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[Effect of Electroacupuncture on Expression of Cortical srGAP 1 and Cdc 42 in Rats with Focal Cerebral Infarction].

AbstractOBJECTIVE:
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.
AuthorsEn-ze Dai, Fei Long, Biao Gong, Quan-hu Guo, Ying Wang, Zhi-hua Zeng
JournalZhen ci yan jiu = Acupuncture research (Zhen Ci Yan Jiu) Vol. 40 Issue 3 Pg. 186-91 (Jun 2015) ISSN: 1000-0607 [Print] China
PMID26237968 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • GTPase-Activating Proteins
  • srGAP1 protein, rat
  • cdc42 GTP-Binding Protein
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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