中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2015年
5期
447-451
,共5页
胡星云%刘珊英%刘晓丹%蒋清凌%严励%李焱
鬍星雲%劉珊英%劉曉丹%蔣清凌%嚴勵%李焱
호성운%류산영%류효단%장청릉%엄려%리염
二肽基肽酶Ⅳ抑制剂%脂多糖%胰岛β细胞
二肽基肽酶Ⅳ抑製劑%脂多糖%胰島β細胞
이태기태매Ⅳ억제제%지다당%이도β세포
Dipeptidyl peptidase-4 inhibitor%Lipopolysaccharide%Pancreatic β-cell
目的 探讨二肽基肽酶Ⅳ(DPP-4)抑制剂对脂多糖诱导的胰岛β细胞数量与功能改变的影响.方法 不同浓度西格列汀(Sitagliptin)与脂多糖处理RINm细胞24 h后,采用CCK-8比色法检测细胞增殖,Annexin V/PI染色流式细胞术检测细胞凋亡,ELISA法检测细胞胰岛素分泌功能,RT-PCR检测白细胞介素6(IL-6)mRNA表达.结果 脂多糖组较对照组明显促进RINm细胞的增殖(0.89±0.04对1.14±0.08,P<0.01),但脂多糖+西格列汀各组与脂多糖组相比差异均无统计学意义;脂多糖+10-1 mmol/L西格列汀组凋亡率较脂多糖组明显减低;各组之间胰岛素基础分泌量无明显差异,但高糖/低糖刺激后,脂多糖组较对照组胰岛素分泌量增加;脂多糖+西格列汀组IL-6 mRNA表达较脂多糖组明显减低(0.77±0.33对1.30±0.41,P=0.006).结论 DPP-4抑制剂对脂多糖诱导β细胞增殖的影响较弱,但一定程度上能够抑制脂多糖对β细胞促凋亡及胰岛素分泌功能的作用,这可能与炎症因子IL-6的表达有关.
目的 探討二肽基肽酶Ⅳ(DPP-4)抑製劑對脂多糖誘導的胰島β細胞數量與功能改變的影響.方法 不同濃度西格列汀(Sitagliptin)與脂多糖處理RINm細胞24 h後,採用CCK-8比色法檢測細胞增殖,Annexin V/PI染色流式細胞術檢測細胞凋亡,ELISA法檢測細胞胰島素分泌功能,RT-PCR檢測白細胞介素6(IL-6)mRNA錶達.結果 脂多糖組較對照組明顯促進RINm細胞的增殖(0.89±0.04對1.14±0.08,P<0.01),但脂多糖+西格列汀各組與脂多糖組相比差異均無統計學意義;脂多糖+10-1 mmol/L西格列汀組凋亡率較脂多糖組明顯減低;各組之間胰島素基礎分泌量無明顯差異,但高糖/低糖刺激後,脂多糖組較對照組胰島素分泌量增加;脂多糖+西格列汀組IL-6 mRNA錶達較脂多糖組明顯減低(0.77±0.33對1.30±0.41,P=0.006).結論 DPP-4抑製劑對脂多糖誘導β細胞增殖的影響較弱,但一定程度上能夠抑製脂多糖對β細胞促凋亡及胰島素分泌功能的作用,這可能與炎癥因子IL-6的錶達有關.
목적 탐토이태기태매Ⅳ(DPP-4)억제제대지다당유도적이도β세포수량여공능개변적영향.방법 불동농도서격렬정(Sitagliptin)여지다당처리RINm세포24 h후,채용CCK-8비색법검측세포증식,Annexin V/PI염색류식세포술검측세포조망,ELISA법검측세포이도소분비공능,RT-PCR검측백세포개소6(IL-6)mRNA표체.결과 지다당조교대조조명현촉진RINm세포적증식(0.89±0.04대1.14±0.08,P<0.01),단지다당+서격렬정각조여지다당조상비차이균무통계학의의;지다당+10-1 mmol/L서격렬정조조망솔교지다당조명현감저;각조지간이도소기출분비량무명현차이,단고당/저당자격후,지다당조교대조조이도소분비량증가;지다당+서격렬정조IL-6 mRNA표체교지다당조명현감저(0.77±0.33대1.30±0.41,P=0.006).결론 DPP-4억제제대지다당유도β세포증식적영향교약,단일정정도상능구억제지다당대β세포촉조망급이도소분비공능적작용,저가능여염증인자IL-6적표체유관.
Objective To investigate the effect of dipeptidyl peptidase-4 (DPP-4) inhibitor on lipopolysaccharide (LPS)-induced changes in the mass and function of pancreatic β-cells.Methods RINm cells were cultured and treated with LPS alone or combined with different concentrations of sitagliptin for 24 h.The proliferation of RINm cells was detected by CCK-8 assay.Apoptotic rate was determined by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide flow cytometry.Insulin secretion was measured by enzyme-linked immunosorbent assay.The expression of IL-6 mRNA was displayed by RT-PCR.Results LPS significantly stimulated the proliferation of RINm cells (0.89 ± 0.04 vs 1.14 ± 0.08,P<0.01),while LPS+sitagliptin showed no significant difference compared with LPS group.The cell apoptotic rate in LPS + 10-1 mmol/L sitagliptin group was significantly lower than that in LPS group.There were no significant differences in basal insulin secretion among all groups,but after the high/low glucose stimulation,LPS increased insulin secretion as compared with the control.The IL-6 mRNA expression in LPS+sitagliptin group was significantly lower than that in LPS group (0.77 ± 0.33 vs 1.30 ± 0.41,P =0.006).Conclusions DPP-4 inhibitor has no influence on LPS-induced proliferation of pancreatic β-cell,but it can inhibit LPS-induced apoptosis and insulin secretion,and IL-6 may be involved in the process.