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Some inflammation inducers like LPS can stimulate astrocytes to produce NO (a main member of RNS) and increase GFAP expression.12 In an in vivo study, a cortical transplantation model was used to mimic glial activation in neurodegenerative diseases and the results suggest that sustained high levels of oxidative stress after transplantation are associated with chronic glial activation.7 MitoQ, a mitochondria‐targeted antioxidant, attenuates excessive reactive astrogliosis in the brains of Alzheimer's disease model of mice.78 Additionally, some amino acid complex, like cysteamine (CSH), promotes mitochondrial oxidative stress in astrocytes and causes astrocyte activation both in vivo and ex vivo, and the authors indicated that intervention of CSH can be used as a model to study reactive astrogliosis induced by ageing and neurodegenerative diseases.74 JAK‐STAT signal pathway is a key direct mediator of astrogliosis.91, 98, 101 Conditional knockout STAT3 in astrocytes leads to inactivation of astrocytes, and there is no glial scar formed in the injury site of astrocytic STAT3 conditional knockout mice in spinal cord injury model.137 The activation of JAK‐STAT signal was reported to be affected by oxidative stress.137 In a Parkinson's disease model, enhanced NOX activity in microglia is able to mediate microglia‐induced reactive astrogliosis by activating STAT1 or STAT3 signalling pathways.45 On the contrary, activation of endogenous antioxidant system like Nrf2‐Keap1‐ARE could inhibit the activation of excessive astrogliosis.47, 141 In conclusion, regulation of oxidative stress may be an effective way to inhibit excessive glial cell activation and glial scar formation
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