METTL14基因敲除对骨质疏松小鼠骨微结构和骨密度及氧化应激的影响

Effects of METTL14 knockdown on bone microarchitecture,bone mineral density and oxidative stress in osteoporotic mice

目的 研究人甲基转移酶样蛋白14(METTL14)基因敲除对骨质疏松小鼠骨微结构、骨密度及氧化应激的影响。方法 12只野生型小鼠随机分为对照组和模型组,每组6只。对照组小鼠切除卵巢附近脂肪组织;模型组小鼠切除双侧卵巢构建骨质疏松小鼠模型;另取6只切除双侧卵巢的METTL14基因敲除小鼠作为敲低组。术后8周,使用micro-CT扫描仪测量小鼠右股骨骨密度和骨微结构相关指标,使用ELISA检测小鼠血清中PINP、CTX、MDA和SOD水平。结果 模型组小鼠骨密度、BV/TV、Tb. N、Tb. Th、SOD、PINP、CTX水平显著低于对照组,差异有统计学意义(P<0.05)。此外,敲低组小鼠骨密度、BV/TV、Tb. N、Tb. Th、SOD、PINP、CTX水平显著低于模型组,差异有统计学意义(P<0.05)。模型组小鼠Tb. Sp、MDA水平显著高于对照组,敲低组小鼠Tb. Sp、MDA水平显著高于模型组,差异有统计学意义(P<0.05)。结论 METTL14基因敲除可抑制骨质疏松小鼠骨密度,破坏骨微结构,并促进氧化应激。

Objective To investigate the effects of METTL14 knockdown on bone microarchitecture,bone mineral density and oxidative stress in osteoporotic mice.Methods Twelve wild⁃type mice were randomly divided into control and model groups,six mice in each group.In the control group,adipose tissue near the ovaries was excised;in the model group,bilateral ovaries were excised to construct an osteoporotic mouse model;six METTL14 knockout mice with bilateral ovaries excised were taken as the knockdown group.At 8 weeks after surgery,the bone density and bone microstructure of the right femur were measured by micro⁃CT scanner,and the levels of PINP,CTX,MDA and SOD in the serum of mice were measured by ELISA.Results The levels of BMD,BV/TV,Tb.N,Tb.Th,SOD,PINP and CTX in the model group were significantly lower than those in the control group,and the differences were statistically significant(P<0.05).In addition,the levels of BMD,BV/TV,Tb.N,Tb.Th,SOD,PINP and CTX in the knock⁃down group were significantly lower than those in the model group,and the differences were statistically significant(P<0.05).The levels of Tb.Sp and MDA in the model group were significantly higher than those in the control group,and the levels of Tb.Sp and MDA in the knockdown group were significantly higher than those in the model group,and the differences were statistically significant(P<0.05).Conclusion METTL14 knockdown can inhibit bone density,disrupt bone microarchitecture and promote oxidative stress in osteoporotic mice.