中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2012年
1期
33-37
,共5页
韩丽萍%聂圆圆%牛文彦%谢云
韓麗萍%聶圓圓%牛文彥%謝雲
한려평%섭원원%우문언%사운
胰高血糖素样肽1%糖原合成酶%糖原合成酶激酶3%肌,骨骼%磷脂酰肌醇3激酶
胰高血糖素樣肽1%糖原閤成酶%糖原閤成酶激酶3%肌,骨骼%燐脂酰肌醇3激酶
이고혈당소양태1%당원합성매%당원합성매격매3%기,골격%린지선기순3격매
Glucagon-like peptide 1%Glycogen synthase%Glycogen synthase kinase 3%Muscle,skeletal%Phosphatidylinositol 3 kinase
目的 研究胰高血糖素样肽-1对大鼠骨骼肌细胞的影响及其机制.方法 体外培养大鼠骨骼肌细胞,采用检测细胞存活和生长的方法(MTT法)检测胰高血糖素样肽-1、胰岛素对骨骼肌细胞存活数量的影响,应用免疫组织化学法测定糖原合成酶和磷酸化糖原合成酶激酶-3α/β表达水平,Western blotting验证胰高血糖素样肽-1对磷脂酰肌醇-3-激酶通路的影响.将骨骼肌细胞分为对照组、胰高血糖素样肽-1组、LY294002组、胰高血糖素样肽-1+LY294002组,于48和72 h分别测定糖原合成酶和磷酸化糖原合成酶激酶-3α/β的表达水平.采用单因素方差分析进行多组间均数比较.结果 Western blotting检测结果显示,胰高血糖素样肽-1刺激后15、30 min、1、2、8h,大鼠骨骼肌细胞出现明显的阳性颗粒表达.与胰高血糖素样肽-1组相比,对照组、LY294002组、胰高血糖素样肽-1+ LY294002组磷酸化糖原合成酶激酶-3α/β表达水平明显降低(分别为0.93±0.11、0.52±0.05、0.65±0.07、0.54±0.21,t值分别为5.751、3.651、2.811,均P＜0.05),糖原合成酶明显降低(分别为0.84±0.14、0.28±0.05、0.34±0.22、0.57±0.08,t值分别为6.390、3.260、2.801,均P＜0.05).结论 本研究证实胰高血糖素样肽-1可通过激活大鼠骨骼肌细胞磷脂酰肌醇-3-激酶通路增加糖原合成酶活性,促进糖原合成.
目的 研究胰高血糖素樣肽-1對大鼠骨骼肌細胞的影響及其機製.方法 體外培養大鼠骨骼肌細胞,採用檢測細胞存活和生長的方法(MTT法)檢測胰高血糖素樣肽-1、胰島素對骨骼肌細胞存活數量的影響,應用免疫組織化學法測定糖原閤成酶和燐痠化糖原閤成酶激酶-3α/β錶達水平,Western blotting驗證胰高血糖素樣肽-1對燐脂酰肌醇-3-激酶通路的影響.將骨骼肌細胞分為對照組、胰高血糖素樣肽-1組、LY294002組、胰高血糖素樣肽-1+LY294002組,于48和72 h分彆測定糖原閤成酶和燐痠化糖原閤成酶激酶-3α/β的錶達水平.採用單因素方差分析進行多組間均數比較.結果 Western blotting檢測結果顯示,胰高血糖素樣肽-1刺激後15、30 min、1、2、8h,大鼠骨骼肌細胞齣現明顯的暘性顆粒錶達.與胰高血糖素樣肽-1組相比,對照組、LY294002組、胰高血糖素樣肽-1+ LY294002組燐痠化糖原閤成酶激酶-3α/β錶達水平明顯降低(分彆為0.93±0.11、0.52±0.05、0.65±0.07、0.54±0.21,t值分彆為5.751、3.651、2.811,均P＜0.05),糖原閤成酶明顯降低(分彆為0.84±0.14、0.28±0.05、0.34±0.22、0.57±0.08,t值分彆為6.390、3.260、2.801,均P＜0.05).結論 本研究證實胰高血糖素樣肽-1可通過激活大鼠骨骼肌細胞燐脂酰肌醇-3-激酶通路增加糖原閤成酶活性,促進糖原閤成.
목적 연구이고혈당소양태-1대대서골격기세포적영향급기궤제.방법 체외배양대서골격기세포,채용검측세포존활화생장적방법(MTT법)검측이고혈당소양태-1、이도소대골격기세포존활수량적영향,응용면역조직화학법측정당원합성매화린산화당원합성매격매-3α/β표체수평,Western blotting험증이고혈당소양태-1대린지선기순-3-격매통로적영향.장골격기세포분위대조조、이고혈당소양태-1조、LY294002조、이고혈당소양태-1+LY294002조,우48화72 h분별측정당원합성매화린산화당원합성매격매-3α/β적표체수평.채용단인소방차분석진행다조간균수비교.결과 Western blotting검측결과현시,이고혈당소양태-1자격후15、30 min、1、2、8h,대서골격기세포출현명현적양성과립표체.여이고혈당소양태-1조상비,대조조、LY294002조、이고혈당소양태-1+ LY294002조린산화당원합성매격매-3α/β표체수평명현강저(분별위0.93±0.11、0.52±0.05、0.65±0.07、0.54±0.21,t치분별위5.751、3.651、2.811,균P＜0.05),당원합성매명현강저(분별위0.84±0.14、0.28±0.05、0.34±0.22、0.57±0.08,t치분별위6.390、3.260、2.801,균P＜0.05).결론 본연구증실이고혈당소양태-1가통과격활대서골격기세포린지선기순-3-격매통로증가당원합성매활성,촉진당원합성.
Objective To investigate the effects and mechanism of glucagon-like peptide-1 ( GLP-1 )on rat skeletal muscles.Methods Rat skeletal muscle cells were cultivated in vitro.MTT method was used to check the effects of GLP-1 and insulin (INS) on survival of skeletal muscle cells.Glycogen synthase (GS) and phospho-glycogen synthase kinase-3α/β (pGSK-3α/β) were measured by using immunohistochemistry.Impact of GLP-1 on phosphatidylinositol 3 kinase (PI3K) pathway was confirmed by Western blotting.Rat skeletal muscle cells were divided into the control group,GLP-1 group,LY294002 group,and GLP-1 + LY294002 group.The expressions of GS and pGSK-3α/β were compared between the groups. Analysis of variance (ANOVA) was used for data analysis. Results Western blotting results indicated that following GLP-1 intervention,positive particles were found in rat skeletal muscle cells at 15 and 30 min,and 1,2 and 8 h.In comparison with the GLP-1 group,the expression of pGSK-3α/β of the control group,LY294002 group,and GLP-1 + LY294002 group was significantly decreased (0.93 ± 0.11,0.52 ±0.05,0.65 ±0.07,and 0.54 ±0.21,respectively; t values were 5.751,3.651,and 2.811,respectively; all P ＜ 0.05 ),and the expression of GS was significantly decreased (0.84 ± 0.14,0.28 ±0.05,0.34 ± 0.22,and 0.57 ± 0.08,respectively; t values were 6.390,3.260,and 2.801,respectively;all P ＜ 0.05 ).Conclusion This study suggests that GLP-1 may increase the activity of GS in skeletal muscle cells through activating GSK-3 pathway.
