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mfat‐1 transgene protects cultured adult neural stem cells against cobalt chloride‐mediated hypoxic injury by activating Nrf2/ARE pathways

Ischemic stroke is a devastating neurological disorder and one of the leading causes of death and serious disability in adults. Adult neural stem cell (NSC) replacement therapy is a promising treatment for both structural and functional neurological recovery. However, for the treatment to work, adult NSCs must be protected against hypoxic‐ischemic damage in the ischemic penumbra. In the present study, we aimed to investigate the neuroprotective effects of the mfat‐1 transgene on cobalt chloride (CoCl2)‐induced hypoxic‐ischemic injury in cultured adult NSCs as well as its underlying mechanisms. The results show that in the CoCl2‐induced hypoxic‐ischemic injury model, the mfat‐1 transgene enhanced the viability of adult NSCs and suppressed CoCl2‐mediated apoptosis of adult NSCs. Additionally, the mfat‐1 transgene promoted the proliferation of NSCs as shown by increased bromodeoxyuridine labeling of adult NSCs. This process was related to the reduction of reactive oxygen species. Quantitative real‐time polymerase chain reaction and Western blot analysis revealed a much higher expression of nuclear factor erythroid 2‐related factor 2 (Nrf2) and its downstream genes (HO‐1, NQO‐1, GCLC). Taken together, our findings show that the mfat‐1 transgene restored the CoCl2‐inhibited viability and proliferation of NSCs by activating nuclear factor erythroid 2‐related factor 2 (Nrf2)/antioxidant response elements (ARE) signal pathway to inhibit oxidative stress injury. Further investigation of the function of the mfat‐1 transgene in adult protective mechanisms may accelerate the development of adult NSC replacement therapy for ischemic stroke.