miRNAs调节的免疫炎性机制在脊髓损伤致骨质疏松症患者发病中的调控机制

Regulatory role of miRNAs in the pathogenesis of osteoporosis induced by spinal cord injury

目的探究微小RNAs(miRNAs)调节的免疫炎性机制在脊髓损伤致骨质疏松症(CSCI-OP)发病中的调控机制。方法收集30例CSCI-OP患者为脊髓损伤组,选50例老年性骨质疏松患者为老年骨质疏松组,选50例健康体检人群为正常对照组。对比各组激素指标、炎症因子、miRNAs表达、生物信息学分析的变化,探究影响CSCI-OP患者发病的主要因素。结果与脊髓损伤组对比,老年骨质疏松组的睾酮(T)、肿瘤坏死因子-α(TNF-α)水平上升,雌二醇(E2)、白细胞介素-6(IL-6)、骨性碱性磷酸酶(BLAP)水平下降(P<0.05);而两组的25羟基维生素D(25-OHD)、甲状旁腺激素(PTH)水平对比,但差异无统计学意义(P>0.05)。单因素分析显示CSCI-OP发生主要与年龄、性别、脊髓损伤病程、糖尿病有关(P<0.05)。与正常对照组相比,老年骨质疏松组、脊髓损伤组的IL-6 miRNA、BLAP miRNA表达升高,TNF-αmiRNA表达下降(P<0.05)。结论miRNAs在CSCI-OP中可有效调节,且通过靶向免疫炎性机制能明显减缓CSCI-OP的发生及发展。

Objective To explore the regulatory role of immunoinflammatory mechanism regulated by tiny RNAs(miRNAs)in the pathogenesis of spinal cord injury-induced osteoporosis(CSCI-OP).Methods Thirty patients with CSCI-OP admitted to our hospital from July 2021 to July 2022 were selected as the observation group,fifty patients with senile osteoporosis were selected as the control group,and fifty healthy people were selected as the normal control group.The three groups were compared in terms of hormone indexes,inflammatory factors,miR-NAs expression and bioinformatics analysis.The main factors affecting the pathogenesis of CSCI-OP patients were detected.Results Compared with the spinal cord injury group,the T and TNF-αlevels were increased,and the E2,IL-6 and BLAP levels were decreased in the senile osteoporosis group(P<0.05),but there was no significant difference in 25-OHD and PTH levels between the two groups(P>0.05).Univariate analysis showed that the incidence of CSCI-OP was mainly related to age,sex,duration of spinal cord injury and diabetes mellitus(P<0.05).Compared with the normal control group,the expression of IL-6 miRNA and BLAP miRNA in the control group and observation group was increased and the expression of TNF-αmiRNA was decreased(P<0.05).Conclusion MiRNAs can be effectively regulated in CSCI-OP.It can significantly slow down the occurrence and development of CSCI-OP through targeted immune inflammatory mechanisms.