Objective To investigate the effect of long non-coding small nucleolar RNA host gene 1 (lncRNA-SNHG1) on the proliferation of human hypertrophic scar fibroblasts. Methods The hypertrophic scar tissue and normal skin tissue adjacent to the scar (within 3 cm near the scar) of 22 patients with hypertrophic scar treated and operated in the Department of Burn and Plastic Surgery of the General Hospital of Ningxia Medical University from 2019 to 2021 were collected, and human primary fibroblasts were isolated and cultured from the hypertrophic scar and normal skin tissue adjacent to the scar, while the expression of SNHG1 and miR-382-3p was detected at the tissue and primary cell levels by using qRT-PCR. Proliferative scar fibroblasts were randomly divided into control group, SNHG1 negative control group (adding empty lentivirus vectors), mimic control group (adding control mimic), SNHG1 negative control + mimic control group (adding empty lentivirus vectors and control mimic), SNHG1 overexpression group (adding overexpression lentivirus), miR-382-3p overexpression group (adding miR-382-3p mimics), SNHG1 overexpression + mimic control group (adding overexpression lentivirus and control mimics) and SNHG1 overexpression + miR-382-3p overexpression group (adding overexpression lentivirus and miR-382-3p mimics). qRT-PCR was used to detect the mRNA expression of SNHG1, PCNA, p27 and miR-382-3p in each group; CCK-8 method to detect the proliferation viability of the cells in each group after transfection; EdU staining method to detect the change of proliferation level of each group of cells after transfection;Western blotting to detect the expression levels of p27 and PCNA proteins in each group of cells after transfection. Results SNHG1 presented high expression in hypertrophic scar tissue (3.21±2.65 vs. 1.14±0.61, P<0.001) and primary cells (0.91±0.08 vs. 0.54±0.08, P<0.01), whereas the expression of miR-382-3p was down-regulated (0.53±0.34 vs. 1.15±0.61, P<0.001; 0.84±0.09 vs. 1.01±0.004, P<0.05). Compared with SNHG1 negative control group, the cell proliferation ability of SNHG1 overexpression group increased (0.23±0.03 vs. 0.16±0.01, P<0.001), the percentage of EdU positive cells significantly increased (30.01%±5.70% vs. 7.13%±4.40%, P<0.001), the expression levels of PCNA mRNA and protein increased (mRNA: 2.97±0.33 vs. 0.98±0.25,P<0.01; protein: 2.20±0.09 vs. 0.88±0.20, P<0.05), the expression levels of p27 mRNA and protein decreased (mRNA: 0.30±0.03 vs. 1.42±0.15, P<0.001; protein: 0.47±0.11 vs. 1.13±0.19, P<0.05), and the expression level of miR-382-3p decreased significantly(0.05±0.01 vs. 1.03± 0.12, P<0.001). Compared with SNHG1 overexpression + mimic control group, the cell proliferation ability of SNHG1 overexpression + miR-382-3p overexpression group decreased (0.15±0.02 vs. 0.26±0.01, P<0.001), the percentage of EdU positive cells decreased (5.97%±0.33% vs. 11.70%±0.87%, P<0.001), the expression levels of PCNA mRNA and protein decreased significantly (mRNA: 0.64±0.09 vs. 3.33±0.38, P<0.001; protein: 1.70±0.36 vs. 2.34±0.16, P<0.05), the expression levels of p27 mRNA and protein increased (mRNA: 1.01±0.44 vs. 0.09±0.04, P<0.05; protein: 1.38±0.31 vs. 0.50±0.09, P<0.05). Conclusion SNHG1 presents high expression in hypertrophic scar and can negatively regulate miR-382-3p expression to promote proliferation of primary hypertrophic scar fibroblasts, which may become a potential new target in the treatment of hypertrophic scar.