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作 者:许心弦[1] 胡月正[1] 柳海晓[1] XU Xinxian;HU Yuezheng;LIU Haixiao(The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University,Zhejiang 325000,China)
出 处:《浙江创伤外科》2023年第9期1601-1604,1608,共5页Zhejiang Journal of Traumatic Surgery
基 金:浙江省温州市科技局基础性医疗卫生科技项目(Y20210397)。
摘 要:目的 探索促红细胞生成素(EPO)通过调节信号转导与转录激活子1(STAT1)-半胱氨酸天冬氨酸蛋白酶3(Caspase3)通路对激素性股骨头坏死SANFH的治疗机制。方法 将40只SD大鼠随机分为阴性对照组、阳性对照组、模型组、治疗组。模型组和治疗组大鼠左臀肌注射地塞米松针,阴性和阳性对照组注射0.9%氯化钠溶液,治疗组和阳性对照组的大鼠尾部静脉分别缓慢注射EPO 500 U/kg。治疗结束后比较各组大鼠病理切片空骨陷窝率,并检测各组骨组织p-STAT1和C-Caspase 3蛋白表达水平,及STAT1和Caspase 3的mRNA表达水平。结果 与两对照组相比,模型组及治疗组中大鼠股骨头空骨陷窝率、骨组织中p-STAT1和C-Caspase 3蛋白表达水平及STAT1和Caspase 3的mRNA表达水平均显著升高(P<0.05)。与模型组比较,治疗组大鼠以上指标均显著降低(P<0.05)。结论 EPO通过抑制关节内STAT1、Caspase 3的表达水平,调控STAT1-Caspase 3信号通路来治疗SANFH。Objective To explore the mechanisms of erythropoietin(EPO)on steroid-induced avascular necrosis of the femoral head(SANFH)by regulating signal transducer and activator of transcription 1(STAT1)-Caspase 3 signaling.Methods 40 SD rats were randomly allocated into negative control group,positive control group,SANFH group and treatment group.SANFH group and treatment group were given injections of dexamethasone in the left hip,two control groups were injected 0.9%sodium chloride,and treatment group and positive control group were given injections of EPO.At the end of treatment,the percentage of empty lacunae was calculated,the protein levels of p-STAT1 and C-Caspase 3 of bone tissues,as well as the mRNA levels of STAT1 and Caspase 3 were detected.Results Compared with the two control groups,the percentages of empty lacunae,the protein levels of p-STAT1 and C-Caspase 3 of bone tissues,and the mRNA levels of STAT1 and Caspase 3 were significantly higher(P<0.05).Compared with SANFH group,the levels of the indicators above in treatment group were all significantly reduced(P<0.05).Conclusion EPO can inhibit the local expression levels of STAT1 and Caspase 3 and regulating the STAT1-Caspase 3 signaling,thus attenuating the progress of SANFH.
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