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Objective To investigate the effect of electro-acupuncture (EA) on vasomotor symptoms in rats with acute cerebral infarction, by observing the changes in the expression of factors related to the phosphatidylinositol (PI) system. Methods Forty-two Wistar rats were randomly divided into 3 groups by a random number table: the control group ( n =6), the model group ( n =18) and the EA group ( n =18). The EA group was given EA treatment at Shuigou (GV 26) instantly after modeling with middle cerebral artery occlusion (MCAO) method, while the model and control groups were not given any treatment. The degrees of neurological deficiency were evaluated using neurological severity scores (NSS) and the brain blood flow was evaluated by a laser scanning confocal microscope. Western blot analysis was conducted to detect the expression levels of G-protein subtype (Gq) and calmodulin (CaM). Competition for protein binding was conducted to detect the expression level of inositol triphosphate (IP3). Thin layer quantitative analysis was conducted to detect the expression level of diacylglycerol (DAG). The expression level of intracellular concentration of free calcium ion ([Ca 2+ ] i ) was detected by flow cytometry. Results The NSS of the model group was significantly higher than the control group at 3 and 6 h after MCAO ( P <0.01), while the EA group was significantly lower than the model group at 6 h ( P <0.01). The cerebral blood flow in the model group was significantly lower than the control group at 1, 3 and 6 h after MCAO ( P <0.01), while for the EA group it was remarkably higher than the model group at the same time points ( P <0.01). The expressions of Gq, CaM, IP3, DAG and [Ca 2+ ] i in the model group were significantly higher than the control group ( P <0.05 or P <0.01), and those in the EA group were significantly lower than the model group at the same time points ( P <0.05 or P <0.01). Conclusion EA treatment at GV 26 can effectively decrease the over-expression of related factors of PI system in rats with acute cerebral infarction, improve cerebral autonomy movement, and alleviate cerebral vascular spasm.

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Background: We aimed to investigate changes into the levels of angiogenesis-associated factors following cerebral infarction and acupuncture intervention and reveal the underlying molecular mechanisms involved in promoting angiogenesis. Methods: Model rats with middle cerebral artery occlusion (MCAO) were randomized into electroacupuncture (EA), model control (MC), and blank control (control) groups. Changes in the degree of neurological impairment following cerebral infarction and angiogenesis in the ischemic center and peripheral area were observed using immunofluorescence double-labeling. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to detect changes in the Ang-1, Ang-2, PDGF-B, and bFGF levels. Moreover, the effects of EA intervention were evaluated. Results: The neurological severity score of each phase in the EA group was lower than that into the simultaneous phase in the MC group. The proliferation of vascular endothelial cells in the EA group was higher than that in the MC group at 12 hours to 7 days. The Ang-1 and Ang-2 mRNA and protein levels in the EA group were significantly higher than those in the MC group. PDGF-B levels in the EA group were significantly higher than those in the MC group at 3 to 6 hours and 3 to 12 days, and protein levels were high at 6 hours and 3 to 12 days. bFGF mRNA levels at 24 hours to 12 days and bFGF protein at 3 to 12 days were significantly elevated in the EA group than those in the MC group. Conclusions: EA at Shui Gou(DU 26) significantly improved the neurological symptoms of MCAO rats, promoted vascular endothelial cell proliferative activity around the infarct area, significantly advanced the time of proliferation of vascular endothelial cells, and upregulated the expression of angiogenesis-related factors, thereby promoting angiogenesis. Thus, EA may significantly improve the prognosis of cerebral infarction. Graphical abstract: http://links.lww.com/AHM/A43.