Department of Orthopedics, Fuzhou Second Hospital Affiliated Xiamen University Fuzhou, Fuzhou, Fujian, China.
Biosci Biotechnol Biochem. 2020 May;84(5):989-996. doi: 10.1080/09168451.2020.1717925. Epub 2020 Jan 26.
Morroniside plays a therapeutic role in knee osteoarthritis (OA) by protecting chondrocytes. PI3K/AKT signaling is involved in the regulation of chondrocytes by Morroniside. PI3K/AKT suppresses autophagy through downstream signaling. However, the regulation of chondrocyte autophagy by Morroniside and the significance of the above effect on protecting chondrocytes aren't clear. The results showed that Morroniside inhibited the autophagiy of human OA chondrocytes. Besides, both PI3K inhibitors and mTOR inhibitors significantly reversed the autophagy reduced by Morroniside, but had no effect on the protective effect of Morroniside on chondrocytes. However, the enhanced autophagy caused by overexpression of autophagic genes enhanced the protective effect of Morroniside on chondrocytes. In conclusion, Morroniside represses the autophagy of human OA chondrocyte, which is related to PI3K/mTOR pathway. Moreover, the upregulation of autophagy further promoted the role of Morroniside in treating chondrocytes. Our data present a potential clue for the therapeutic strategies of Morroniside in treating OA.
山柰酚通过保护软骨细胞在膝骨关节炎（OA）中发挥治疗作用。PI3K/AKT 信号通路参与了山柰酚对软骨细胞的调节。PI3K/AKT 通过下游信号抑制自噬。然而，山柰酚对软骨细胞自噬的调节以及上述对保护软骨细胞的影响的意义尚不清楚。结果表明，山柰酚抑制了人 OA 软骨细胞的自噬。此外，PI3K 抑制剂和 mTOR 抑制剂均能显著逆转山柰酚引起的自噬减少，但对山柰酚保护软骨细胞的作用没有影响。然而，自噬基因过表达引起的自噬增强增强了山柰酚对软骨细胞的保护作用。总之，山柰酚抑制人 OA 软骨细胞的自噬，与 PI3K/mTOR 通路有关。此外，自噬的上调进一步促进了山柰酚在治疗软骨细胞中的作用。我们的数据为山柰酚治疗 OA 的治疗策略提供了一个潜在的线索。
