2022, Vol. 26 ›› Issue (25): 3999-4003

Effect of N-arachidonylethanolamine on axon regeneration of the dorsal root ganglion

Zhang Haonan1, Wang Xingran2, Li Meimei2, Ma Jinjin2, Ma Yanxia2, Saijilafu1, 2   

Abstract: BACKGROUND: Nerve axon regeneration is mainly affected by its own regenerative ability and inhibitory external environment. N-arachidonylethanolamine has been proven to regulate axon regeneration in C. elegans, but its role in mammals is still unknown.  
OBJECTIVE: To explore the effect of N-arachidonylethanolamine on axon regeneration of mouse dorsal root ganglion neurons.
METHODS:   Dorsal root ganglion tissues were taken from L4-L5 of ICR mice aged 6-8 weeks, digested with collagenase and trypsin, and divided into URB597 group, N-arachidonylethanolamine group, methyl-sulfoxide control group, and electroporated green fluorescent protein and specific siRNA mixture group. After 3 days of in vitro culture, the axons were labeled by neuron-specific immunoassay. Axon length, and the number of primary and secondary branches were measured, and the statistics was performed to determine the regulatory effect of N-arachidonylethanolamine on the regeneration of dorsal root ganglion neuron axon.  
RESULTS AND CONCLUSION: (1) After inhibiting fatty acid amide hydrolase activity, there was no obvious change in dorsal root ganglion cell axon regeneration and URB597 had no cytotoxic effect on dorsal root ganglion neuron cells (P > 0.05). (2) After fatty acid amide hydrolase knockdown, dorsal root ganglion cell axon regeneration had no obvious change (P > 0.05). (3) Exogenous N-arachidonylethanolamine had no obvious regulatory effect on dorsal root ganglion cell axon regeneration and N-arachidonylethanolamine had no cytotoxic effect on dorsal root ganglion neuron cells (P > 0.05). (4) Inhibiting fatty acid amide hydrolase activity or adding exogenous N-arachidonylethanolamine has no effect on dorsal root ganglion neuron axon branches (P > 0.05).
Key words: dorsal root ganglion, neurons, N-arachidylethanolamine, fatty acid amide hydrolase, axon regeneration, cytotoxicity