Background:Hypertrophy of the ligamentumflavum(HLF)is a common contributor to spinal stenosis which results in significant neurological impairments.Circular RNA(circRNA)circ_0003609 has been linked to HLF;however,the ex...Background:Hypertrophy of the ligamentumflavum(HLF)is a common contributor to spinal stenosis which results in significant neurological impairments.Circular RNA(circRNA)circ_0003609 has been linked to HLF;however,the exact mechanism by which it causes this disease is unclear.Methods:Circ_0003609 expressions were regulated in HLF cells by overexpression vectors and RNA interference.Cell proliferation andfibrosis-related gene expression were checked by the Cell Counting Kit-8(CCK-8)assay and western blotting.CircBank’s prediction of the association between miR-155 and circ_0003609 was supported by a dual-luciferase reporter experiment.The function of the miR-155/sirtuin 1(SIRT1)axis in controlling HLFfibrosis was further examined.Results:Overexpression of circ_0003609 suppressed HLF cell propagation andfibrosis compared to its silencing.It was found that circ_0003609 served as the sponge for miR-155 and that the circ_0003609/miR-155 axis controlled thefibrosis of HLF cells.It was found that circ_0003609 acted as a sponge for miR-155,regulating thefibrosis of HLF cells.Further,miR-155 targets SIRT1,and the miR-155/SIRT1 axis promotes HLF cellfibrosis.Conclusion:Circ_0003609 ameliorates hypertrophied ligamentumflavum(LF)by modulating the miR-155/SIRT1 axis,indicating a potential treatment approach for HLF.展开更多
目的探讨九味白术汤对溃疡性结肠炎(UC)大鼠肠黏膜免疫屏障及微小RNA(miR)-155/细胞因子信号转导抑制因子-1(SOCS-1)轴的影响。方法将大鼠随机分为对照组、模型组、药物组、药物+阴性对照组、药物+miR-155过表达组,每组8只,以2,4,6-三...目的探讨九味白术汤对溃疡性结肠炎(UC)大鼠肠黏膜免疫屏障及微小RNA(miR)-155/细胞因子信号转导抑制因子-1(SOCS-1)轴的影响。方法将大鼠随机分为对照组、模型组、药物组、药物+阴性对照组、药物+miR-155过表达组,每组8只,以2,4,6-三硝基苯磺酸(TNBS)诱导建立UC模型,给药7 d后,检测疾病活动指数(DAI)评分,HE染色观察结肠黏膜组织形态变化,ELISA法检测结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,RT-qPCR法检测结肠黏膜组织miR-155表达,Western blot法检测结肠黏膜组织SOCS-1、GP130、iNOS、RORγt、STAT3蛋白表达。结果与对照组比较,模型组大鼠1、2、3、4、5、6、7 d DAI评分升高(P<0.05);与模型组比较,药物组大鼠5、6、7 d DAI评分降低(P<0.05)。与对照组比较,模型组大鼠结肠黏膜损伤评分,结肠黏膜组织病理学评分,结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,miR-155表达,GP130、iNOS、RORγt、STAT3蛋白表达均升高(P<0.05),SOCS-1蛋白表达降低(P<0.05);与模型组比较,药物组、药物+阴性对照组大鼠结肠黏膜损伤评分,结肠黏膜组织病理学评分,结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,miR-155表达,GP130、iNOS、RORγt、STAT3蛋白表达均降低(P<0.05),SOCS-1蛋白表达升高(P<0.05)。结论九味白术汤对UC大鼠肠黏膜免疫屏障具有保护作用,该作用可能与抑制miR-155表达从而促进SOCS-1表达有关。展开更多
基金This research was supported by the Shanghai Natural Science Fund(No.21ZR1447500)Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital Baoshan Branch Medical Key Specialty Construction Project(No.rbzdzk-2023-001).
文摘Background:Hypertrophy of the ligamentumflavum(HLF)is a common contributor to spinal stenosis which results in significant neurological impairments.Circular RNA(circRNA)circ_0003609 has been linked to HLF;however,the exact mechanism by which it causes this disease is unclear.Methods:Circ_0003609 expressions were regulated in HLF cells by overexpression vectors and RNA interference.Cell proliferation andfibrosis-related gene expression were checked by the Cell Counting Kit-8(CCK-8)assay and western blotting.CircBank’s prediction of the association between miR-155 and circ_0003609 was supported by a dual-luciferase reporter experiment.The function of the miR-155/sirtuin 1(SIRT1)axis in controlling HLFfibrosis was further examined.Results:Overexpression of circ_0003609 suppressed HLF cell propagation andfibrosis compared to its silencing.It was found that circ_0003609 served as the sponge for miR-155 and that the circ_0003609/miR-155 axis controlled thefibrosis of HLF cells.It was found that circ_0003609 acted as a sponge for miR-155,regulating thefibrosis of HLF cells.Further,miR-155 targets SIRT1,and the miR-155/SIRT1 axis promotes HLF cellfibrosis.Conclusion:Circ_0003609 ameliorates hypertrophied ligamentumflavum(LF)by modulating the miR-155/SIRT1 axis,indicating a potential treatment approach for HLF.
文摘目的探讨九味白术汤对溃疡性结肠炎(UC)大鼠肠黏膜免疫屏障及微小RNA(miR)-155/细胞因子信号转导抑制因子-1(SOCS-1)轴的影响。方法将大鼠随机分为对照组、模型组、药物组、药物+阴性对照组、药物+miR-155过表达组,每组8只,以2,4,6-三硝基苯磺酸(TNBS)诱导建立UC模型,给药7 d后,检测疾病活动指数(DAI)评分,HE染色观察结肠黏膜组织形态变化,ELISA法检测结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,RT-qPCR法检测结肠黏膜组织miR-155表达,Western blot法检测结肠黏膜组织SOCS-1、GP130、iNOS、RORγt、STAT3蛋白表达。结果与对照组比较,模型组大鼠1、2、3、4、5、6、7 d DAI评分升高(P<0.05);与模型组比较,药物组大鼠5、6、7 d DAI评分降低(P<0.05)。与对照组比较,模型组大鼠结肠黏膜损伤评分,结肠黏膜组织病理学评分,结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,miR-155表达,GP130、iNOS、RORγt、STAT3蛋白表达均升高(P<0.05),SOCS-1蛋白表达降低(P<0.05);与模型组比较,药物组、药物+阴性对照组大鼠结肠黏膜损伤评分,结肠黏膜组织病理学评分,结肠黏膜组织TNF-α、IL-23、IL-6、IL-1β水平,miR-155表达,GP130、iNOS、RORγt、STAT3蛋白表达均降低(P<0.05),SOCS-1蛋白表达升高(P<0.05)。结论九味白术汤对UC大鼠肠黏膜免疫屏障具有保护作用,该作用可能与抑制miR-155表达从而促进SOCS-1表达有关。
