【摘 要】
：
Epilepsy is a brain condition characterized by the recurrence of unprovoked seizures.Recent studies have shown that complement component 3 (C3) aggravate the neuronal injury in epilepsy.And our previous studies revealed that TRPV1 (transient receptor pote
【机 构】
：
Department of Physiology,Hubei Provincial Key Laboratory of Developmentally Originated Disease,Schoo
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Epilepsy is a brain condition characterized by the recurrence of unprovoked seizures.Recent studies have shown that complement component 3 (C3) aggravate the neuronal injury in epilepsy.And our previous studies revealed that TRPV1 (transient receptor potential vanilloid type 1) is involved in epilepsy.Whether complement C3 regulation of neuronal injury is related to the activation of TRPV 1 during epilepsy is not fully understood.We found that in a mouse model of status epilepticus (SE),comple-ment C3 derived from astrocytes was increased and aggravated neuronal injury,and that TRPVl-knockout rescued neurons from the injury induced by complement C3.Circular RNAs are abundant in the brain,and the reduction of circRad52 caused by complement C3 pro-moted the expression of TRPV1 and exacerbated neuronal injury.Mechanistically,disorders of neuron-glia interaction mediated by the C3-TRPV1 signaling pathway may be important for the induction of neuronal injury.This study provides support for the hypothesis that the C3-TRPV1 pathway is involved in the prevention and treat-ment of neuronal injury and cognitive disorders.
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