Neuroprotective Effects of Exogenous Irisin in Kainic Acid-Induced Status Epilepticus

• Main Authors: Yao Cheng, Yaru Cui, Yujie Zhai, Wenyu Xin, Yan Yu, Jia Liang, Shucui Li, Hongliu Sun
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2021-10-01
• Series: Frontiers in Cellular Neuroscience
• Subjects: irisin; status epilepticus; mitophagy; mitochondrial oxidative stress; neuronal injury
• Online Access: https://www.frontiersin.org/articles/10.3389/fncel.2021.738533/full

Elevated reactive oxygen species (ROS) level is considered a crucial causative factor for neuronal damage in epilepsy. Irisin has been reported to ameliorate mitochondrial dysfunction and to reduce ROS levels; therefore, in this study, the effect of exogenous irisin on neuronal injury was evaluated in rats with kainic acid (KA)-induced status epilepticus (SE). Our results showed that exogenous irisin treatment significantly increased the expression of brain-derived neurotrophic factor (BDNF) and uncoupling protein 2 (UCP2), and reduced the levels of neuronal injury and mitochondrial oxidative stress. Additionally, an inhibitor of UCP2 (genipin) was administered to investigate the underlying mechanism of irisin-induced neuroprotection; in rats treated with genipin, the neuroprotective effects of irisin on KA-induced SE were found to be partially reversed. Our findings confirmed the neuroprotective effects of exogenous irisin and provide evidence that these effects may be mediated via the BDNF/UCP2 pathway, thus providing valuable insights that may aid the development of exogenous irisin treatment as a potential therapeutic strategy against neuronal injury in epilepsy.