Background: Intervertebral disc degeneration (IVDD) is regarded as the leading cause of low back pain, resulting in disability and a heavy burden on public health. Several studies have unveiled that long noncoding RNAs (lncRNAs) play a key role in the pathogenesis and progression of IVDD. In this study, we aimed to investigate the biological function and latent molecular mechanism of the lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) in IVDD development. Methods: Firstly, we established an IVDD model in rats using advanced glycation end products (AGEs) intradiscal injection. Subsequently, gain-of-function assays were conducted to investigate the role of FAM83H-AS1 in the progression of IVDD. Bioinformatics analysis, RNA pull down assay and rescue experiments were employed to shed light on the molecular mechanism underlying FAM83H-AS1 involving in IVDD. Results: Our findings verified that AGEs treatment aggravated IVDD damage, and FAM83H-AS1 was downregulated in the IVDD group. Additionally, overexpression of FAM83H-AS1 contributed to the growth of nucleus pulposus (NP) cells and ameliorated IVDD injury. It was revealed that FAM83H-AS1 possessed the speculated binding sites of miR-22-3p. More importantly, we confirmed that FAM83H-AS1 functioned as a sponge of miR-22-3p in IVDD. Lastly, we demonstrated that miR-22-3p mediated the impact of FAM83H-AS1 on cell proliferation, ECM degradation, and inflammation. Conclusions: Our study indicated that FAM83H-AS1 relieved IVDD deterioration through sponging miR-22-3p, and provides novel insights into the mechanisms underlying FAM83H-AS1 in IVDD progression.