| Objective To investigate the effects of long non coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1)/microRNA-101-3p (miR-101-3p) /high mobility group protein A2 (HMGA2) on osteogenic differentiation in osteoporosis (OP) rats. Methods An OP rat model was constructed and the osteoblasts were extracted, and the relative expression levels of LncRNA SNHG1 and miR-101-3p were detected using qRT-PCR. The cells were grouped into Control group, Model group, sh-NC group, sh-SNHG1 group, sh-SNHG1+inhibitor NC group, and sh-SNHG1+miR-101-3p inhibitor group. The relative expression levels of LncRNA SNHG1, miR-101-3p, and HMGA2 mRNA in osteoblasts (qRT-PCR method), cell proliferation ability (CCK-8 kit method), apoptosis status (flow cytometry method), relative activity of ALP in osteoblasts (ALP kit), mineralization ability of osteoblasts (eosin staining), and protein expression levels of HMGA2, Bax, and Bcl-2 in osteoblasts were measured. Relevant experiments verified the targeting relationship between miR-101-3p and LncRNA SNHG1 and HMGA2. Results Compared with the Control group, the relative expression levels of LncRNA SNHG1 and HMGA2 mRNA, the expression levels of HMGA2 and Bax proteins, and the apoptosis rate in osteoblasts were greatly higher in the Model group, the relative expression level of miR-101-3p, the expression level of Bcl-2 protein, cell viability, ALP relative activity, and mineralization ability were greatly lower (P<0.05). Compared with the sh-NC group, the relative expression levels of LncRNA SNHG1 and HMGA2 mRNA, the expression levels of HMGA2 and Bax proteins, and the apoptosis rate in osteoblasts were greatly lower in the sh-SNHG1 group, the relative expression level of miR-101-3p, the expression level of Bcl-2 protein, cell viability, ALP relative activity, and mineralization ability were greatly higher (P<0.05). Compared with the sh-SNHG1+inhibitor NC group, the relative expression levels of LncRNA SNHG1 and HMGA2 mRNA, the expression levels of HMGA2 and Bax proteins, and the apoptosis rate in osteoblasts were greatly higher in the sh-SNHG1+miR-101-3p inhibitor group, the relative expression level of miR-101-3p, the expression level of Bcl-2 protein, cell viability, ALP relative activity, and mineralization ability were greatly lower (P<0.05). Conclusion The expression level of LncRNA SNHG1 is greatly upregulated in OP rat osteoblasts. Silencing the expression of LncRNA SNHG1 can upregulate the expression of miR-101-3p and inhibit the expression of HMGA2, thereby reducing osteoblast apoptosis, enhancing osteoblast mineralization ability and ALP activity, and promoting their proliferation and differentiation. |