In the present study, model rat showed significant increases of GFAP and C3, which indicated the activation of excessive A1 ACs by CNTF at the later stage of stroke, while LCH not only alleviated the activation to a certain extent via reducing the expression of CNTF but also guided the transformation of reactive ACs from A1 to A2, which reversely promoted the release of some neurotrophic factors, such as BDNF. The gene discussed is CNTF; the disease is stroke disorder.