Leukemia inhibitory factor receptor(LIFR),as a neuroregulatory cytokine receptor,generally shows a neuroprotective effect in central nervous system injuries.In this study,to understand the effect of LIFR on pathogenes...Leukemia inhibitory factor receptor(LIFR),as a neuroregulatory cytokine receptor,generally shows a neuroprotective effect in central nervous system injuries.In this study,to understand the effect of LIFR on pathogenesis of neural tube defects,we explored spatiotemporal expression of LIFR at different stages of fetal development in normal and neural tube defect embryos.Spina bifida aperta was induced with all-trans retinoic acid on embryonic day 10 in rats,and the spatiotemporal expression of LIFR was investigated in spina bifida aperta rats and healthy rats from embryonic day 11 to 17.Real time-polymerase chain reaction and western blot assay were used to examine mRNA and protein expression of LIFR in healthy control and neural tube defect embryos.Results of the animal experiment demonstrated that expression of LIFR protein and mRNA in the spinal cords of normal rat embryos increased with embryonic development.LIFR was significantly downregulated in the spinal cords of spina bifida aperta rats compared with healthy rats from embryonic days 11 to 17.Immunohistochemical staining showed that the expression of LIFR in placenta and spinal cord in spina bifida aperta rat embryos was decreased compared with that in control embryos at embryonic day 15.Results from human embryo specimens showed that LIFR mRNA expression was significantly down-regulated in spinal cords of human fetuses with neural tube defects compared with normal controls at a gestational age of 24 to 33 weeks.The results were consistent with the down-regulation of LIFR in the animal experiments.Our study revealed spatiotemporal changes in expression of LIFR during embryonic neurulation.Thus,LIFR might play a specific role in neural tube development.All animal and human experimental procedures were approved by the Medical Ethics Committee of Shengjing Hospital of China Medical University,China(approval No.2016PS106K)on February 25,2016.展开更多
目的研究血清硒蛋白P(SEPP)、摄食抑制因子-1(Nesfatin-1)、肿瘤坏死因子-α(TNF-α)水平与妊娠糖尿病患者胰岛素抵抗的关系。方法回顾性选取2018年1月至2021年6月邢台医学高等专科学校第二附属医院收治的120例妊娠糖尿病患者为观察组,...目的研究血清硒蛋白P(SEPP)、摄食抑制因子-1(Nesfatin-1)、肿瘤坏死因子-α(TNF-α)水平与妊娠糖尿病患者胰岛素抵抗的关系。方法回顾性选取2018年1月至2021年6月邢台医学高等专科学校第二附属医院收治的120例妊娠糖尿病患者为观察组,选择同期健康体检产妇120名为对照组。比较两组血糖指标[空腹血糖(FBG)、餐后30 min血糖(30 min PG)、餐后1 h血糖(1 h PG)、餐后2 h血糖(2 h PG)]及胰岛素分泌指标[空腹胰岛素(FINS)、餐后30 min胰岛素(30 min INS)、餐后1 h胰岛素(1 h INS)、餐后2 h胰岛素(2 h INS)],对比两组胰岛素抵抗相关指数[胰岛素抵抗指数(HOMA-IR)、胰岛素β细胞功能指数(HOMA-β)、早期胰岛素分泌功能指数(△I_(30)/△G_(30))];比较两组血清SEPP、Nesfatin-1、TNF-α水平;分析血清SEPP、Nesfatin-1、TNF-α水平与妊娠糖尿病患者胰岛素抵抗的相关性。结果观察组FBG、30 min PG、1 h PG、2 h PG水平均高于对照组,差异均有统计学意义(P<0.05)。观察组FINS、1 h INS、2 h INS水平高于对照组,差异均有统计学意义(P<0.05),30 min INS较对照组比较差异无统计学意义(P>0.05)。观察组HOMA-IR高于对照组,HOMA-β、△I_(30)/△G_(30)低于对照组,差异均有统计学意义(P<0.05)。观察组Nesfatin-1、TNF-α水平高于对照组,SEPP水平低于对照组,差异均有统计学意义(P<0.05)。经Pearson检验,SEPP与HOMA-β、△I_(30)/△G_(30)呈正相(P<0.05),与HOMA-IR呈负相关(P<0.05);Nesfatin-1、TNF-α与HOMA-IR呈正相关(P<0.05),与HOMA-β、△I_(30)/△G_(30)呈负相关(P<0.05)。结论妊娠糖尿病患者血清Nesfatin-1、TNF-α水平明显上升,SEPP水平明显降低,且与胰岛素抵抗存在一定相关性。展开更多
基金supported by the National Natural Science Foundation of China,No.81601292(to DA),No.81671469(to ZWY)the National Basic Research Program of China(973 Program),No.2013CB945402(to ZWY)the National Key Research and Development Program of China,No.2016YFC1000505(to ZWY)
文摘Leukemia inhibitory factor receptor(LIFR),as a neuroregulatory cytokine receptor,generally shows a neuroprotective effect in central nervous system injuries.In this study,to understand the effect of LIFR on pathogenesis of neural tube defects,we explored spatiotemporal expression of LIFR at different stages of fetal development in normal and neural tube defect embryos.Spina bifida aperta was induced with all-trans retinoic acid on embryonic day 10 in rats,and the spatiotemporal expression of LIFR was investigated in spina bifida aperta rats and healthy rats from embryonic day 11 to 17.Real time-polymerase chain reaction and western blot assay were used to examine mRNA and protein expression of LIFR in healthy control and neural tube defect embryos.Results of the animal experiment demonstrated that expression of LIFR protein and mRNA in the spinal cords of normal rat embryos increased with embryonic development.LIFR was significantly downregulated in the spinal cords of spina bifida aperta rats compared with healthy rats from embryonic days 11 to 17.Immunohistochemical staining showed that the expression of LIFR in placenta and spinal cord in spina bifida aperta rat embryos was decreased compared with that in control embryos at embryonic day 15.Results from human embryo specimens showed that LIFR mRNA expression was significantly down-regulated in spinal cords of human fetuses with neural tube defects compared with normal controls at a gestational age of 24 to 33 weeks.The results were consistent with the down-regulation of LIFR in the animal experiments.Our study revealed spatiotemporal changes in expression of LIFR during embryonic neurulation.Thus,LIFR might play a specific role in neural tube development.All animal and human experimental procedures were approved by the Medical Ethics Committee of Shengjing Hospital of China Medical University,China(approval No.2016PS106K)on February 25,2016.
文摘目的研究血清硒蛋白P(SEPP)、摄食抑制因子-1(Nesfatin-1)、肿瘤坏死因子-α(TNF-α)水平与妊娠糖尿病患者胰岛素抵抗的关系。方法回顾性选取2018年1月至2021年6月邢台医学高等专科学校第二附属医院收治的120例妊娠糖尿病患者为观察组,选择同期健康体检产妇120名为对照组。比较两组血糖指标[空腹血糖(FBG)、餐后30 min血糖(30 min PG)、餐后1 h血糖(1 h PG)、餐后2 h血糖(2 h PG)]及胰岛素分泌指标[空腹胰岛素(FINS)、餐后30 min胰岛素(30 min INS)、餐后1 h胰岛素(1 h INS)、餐后2 h胰岛素(2 h INS)],对比两组胰岛素抵抗相关指数[胰岛素抵抗指数(HOMA-IR)、胰岛素β细胞功能指数(HOMA-β)、早期胰岛素分泌功能指数(△I_(30)/△G_(30))];比较两组血清SEPP、Nesfatin-1、TNF-α水平;分析血清SEPP、Nesfatin-1、TNF-α水平与妊娠糖尿病患者胰岛素抵抗的相关性。结果观察组FBG、30 min PG、1 h PG、2 h PG水平均高于对照组,差异均有统计学意义(P<0.05)。观察组FINS、1 h INS、2 h INS水平高于对照组,差异均有统计学意义(P<0.05),30 min INS较对照组比较差异无统计学意义(P>0.05)。观察组HOMA-IR高于对照组,HOMA-β、△I_(30)/△G_(30)低于对照组,差异均有统计学意义(P<0.05)。观察组Nesfatin-1、TNF-α水平高于对照组,SEPP水平低于对照组,差异均有统计学意义(P<0.05)。经Pearson检验,SEPP与HOMA-β、△I_(30)/△G_(30)呈正相(P<0.05),与HOMA-IR呈负相关(P<0.05);Nesfatin-1、TNF-α与HOMA-IR呈正相关(P<0.05),与HOMA-β、△I_(30)/△G_(30)呈负相关(P<0.05)。结论妊娠糖尿病患者血清Nesfatin-1、TNF-α水平明显上升,SEPP水平明显降低,且与胰岛素抵抗存在一定相关性。
