ObjectiveTo observe the effect of penetrative needling from"Baihui"(GV20)to"Qubin"(GB7)on neurological function and expression of autophagy related protein microtubule-associated protein

light chain 3(LC3)in rats with hemorrhagic stroke

so as to explore its mechanism underlying improvement of hemorrhagic stroke.MethodsA total of 120 male SD rats were randomly divided into sham operation

model

non-acupoint

acupuncture and medication(Rapamycin) groups which were further divided into two time-point subgroups(3

7 days after modeling

n=12/subgroup). The intracerebral hemorrhage model was established by injection of the rat's auto-blood(50 μL)into the putaman region. Penetrative needling from GV20 to GB7 or sham acupoints(about 1 cm beside GV20 and GB7)was conducted for 30 min

twice daily for 7 days. For rats of the medication group

Rapamycin solution(7 μmol/L)was injected into the right lateral ventricle. The neurological functions(locomotor and balance deficits)were evaluated according to suspended wire test(0-6 points)and horizontal board walking test(0-6 points). Immunohistochemistry and Western blot were used to detect the expression of total LC3 and expression of LC3-Ⅰ and LC3-Ⅱ proteins in the ischemic penumbra region of brain tissue

respectively.ResultsAfter modeling

the neurological function scores were significantly decreased on day 3 and 7

the levels of LC3-Ⅱ/Ⅰ and LC3 protein on day 3 and 7 were significantly increased in the model group relevant to the sham operation group(P<0. 05). Following the interventions

the neurological function scores as well as LC3-Ⅱ/Ⅰ and LC3 protein expression were significantly increased in both acupuncture and medication groups compared with the model group(P<0. 05). The effect of Rapamycin was obviously stronger than that of penetrative needling in up-regulating the expression of LC3-Ⅱ/Ⅰ and LC3 protein(P<0. 05).ConclusionPenetrative needling can improve neurologic function in hemorrhagic stroke rats

which is related with its effect in up-regulating the expression of autophagy-related protein LC3.