PI3K/AKT/mTOR通路
自噬
骨细胞
糖皮质激素
蛋白激酶B
化学
细胞凋亡
细胞生物学
皮诺森布林
内分泌学
内科学
医学
生物
成骨细胞
生物化学
体外
抗氧化剂
类黄酮
作者
Xinyuan Wang,Linjing Gong,Jian Huang,Jiang Chang,Zuoqin Yan
标识
DOI:10.1016/j.ejphar.2020.173212
摘要
Glucocorticoids are widely used in clinical practice, but are associated with potentially severe side effects like glucocorticoid-induced osteoporosis (GIOP) and glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH). Glucocorticoid-induced osteocyte apoptosis plays critical roles in the pathological processes of both GIOP and GA-ONFH. Pinocembrin is a natural flavonoid that may exert protective effects on osteocytes. The present study investigated the effects of pinocembrin on glucocorticoid-induced apoptosis of murine long bone osteocyte Y4 (MLO-Y4) cells and sought to elucidate the underlying molecular mechanism. We found that pinocembrin attenuated glucocorticoid-induced cell viability injury and apoptosis of MLO-Y4 cells. Moreover, pinocembrin increased Beclin-1 and LC3B-II level, but decreased p62 expression, suggesting that pinocembrin activates autophagy in glucocorticoid-treated MLO-Y4 cells. The protective effects of pinocembrin on glucocorticoid-induced apoptosis of MLO-Y4 cells were mimicked by a known stimulator of autophagy but prevented by a known inhibitor of autophagy. Pinocembrin also suppressed the PI3K/Akt/mTOR signaling pathway, which regulates cell autophagy, in glucocorticoid-treated MLO-Y4 cells. In conclusion, the results indicate that pinocembrin alleviates glucocorticoid-induced osteocyte apoptosis by activating autophagy via suppressing the PI3K/Akt/mTOR pathway. Pinocembrin may represent a potential natural agent for preventing and treating GIOP and GA-ONFH.
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