Over-expressed LOC101927196 suppressed oxidative stress levels and neuron cell proliferation in a rat model of autism through disrupting the Wnt signaling pathway by targeting FZD3

Accumulating evidence indicates that long non-coding RNAs (lncRNAs) play an important role in autism. Herein, we delineated the functions of LOC101927196 and its potential mitigation effect on a rat model of autism. We retrieved various bioinformatics databases and websites to screen differentially expressed lncRNAs associated with autism. Next, a rat model of autism was established with the neuron cells extracted for transfection of different plasmids. The regulatory effect of LOC101927196 on neuron cell proliferation, apoptosis as well as oxidative stress was also investigated. Firstly, microarray dataset GSE18123 revealed that LOC101927196 was poorly expressed in a rat model of autism. Poor development and growth and oxidative stress disorder were also observed in a rat model of autism. In addition, LOC101927196 targeting FZD3 played a vital role in a rat model of autism through the Wnt signaling pathway. Furthermore, we further demonstrated that over-expressed LOC101927196 blocked neuron cell proliferation and reduced oxidative stress levels, while promoting apoptosis by suppressing the activation of the Wnt signaling pathway. Our findings illustrate that up-regulated LOC101927196 attenuated oxidative stress disorder in a rat model of autism through suppressing the activation of Wnt signaling pathway by targeting FZD3. •We first explored the role of LOC101927196 in autistic rats.•LOC101927196 was decreased in brain tissues of autistic rats.•Forced LOC101927196 inhibits oxidative stress and neuron proliferation.•Upregulated LOC101927196 repressed Wnt signaling pathway.•It gives a promising direction for understanding oxidative stress disorder in autism.