The Effect of Hoxa11-as on the Differentiation of Osteoblasts in Osteoporosis by Regulating Cellular Autophagy

Objective: To investigate the effect of long non-coding RNA (lncRNA) Hoxa11-as on the osteogenic differentiation in osteoporosis (OP) through the regulation of cellular autophagy. Methods: Establish a rat model of osteoporosis. Divide 12-week-old male rats into a blank group, a Hoxa11-as group, and a si-Hoxa11-as group, with 10 rats in each group. To establish glucocorticoid-induced osteoporosis, the required concentration is 1 ml/kg. The average body weight of this batch of rats is 500 g. The glucocorticoid is intraperitoneally injected at a dose of 0.5 ml/kg per day, and the intraperitoneal injection is continued for 8 weeks. After successfully establishing the rat model of osteoporosis, a bone rotary drill is used to create a 1-mm defect at the distal end of the femur of the model. At the same time, a hydrogel containing Hoxa11-as and si-Hoxa11-as plasmids is placed. After continuing the culture for 4 weeks, the samples are collected. Perform immunohistochemistry (IHC) and Real-time quantitative polymerase chain reaction (qPCR) experiments on the specimens to detect the protein expression levels of Hoxa11-as, LC3, Beclin1, and Runx2 factors. Results: The results of qPCR indicated that in the Hoxa11-as group, there were statistically significant differences in the mRNA expression levels of Hoxa11-as, LC3, Beclin1 and Runx2 (P < 0.05); in the si-Hoxa11-as group, there were also statistically significant differences in the mRNA expression levels of Hoxa11-as, LC3, Beclin1 and Runx2 (P < 0.05). Conclusion: Hoxa11-as has an inhibitory effect on cellular autophagy, while si-Hoxa11-as can activate cellular autophagy and enhance the differentiation level of osteoblasts.