Electro-acupuncture at LI11 and ST36 acupoints exerts neuroprotective effects via reactive astrocyte proliferation after ischemia and reperfusion injury in rats

- A subpopulation of GFAP/Vimentin/Nestin-posivie reactive astrocytes.
- EA promotes the proliferation of reactive astrocytes.
- EA attenuates neurological deficit and motor impairment.
- EA regulates CyclinDl control of the G1/S cell cycle phase transition.
- EA protects cerebral infarct via secretion of reactive astrocytes-derived BDNF.

Reactive astrogliosis is a common phenomenon in central nervous system (CNS) injuries such as ischemic stroke. The present study aimed to deeply investigate the relationships between the neuroprotective effect of electro-acupuncture (EA) and reactive astrocytes following cerebral ischemia. EA treatment at the Quchi (LI11) and Zusanli (ST36) acupoints at Day 3 attenuated neurological deficits and cerebral infarct volume in ischemia and reperfusion (I/R) injured rats. Animal behavior assessments found that the speed of Catwalk gait, equilibrium and coordination of Rotarod test were improved. Furthermore, EA treatment exerted neuroprotective effects via activation of glial fibrillary acidic protein (GFAP), vimentin and nestin positive cells. Simultaneously, an obvious increase in GFAP/vimentin, GFAP/nestin and GFAP/BrdU co-labeling appeared in the peri-infract cortex and striatum, suggesting EA can promote the proliferation of GFAP/vimentin/nestin-positive reactive astrocytes. The expression of cell cycle-associated proteins Cyclin Dl, CDK4 and phospho-Rb were increased in the peri-infract cortex and striatum, indicating proliferated reactive astrocytes-mediated CyclinDl/CDK4 regulation of the transition of the G1-to-S cell cycle phases. In addition, EA enhanced the localized expression of brain-derived neurotrophic factor (BDNF) in the peri-infract cortex and striatum. These results demonstrated that EA treatment at the LI11 and ST36 acupoints on Day 3 exerted neuroprotection via proliferation of GFAP/vimentin/nestin-positive reactive astrocytes and, potentially, secretion of reactive astrocytes-derived BDNF in I/R injured rats.