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• W2983078506 abstract "This study aimed to elucidate the mechanism of autophagy in bone metabolism in high-glucose environments and its relationship with Toll-like receptor 4 (TLR4).A TLR4 knockout diabetic rat model and MC3T3-E1 with TLR4 silencing by small interfering RNA were used to observe the protective mechanism of TLR4 knockdown or silencing in hyperglycemia-induced bone injury.The inhibition of TLR4 expression improved bone metabolism and bone structure; promoted alkaline phosphatase (ALP) and osteocalcin (OCN) secretion, enhanced bone morphogenic protein (BMP)-2 expression, promoted bone mineralization, and reduced hyperglycemia-induced osteoblast apoptosis. TLR4 knockdown or silencing reduced the levels of inflammatory factors interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha at the animal and cell levels, inhibited the expression of inflammatory pathway proteins, and downregulated the expression of Beclin 1 and LC3II/LC-1 proteins. The inhibition of autophagic activity enhanced the osteoprotective effect of TLR4 knockdown, improved cell viability, reduced the apoptosis rate of osteoblasts, and promoted the BMP-2 protein level and ALP and OCN secretion. Conversely, the activation of autophagy significantly aggravated osteoblast apoptosis, reduced BMP-2 protein levels, and inhibited ALP and OCN secretion.Taken together, the experimental results supported the hypothesis that TLR4 deficiency might alleviate hyperglycemia-induced apoptosis and differentiation suppression in osteoblasts and exert osteoprotective effects via autophagic inhibition." @default.
• W2983078506 created "2019-11-22" @default.
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• W2983078506 date "2020-01-01" @default.
• W2983078506 modified "2023-09-25" @default.
• W2983078506 title "Toll-like receptor 4 knockout protects against diabetic-induced imbalance of bone metabolism via autophagic suppression" @default.
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• W2983078506 doi "https://doi.org/10.1016/j.molimm.2019.10.025" @default.
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