位于青藏高原与黄土高原过渡带的甘肃武都万象洞石笋WXSM51和WXSM52提供了M IS 5(118~79kaB.P.)高分辨率的1δ8O记录。研究表明,万象洞石笋1δ8O值与夏季风强度呈负相关关系,与我国西南部的贵州董歌洞石笋1δ8O记录有良好的对应关系,并...位于青藏高原与黄土高原过渡带的甘肃武都万象洞石笋WXSM51和WXSM52提供了M IS 5(118~79kaB.P.)高分辨率的1δ8O记录。研究表明,万象洞石笋1δ8O值与夏季风强度呈负相关关系,与我国西南部的贵州董歌洞石笋1δ8O记录有良好的对应关系,并与高纬度的格陵兰NGR IP冰芯1δ8O记录和65°N太阳辐射强度有很好的一致性,说明万象洞石笋1δ8O记录了118~79kaB.P.期间亚洲季风强度的变化,同时也说明东亚季风强度的变化和全球气候变化同步,而且主要受控于北半球太阳辐射强度的变化。同时它与地中海碳酸盐记录有很好的相似性,和巴西石笋1δ8O记录在千年尺度上表现出相反的变化趋势,说明东亚季风区、地中海地区以及巴西季风区之间存在密切的联系,指示了南北半球气候在千年尺度上存在“跷跷板”(seesaw)现象。万象洞石笋1δ8O记录的M IS 5b与M IS 5 a突发性转换,与NGR IP冰芯1δ8O记录相似,而与神农架记录存在差异,说明万象洞地区对亚洲季风强度的响应更为敏感。展开更多
AIM To evaluate the levels of mi R-192-5 p in non-alcoholic fatty liver disease(NAFLD) models and demonstrate the role of mi R-192-5 p in lipid accumulation. METHODS Thirty Sprague Dawley rats were randomly divided in...AIM To evaluate the levels of mi R-192-5 p in non-alcoholic fatty liver disease(NAFLD) models and demonstrate the role of mi R-192-5 p in lipid accumulation. METHODS Thirty Sprague Dawley rats were randomly divided into three groups, which were given a standard diet, a high-fat diet(HFD), and an HFD with injection of liraglutide. At the end of 16 weeks, hepatic mi R-192-5 p and stearoyl-Co A desaturase 1(SCD-1) levels were measured. Mi R-192-5 p mimic and inhibitor and SCD-1 si RNA were transfected into Huh7 cells exposed to palmitic acid(PA). Lipid accumulation was evaluated by oil red O staining and triglyceride assays. Direct interaction was validated by dual-luciferase reporter gene assays.RESULTS The HFD rats showed a 0.46-fold decrease and a 3.5-fold increase in hepatic mi R-192-5 p and SCD-1 protein levels compared with controls, respectively, which could be reversed after disease remission by liraglutide injection(P < 0.01). The Huh7 cells exposed to PA also showed down-regulation and up-regulation of mi R-192-5 p and SCD-1 protein levels, respectively(P < 0.01). Transfection with mi R-192-5 p mimic and inhibitor in Huh7 cells induced dramatic repression and promotion of SCD-1 protein levels, respectively(P < 0.01). Luciferase activity was suppressed and enhanced by mi R-192-5 p mimic and inhibitor, respectively, in wild-type SCD-1(P < 0.01) but not in mutant SCD-1. Mi R-192-5 p overexpression reduced lipid accumulation significantly in PA-treated Huh7 cells, and SCD-1 si RNA transfection abrogated the lipid deposition aggravated by mi R-192-5 p inhibitor(P < 0.01).CONCLUSION This study demonstrates that mi R-192-5 p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1.展开更多
文摘位于青藏高原与黄土高原过渡带的甘肃武都万象洞石笋WXSM51和WXSM52提供了M IS 5(118~79kaB.P.)高分辨率的1δ8O记录。研究表明,万象洞石笋1δ8O值与夏季风强度呈负相关关系,与我国西南部的贵州董歌洞石笋1δ8O记录有良好的对应关系,并与高纬度的格陵兰NGR IP冰芯1δ8O记录和65°N太阳辐射强度有很好的一致性,说明万象洞石笋1δ8O记录了118~79kaB.P.期间亚洲季风强度的变化,同时也说明东亚季风强度的变化和全球气候变化同步,而且主要受控于北半球太阳辐射强度的变化。同时它与地中海碳酸盐记录有很好的相似性,和巴西石笋1δ8O记录在千年尺度上表现出相反的变化趋势,说明东亚季风区、地中海地区以及巴西季风区之间存在密切的联系,指示了南北半球气候在千年尺度上存在“跷跷板”(seesaw)现象。万象洞石笋1δ8O记录的M IS 5b与M IS 5 a突发性转换,与NGR IP冰芯1δ8O记录相似,而与神农架记录存在差异,说明万象洞地区对亚洲季风强度的响应更为敏感。
基金Supported by National Key R&D Program of China No.2017YFC0908900National Key Basic Research Project,No.2012CB517501National Natural Science Foundation of China,No.81470840 and No.81600464
文摘AIM To evaluate the levels of mi R-192-5 p in non-alcoholic fatty liver disease(NAFLD) models and demonstrate the role of mi R-192-5 p in lipid accumulation. METHODS Thirty Sprague Dawley rats were randomly divided into three groups, which were given a standard diet, a high-fat diet(HFD), and an HFD with injection of liraglutide. At the end of 16 weeks, hepatic mi R-192-5 p and stearoyl-Co A desaturase 1(SCD-1) levels were measured. Mi R-192-5 p mimic and inhibitor and SCD-1 si RNA were transfected into Huh7 cells exposed to palmitic acid(PA). Lipid accumulation was evaluated by oil red O staining and triglyceride assays. Direct interaction was validated by dual-luciferase reporter gene assays.RESULTS The HFD rats showed a 0.46-fold decrease and a 3.5-fold increase in hepatic mi R-192-5 p and SCD-1 protein levels compared with controls, respectively, which could be reversed after disease remission by liraglutide injection(P < 0.01). The Huh7 cells exposed to PA also showed down-regulation and up-regulation of mi R-192-5 p and SCD-1 protein levels, respectively(P < 0.01). Transfection with mi R-192-5 p mimic and inhibitor in Huh7 cells induced dramatic repression and promotion of SCD-1 protein levels, respectively(P < 0.01). Luciferase activity was suppressed and enhanced by mi R-192-5 p mimic and inhibitor, respectively, in wild-type SCD-1(P < 0.01) but not in mutant SCD-1. Mi R-192-5 p overexpression reduced lipid accumulation significantly in PA-treated Huh7 cells, and SCD-1 si RNA transfection abrogated the lipid deposition aggravated by mi R-192-5 p inhibitor(P < 0.01).CONCLUSION This study demonstrates that mi R-192-5 p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1.
