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
2014年
4期
321-325
,共5页
侯粲%王燕飞%蔺怡%梁功平%陆前进%周智广
侯粲%王燕飛%藺怡%樑功平%陸前進%週智廣
후찬%왕연비%린이%량공평%륙전진%주지엄
胰岛β细胞%白细胞介素-1β%干扰素-γ%曲古霉素A%5-氮杂胞苷
胰島β細胞%白細胞介素-1β%榦擾素-γ%麯古黴素A%5-氮雜胞苷
이도β세포%백세포개소-1β%간우소-γ%곡고매소A%5-담잡포감
Pancreatic β-cells%Interleukin-1 β%Interferon-γ%Trichostatin A%5-azacitidine
目的 探讨细胞因子白细胞介素-1β和干扰素-γ诱导下曲古霉素A(TSA)、5-氮杂胞苷(5-AzaC)及其联合干预对胰岛p细胞增殖、凋亡及功能的影响.方法 采用白细胞介素-1β和干扰素-γ诱导大鼠胰岛素瘤细胞(RIN-m5f)损伤,用TSA、5-AzaC对其进行干预.具体分组:空白对照组、细胞因子诱导组、0.05/0.10 μmol/L TSA干预组、0.63/1.25 μmol/L 5-AzaC干预组、0.10 μmol/L TSA+ 1.25 μmol/L5-AzaC联合干预组.用MTT法检测RIN-m5f细胞的增殖活性,流式细胞技术检测细胞凋亡率及酶联免疫吸附法测定葡萄糖刺激胰岛素分泌能力.结果 0.05/0.10 μmol/L TSA干预组、0.63/1.25μmol/L 5-AzaC干预组、0.10 μmol/L TSA+ 1.25tμmol/L 5-AzaC联合干预组细胞增殖活性分别为70.1%/79.2%、67.3%/82.9%和89.1%,高于细胞因子诱导组的33.9%(P<0.05);其凋亡率分别为10.3%/10.5%、7.9%/9.6%和8.2%,低于细胞因子诱导组的16.6%(P<0.05);各组葡萄糖刺激胰岛素分泌能力均比细胞因子诱导组升高(P<0.05).结论 TSA和5-AzaC可以促进细胞因子诱导的胰岛β细胞增殖,抑制其凋亡和恢复p细胞的胰岛素分泌功能.
目的 探討細胞因子白細胞介素-1β和榦擾素-γ誘導下麯古黴素A(TSA)、5-氮雜胞苷(5-AzaC)及其聯閤榦預對胰島p細胞增殖、凋亡及功能的影響.方法 採用白細胞介素-1β和榦擾素-γ誘導大鼠胰島素瘤細胞(RIN-m5f)損傷,用TSA、5-AzaC對其進行榦預.具體分組:空白對照組、細胞因子誘導組、0.05/0.10 μmol/L TSA榦預組、0.63/1.25 μmol/L 5-AzaC榦預組、0.10 μmol/L TSA+ 1.25 μmol/L5-AzaC聯閤榦預組.用MTT法檢測RIN-m5f細胞的增殖活性,流式細胞技術檢測細胞凋亡率及酶聯免疫吸附法測定葡萄糖刺激胰島素分泌能力.結果 0.05/0.10 μmol/L TSA榦預組、0.63/1.25μmol/L 5-AzaC榦預組、0.10 μmol/L TSA+ 1.25tμmol/L 5-AzaC聯閤榦預組細胞增殖活性分彆為70.1%/79.2%、67.3%/82.9%和89.1%,高于細胞因子誘導組的33.9%(P<0.05);其凋亡率分彆為10.3%/10.5%、7.9%/9.6%和8.2%,低于細胞因子誘導組的16.6%(P<0.05);各組葡萄糖刺激胰島素分泌能力均比細胞因子誘導組升高(P<0.05).結論 TSA和5-AzaC可以促進細胞因子誘導的胰島β細胞增殖,抑製其凋亡和恢複p細胞的胰島素分泌功能.
목적 탐토세포인자백세포개소-1β화간우소-γ유도하곡고매소A(TSA)、5-담잡포감(5-AzaC)급기연합간예대이도p세포증식、조망급공능적영향.방법 채용백세포개소-1β화간우소-γ유도대서이도소류세포(RIN-m5f)손상,용TSA、5-AzaC대기진행간예.구체분조:공백대조조、세포인자유도조、0.05/0.10 μmol/L TSA간예조、0.63/1.25 μmol/L 5-AzaC간예조、0.10 μmol/L TSA+ 1.25 μmol/L5-AzaC연합간예조.용MTT법검측RIN-m5f세포적증식활성,류식세포기술검측세포조망솔급매련면역흡부법측정포도당자격이도소분비능력.결과 0.05/0.10 μmol/L TSA간예조、0.63/1.25μmol/L 5-AzaC간예조、0.10 μmol/L TSA+ 1.25tμmol/L 5-AzaC연합간예조세포증식활성분별위70.1%/79.2%、67.3%/82.9%화89.1%,고우세포인자유도조적33.9%(P<0.05);기조망솔분별위10.3%/10.5%、7.9%/9.6%화8.2%,저우세포인자유도조적16.6%(P<0.05);각조포도당자격이도소분비능력균비세포인자유도조승고(P<0.05).결론 TSA화5-AzaC가이촉진세포인자유도적이도β세포증식,억제기조망화회복p세포적이도소분비공능.
Objective To investigate the effect of trichostatin A (TSA) and 5-azacitidine (5-AzaC) on pancreatic β-cells impaired by cytokine,via measuring the proliferation,apoptosis,and function of pancreatic β-cells.Methods RIN-m5f was impaired by interleukin-1β and interferon-γin vitro,and treated with TSA and 5-AzaC.Experiment groups included blank control group,cytokine induction group,0.05/0.10 μmoL/L TSA group,0.63/1.25 μmoL/L 5-AzaC group,and0.10 μmol/L TSA plus 1.25 μmol/L 5-AzaC group.The viability of RIN-m5f cells was detected by MTT assay.Apoptotic rate was determined by Annexin V-fluorescein isothiocyanate (FITC) /propidium iodide flow cytometry.Insulin secretion was measured by enzyme-linked immunosorbent assay.Results The viability of RIN-m5f cells in 0.05/0.10 μmoL/L TSA group,0.63/1.25 μmol/L 5-AzaC group,and 5-AzaC plus TSA group was 70.1%/79.2 %,67.3 %/82.9 %,and 89.1% respectively,being higher than that in the cytokine group (33.9%,P<0.05) ; the apoptosis rate was 10.3%/10.5%,7.9%/9.6%,and 8.2%,being lower than that in the cytokine group (16.6%,P<0.05) ; the capacity of glucose-stimulated insulin secretion of all the treated groups was higher than that in the cytokine group (P<0.05).Conclusion TSA and 5-AzaC might promote the proliferation of pancreatic β-cells impaired by cytokines,inhibit its apoptosis and recover its insulin secretion.