Objective To observe the protective effect of electroacupuncture(EA) on neurovascular unit

neurological function in rats with cerebral ischemia(CI)

so as to explore its mechanisms underlying improvement of ischemic cerebral tissue. Methods Male SD rats

SPF grade

were randomly and equally divided into sham operation group

model group

EA group Ⅰ and EA group Ⅱ

27 rats in each group. The CI model was established by occlusion of the middle cerebral artery(MCAO). EA(2 Hz/20 Hz

0.5 mA) was applied to “Quchi”(LI11)

“Hegu”(LI4)

“Zusanli”(ST36) and “Shuigou”(GV26) for rats of the EA group Ⅰ

and to “Baihui”(GV26)

“Fengfu”(GV16)

“Neiguan”(PC26) and “Xinshu”(BL15) for rats of the EA group Ⅱ for 20 min

once a day for 14 days. The modified neurologic severity score(mNSS) was calculated according to the state of locomotor

sensory

and reflex parameters. Transmission electron microscope(TEM) was used to observe the neuronal structure of the ischemic cerebral area. The CD34 positive cells(for microvessels) of the ischemic brain tissue were detected by using immunohistochemistry

and the expression levels of cerebral phosphatidylinositol-3 kinase(PI3 K) and protein kinase B(Akt) mRNAs were detected by quantitative real-time-PCR

respectively. Results Along with the extension of time

the mNSS at 4 h

and 3

7 and 14 d after CI were apparently decreased

and the number of CD34 positive cells from 3 d to 14 d after CI

and the expression of PI3 K mRNA and Akt mRNA from 3 d to 7 d were significantly increased in the model

EAⅠand EA Ⅱ group(P<0.01

P<0.05). Compared with the sham operation group

the mNSS at 4 h

and 3

7 and 14 d

and CD34-positive number and PI3 K mRNA and Akt mRNA expression levels at 3

7 and 14 d were significantly increased in the model group(P<0.01

P<0.05). In comparison with the model group

the mNSS at 3

7 and 14 d were obviously decreased(P<0.01)

and the CD34-positive number and PI3 K and Akt mRNA expression levels at 3

7 and 14 d considerably increased in both EA group Ⅰ and Ⅱ(P<0.01

P<0.05). The therapeutic effect of EA group Ⅱ was significantly superior to that of EA group Ⅰ in lowering mNSS at 14 d

up-regulating the CD34-positive number at 7 and 14 d

and PI3 K mRNA at 3

7 and 14 d and Akt mRNA at 3 and 7 d(P<0.05

P<0.01). Results of TEM showed an irregular shape of neurons with nuclear pyknosis

non-uniform chromatin

more organelle loss

swollen mitochondrial Golgi complex and expansion of rough endoplasmic reticulum

being relatively milder in the EA group Ⅰ

particularly in the EA group Ⅱ. Conclusion EA therapy can improve the neurological function in cerebral ischemia rats

which may be related to its effects in protecting the neurovascular unit and up-regulating PI3 K/Akt signal pathway. The effects of EA at GV26

GV16

PC26 and BL15 are better than those of EA at LI11

LI4

ST36 and GV26.