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　LOCI　01　9271　96　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.