Western blot assay indicated that the expression level of srGAP 1 in the model group was significantly higher than that of the control group( P<0. 01) ,and that of the EA group was much lower than those of the model group and non- acupoint EA group(P<0. 01). There was no significant difference of srGAP 1 expression levels between the non- acupoint EA group and the model group(P>0. 05). Additionally, the protein expression of Cdc 42 in the model group was slightly higher than that of the control group(P>0. 05), and that of the EA group was significantly higher than those of the model group and non- acupoint EA group(P<0. 01). There was no significant difference of Cdc 42 expression levels between the non- acupoint EA group and the model group(P>0. 05). CONCLUSION:
Cerebral infarction induced increase of cerebral srGAP 1 and decrease of Cdc 42 can be reversed by acupoint EA intervention in CIRI rats, which may be responsible for its effect in improving impaired neurological function after cerebral infarction.
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Authors | En-ze Dai, Fei Long, Biao Gong, Quan-hu Guo, Ying Wang, Zhi-hua Zeng |
Journal | Zhen ci yan jiu = Acupuncture research
(Zhen Ci Yan Jiu)
Vol. 40
Issue 3
Pg. 186-91
(Jun 2015)
ISSN: 1000-0607 [Print] China |
PMID | 26237968
(Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- GTPase-Activating Proteins
- srGAP1 protein, rat
- cdc42 GTP-Binding Protein
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Topics |
- Animals
- Cerebral Infarction
(enzymology, genetics, therapy)
- Disease Models, Animal
- Electroacupuncture
- GTPase-Activating Proteins
(genetics, metabolism)
- Humans
- Male
- Rats
- Rats, Sprague-Dawley
- cdc42 GTP-Binding Protein
(genetics, metabolism)
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