| Objective To explore the effect and mechanism of the Guben Huoxue Zhuanggu Formula (GBHX) in the treatment of glucocorticoid induced osteoporosis (GIOP). Methods 8-week-old SD rats were randomly divided into a blank group, a model group, a western medicine group, and a traditional Chinese medicine group (n=10).By serological detection of B-ALP and BGP,bone tissue pathology HE staining, Micro-CT scanning to detect bone density and microstructure in rats, immunofluorescence dual labeling method and Western blot to detect the expression of autophagy related proteins Beclin1, LC3, p62 and PI3K-Akt signaling pathway related proteins in femoral tissue of rats in each group, the effect and mechanism of GBHX in improving GIOP were verified. Results The experimental research results showed that in the model group, the thickness of the femoral cortex became thinner, the bone trabeculae became thinner, and even fractured, with widened spacing and increased vacuolar fat. Compared with the blank group, the B-ALP, Tb.Sp, SMI, p-Akt, p-PI3K, LC3, and Beclin1 levels in the model group rats increased(P<0.05), BV/TV, Tb. Th, and BMD decreased(P<0.05); The blue fluorescence of the model group weakened, while the green fluorescence expression of LC3 and Beclin1 increased. Compared with the model group, the Western medicine group and the traditional Chinese medicine group showed thickening of the cortical bone, increased continuity of bone trabeculae, increased quantity and shape, reduced spacing, and decreased fat vacuoles. The levels of B-ALP, Tb.Sp, SMI, p-Akt, p-PI3K, LC3,and Beclin1 decreased in the traditional Chinese medicine group (P<0.05), while BV/TV, Tb. Th, BMD, and p62 increased in the traditional Chinese medicine group(P<0.05).The blue fluorescence of both the Western medicine group and the Chinese medicine group increased to varying degrees, while the expression of LC3 and Beclin1 green fluorescence in the Chinese medicine group and the Western medicine group decreased significantly. Conclusion GBHX can promote bone formation and effectively improve bone quality in GIOP rats. Its mechanism may be related to the autophagy of BMSCs mediated by the PI3K/Akt signaling pathway. |