中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2011年
4期
298-301
,共4页
陈松锦%曹筱佩%陈说%肖海鹏%李延兵
陳鬆錦%曹篠珮%陳說%肖海鵬%李延兵
진송금%조소패%진설%초해붕%리연병
胰升血糖素样肽1%胰腺衍生因子%游离脂肪酸%胰岛细胞%凋亡
胰升血糖素樣肽1%胰腺衍生因子%遊離脂肪痠%胰島細胞%凋亡
이승혈당소양태1%이선연생인자%유리지방산%이도세포%조망
GLP-1%PANDER% FFA% Islet cells% Apoptosis
目的 观察棕桐酸盐对胰岛β细胞凋亡及胰腺衍生因子(PANDER)的影响,并观察胰升血糖素样肽1(GLP-1)对其的干预.方法 培养β-TC3细胞分别以PA、PA+GLP-1以及空白处理24h,以MTT法、Annexin-V/PI荧光染色流式细胞术、Tunel荧光染色法检测细胞凋亡,以RT-PCR法测定PANDER mRNA的表达.结果 PA浓度达0.25mmol/L时细胞存活率开始显著下降,并随浓度上升逐渐下降(P<0.05).GLp-1能显著拮抗PA致胰岛β细胞凋亡;PA能明显增加PANDER mRNA的水平,而GLp-1能显著抑制PA对PANDER的作用.结论 PA在诱导胰岛β细胞凋亡的同时刺激PANDER表达,GLP-1拮抗PA致胰岛β细胞凋亡及PANDER的表达;PANDER可能是GLP-1拮抗胰岛β细胞脂性凋亡的靶点之一.
目的 觀察棕桐痠鹽對胰島β細胞凋亡及胰腺衍生因子(PANDER)的影響,併觀察胰升血糖素樣肽1(GLP-1)對其的榦預.方法 培養β-TC3細胞分彆以PA、PA+GLP-1以及空白處理24h,以MTT法、Annexin-V/PI熒光染色流式細胞術、Tunel熒光染色法檢測細胞凋亡,以RT-PCR法測定PANDER mRNA的錶達.結果 PA濃度達0.25mmol/L時細胞存活率開始顯著下降,併隨濃度上升逐漸下降(P<0.05).GLp-1能顯著拮抗PA緻胰島β細胞凋亡;PA能明顯增加PANDER mRNA的水平,而GLp-1能顯著抑製PA對PANDER的作用.結論 PA在誘導胰島β細胞凋亡的同時刺激PANDER錶達,GLP-1拮抗PA緻胰島β細胞凋亡及PANDER的錶達;PANDER可能是GLP-1拮抗胰島β細胞脂性凋亡的靶點之一.
목적 관찰종동산염대이도β세포조망급이선연생인자(PANDER)적영향,병관찰이승혈당소양태1(GLP-1)대기적간예.방법 배양β-TC3세포분별이PA、PA+GLP-1이급공백처리24h,이MTT법、Annexin-V/PI형광염색류식세포술、Tunel형광염색법검측세포조망,이RT-PCR법측정PANDER mRNA적표체.결과 PA농도체0.25mmol/L시세포존활솔개시현저하강,병수농도상승축점하강(P<0.05).GLp-1능현저길항PA치이도β세포조망;PA능명현증가PANDER mRNA적수평,이GLp-1능현저억제PA대PANDER적작용.결론 PA재유도이도β세포조망적동시자격PANDER표체,GLP-1길항PA치이도β세포조망급PANDER적표체;PANDER가능시GLP-1길항이도β세포지성조망적파점지일.
Objective To observe the effects of palmitate (PA) on the pancreatic β-cell apoptosis and PANDER mRNA expression, and the effects of GLP-1 on fatty acid-induced pancreatic β-cell apoptosis and PANDER expression. Methods β-TC3 cells were cultured with vehicle (control), 0.5 mmol/L PA, 0.5 mmol/L PA + 10 nmol/L GLP-1, respectively for 24 hours. Cell apoptosis were evaluated with MTT, Annexin-V-FITC/PI FACS and Tunel assay. PANDER mRNA expression were measured by RT-PCR. Results MTT analysis showed that PA inhibited β-TC3 cell viability in a dose dependent manner with the significantly viability decrease beginning at 0.25 mmol/L PA.GLP-1 counteracted the apoptotic effects of PA on β-TC3 cell. PANDER mRNA increased significantly in PA treated cells (vs control,P<0.05), while GLP-1 inhibited PA induced PANDER mRNA over expression. Conclusion FFA induces pancreatic β-cells apoptosis and PANDER over expression, GLP-1 counteracts the effects of FFA on pancreatic β-cell and PANDER expression. PANDER may be an important mediator in the signaling pathway of lipoapoptosis of pancreatic beta-cell.