大鼠胰腺β细胞分泌颗粒内钙离子超微结构定位的研究

目的: 观察大鼠胰腺β细胞内钙离子在亚细胞水平的分布情况.方法: 用胶原酶原位灌注法分离大鼠胰岛,在含100 mL/L胎牛血清、11.1 mmol/L葡萄糖的RPMI-1640培养基中培养过夜后,离心,将胰岛细胞团分为实验组(外源性胰岛素100 mU/L孵育240 min)和对照组(外源性胰岛素100 mIU/L孵育0 min),采用改进的焦锑酸钾沉淀的细胞化学方法对胰腺β细胞分泌颗粒内钙离子进行超微结构定位.结果: 超微结构显示胰腺β细胞内钙离子呈高电子密度的黑色颗粒状.对照组的胰岛素分泌颗粒内钙离子沉积明显高于实验组,并伴有钙离子外排.实验组胰腺β细胞靠近细胞膜区钙离子沉积增加.结论: 离子细胞化学定位法是研究组织中钙离子分布的有效方法.胰腺β细胞的分泌功能可能与胰岛素分泌颗粒内钙离子浓度密切相关.     

HbA1c检测及胰岛素释放试验诊断2型糖尿病临床研究

目的分析糖化血红蛋白(HbA1c)检测及胰岛素释放试验诊断2型糖尿病的临床价值。方法选取2018年1月‐2018年9月该院收治的2型糖尿病患者114例为研究对象,根据患者空腹胰岛素分泌水平将其分为研究A组和研究B组,各57例,另选取同期在该院健康体检者57例为对照组。分别检测3组HbA1c、胰岛素释放水平、空腹血糖、空腹胰岛素、胰岛素抵抗指数及胰岛β细胞功能指数等指标。结果研究A组、研究B组空腹血糖、HbA1c、稳态模型胰岛素抵抗指数(HOMA-IR)高于对照组,胰岛β细胞功能指数(HOMA-β)低于对照组(P 0.05);研究A组空腹胰岛素高于对照组,研究B组空腹胰岛素低于对照组(P 0.05);研究A组空腹胰岛素、HOMA-β高于研究B组,HbA1c低于研究B组(P 0.05);研究A组、B组空腹时、30 min、60 min胰岛素释放水平均低于对照组,180 min胰岛素释放水平高于对照组(P 0.05);研究A组120 min胰岛素释放水平高于对照组,研究B组低于对照组(P 0.05);研究A组空腹时、30 min、60 min、120 min、180 min胰岛素释放水平均高于研究B组(P 0.05)。结论 HbA1c检测及胰岛素释放试验可进一步分析胰岛素β细胞功能变化情况,可指导2型糖尿病的诊治。     

免疫抑制剂对成人胰岛细胞的毒性作用的体外观察

目的探讨免疫抑制剂对成人胰岛细胞的毒性作用,旨在筛选适用于成人胰岛细胞移植的免疫抑制剂。方法通过成人胰岛细胞与不同免疫抑制剂分别共培养后的糖刺激胰岛素释放试验,ELISA检测培养液中胰岛素含量比较,探讨免疫抑制剂对胰岛细胞的毒性作用。结果高浓度MMF(骁悉)和FK506(普乐可复)均引起成人胰岛细胞胰岛素分泌明显减少,与对照组比较,具有显著性差异,P<0.05。中低浓度MMF和FK506对成人胰岛细胞胰岛素释放无明显抑制作用。FTY720和Rapamycin(雷帕霉素)对成人胰岛细胞胰岛素分泌无明显影响,与对照组比较,差异无显著,P>0.05。结论中低剂量MMF和FK506不影响人胰岛细胞胰岛素的分泌,高剂量MMF和FK506明显抑制胰岛素的分泌。FTY720和Rapamycin对人胰岛细胞胰岛素的分泌无明显影响。FTY720和Rapamycin有可能作为临床胰岛细胞移植的主要免疫抑制剂使用。胰岛细胞移植时亦可使用中低剂量MMF和FK506。     

促红细胞生成素对新生猪胰岛细胞 增殖分化和凋亡的影响

［摘要］目的：研究促红细胞生成素在体外对新生猪胰岛细胞增殖分化和凋亡的影响。方法：采用胶原酶消化和组织培养方法分离纯化新生猪胰岛细胞,检测其纯度和活性,再分为实验组和对照组。实验组培养基中添加促红细胞生成素（10.0 μmol/L）,对照组不添加促红细胞生成素,培养5 d后行低糖和高糖刺激胰岛素释放试验;并行细胞计数及MTT比色法测细胞增殖活性;流式细胞仪和EB/AO染色荧光检测细胞凋亡百分率,流式细胞仪分析细胞周期,RT-PCR法检测胰岛细胞胰岛素促进因子-1(PDX-1),葡萄糖转运载体2（GlUT-2）,bcl-2,bax,caspase-3 mRNA的表达。结果：促红细胞生成素干预后新生猪胰岛细胞不改变形态和功能,对葡萄糖刺激胰岛素分泌的反应正常;细胞计数示实验组新生猪胰岛细胞数目均比对照组增多（P＜0.05）;随着培养时间延长,实验组和对照组吸光度值均呈上升趋势,且实验组的吸光度值均高于对照组（P＜0.05）,实验组PDX-1 mRNA表达稍有上调（P＜0.05）,而GlUT-2 mRNA表达无明显差别（P=0.34）。流式细胞仪和EB/AO染色荧光检测实验组的凋亡百分率均较对照组降低（P＜0.01）。RT-PCR示实验组bcl-2 mRNA较对照组上调,而bax和 caspase-3 mRNA明显下调（P＜0.01）。结论：促红细胞生成素在体外能促进新生猪胰岛细胞的增殖分化,对形态和功能无影响。促红细胞生成素对新生猪胰岛细胞有抗凋亡保护作用,可能是通过上调bcl-2 mRNA的表达,下调bax, caspase-3 mRNA的表达来实现的。     

氯化锂对培养人胎胰岛细胞胰岛素释放及DNA合成的作用

微元量素锂对糖代谢的影响尚未完全明了。 192 4年 ,Ｗｅｉｓｓ等曾报道用锂盐治疗糖尿病可改善糖耐量 ,嗣后 ,关于锂盐与糖尿病、糖代谢关系的报道逐渐增多。Ｒｏｓｓｅｔｔｉ等认为 ,锂具有胰岛素样作用 ,并可改善胰岛素敏感性[1] 。胡敏等[2 ] 观察小剂量 6个月的锂处理能改善糖尿病中国地鼠糖代谢 ,而锂对胰岛素合成与分泌的作用意见不一。锂能减少中国地鼠胰岛 β细胞内胰岛素 (原 )合成 ,抑制葡萄糖、Ｄ860 等刺激的大鼠胰腺胰岛素释放 ;有人认为 ,锂不能增加单个胰岛细胞胰岛素合成与分泌 ,但可促进培养的胎鼠胰岛细胞ＤＮＡ的复制 ,使胰岛素合成与分泌增加[3] 。锂对人胎胰岛细胞胰岛     

胰高血糖素样肽-1 对胰岛β细胞功能的影响

目的:探讨胰高血糖素样肽(GLP)-1对胰岛β细胞功能的影响?方法:Wistar雄性大鼠20只,随机分为对照组(生理盐水)和实验组[GLP-1 (7-36) NH2],每组各10只?分别在注射生理盐水?GLP-1 (7-36)NH2前及结束后5?10 min时测尾部血糖?胰岛素?应用半定量逆转录聚合酶链式反应(RT-PCR)检测胰岛素mRNA表达强度?结果:注射前,对照组与实验组血糖?血胰岛素浓度差异均无统计学意义(P>0.05);注射后5?10 min时实验组血糖显著低于对照组(P<0.05);5 min时实验组胰岛素水平显著高于对照组(P<0.05);10 min时对照组与实验组血胰岛素水平差异无统计学意义(P>0.05)?胰岛素mRNA表达强度实验组显著高于对照组(P<0.05)?结论:静脉注射GLP-1 (7-36) NH2能促进胰岛素基因转录,升高胰腺胰岛素mRNA水平,促进胰岛素的合成与分泌,迅速升高血胰岛素水平,降低血糖,从而保护胰岛β细胞功能?     

人胎胰岛组织培养及活性测定

人胎胰岛组织临床移植治疗Ⅰ型糖尿病有效,本文报告培养方法及对胰岛β细胞和外分泌细胞活性和功能的检测,发现人胎胰岛组织在体外培养过程中,培养液内胰岛素量逐渐降低,每毫克湿重组织内胰岛素含量逐渐升高。随培养时间不同,茶碱增强葡萄糖诱导胰岛素的释放量不同。胎胰组织及培养液内未测到淀粉酶。     

柯萨奇B4病毒感染对人胚胰岛的影响

目的：研究柯萨奇B₄病毒感染对人胚胰岛的影响。方法：采用中国流行的柯萨奇B₄病毒感染体外培养的人胚胰岛细胞,电镜观察其形态变化,并进行糖刺激的胰岛素释放量试验。结果：病毒可直接攻击胰岛,突破胰岛胞膜,侵犯胰岛β细胞,可在β细胞内繁殖,使β细胞脱颗粒。糖刺激的胰岛素释放量在感染后24 h增加,以后呈逐渐降低趋势。感染组在感染24 h时低糖及高糖刺激的胰岛素释放量分别为（64.50±9.20）mU•L^-1,（87.85±8.50）mU•L^-1,均高于对照组（P<0.05）。48 h~6 d高糖及低糖刺激的胰岛素释放量均显著低于对照组（P<0.05或P<0.01）。结论：柯萨奇B₄病毒可在体外感染人胚胰岛细胞,并损害胰岛β细胞合成胰岛素的功能。     

高血糖对体外培养的胎鼠胰岛Pdx-1基因的影响

目的：研究在体外培养时，高血糖对胎鼠胰岛胰和十二指肠同源盒基因-1（Pdx-1)和胰岛素基因的影响。方法：胶原酶法分离胎鼠胰岛，分别在葡萄糖浓度为5.5mmol/L,11.1mmol/L,33.3mmol/L的条件下培养24h。采用胰岛素含量测定、胰岛素释放实验评价胰岛功能；免疫细胞化学染色检测Pdx-1在细胞内的表达；逆转录PCR（RT-PCR）检测Pdx-1和胰岛素mRNA表达水平。结果：高血糖组1（11.1mmol/L)胎鼠单位重量胰岛细胞内胰岛素水平和刺激指数高于低糖组（5.5mmol/L)和高血糖组2（33.3mmol/L)。而且，高血糖组胎鼠胰岛Pdx-1蛋白的核移位率和mRNA表达水平均高于低糖组，但是高糖组2胰岛素mRNA表达低于高血糖组1，与低糖组无显著性差异。结论：高血糖刺激可以促进胎鼠Pdx-1表达和转录活性，可能是影响胰岛功能和β细胞对葡萄糖刺激敏感性增加的原因之一。     

优化细胞因子诱导胎盘源间充质干细胞向胰岛β样细胞分化的实验研究

目的优化多种细胞因子联合诱导人胎盘源间充质干细胞分化为胰岛β样细胞的实验条件。方法从胎盘中分离、扩增间充质干细胞;扩增后的细胞采用激活素A、表皮生长因子(EGF)等多种细胞因子联合诱导;在诱导过程中运用消化重悬、调节葡萄糖浓度等方法优化诱导方案,促进细胞形成胰岛样细胞团,向胰岛β样细胞的分化;比较不同诱导条件下,诱导后的细胞在胰岛素、C肽分泌及胰岛素释放实验中的差异,筛选出最佳方案。结果经诱导后的细胞,免疫荧光染色及免疫细胞化学染色均能检测出PDX-1及胰岛素表达;优化方案3诱导后的细胞不仅胰岛素分泌量明显提高至(222.00±38.00)mU/L,还能分泌C肽至(0.45±0.22)ng/mL,而且对胰岛素释放实验敏感,胰岛素刺激释放指数为(5.93±0.79)。结论经多种细胞因子联合诱导后,人胎盘源间充质干细胞可分化为胰岛β样细胞,胰岛样细胞团的形成有助于胰岛β样细胞的分化发育。     

胰淀素致大鼠胰岛细胞功能损伤的实验研究

OBJECTIVE: To investigate the effect of amylin on the functions of pancreatic islet cells in vitro. METHODS: In vitro cultured pancreatic islet cells from neonatal rats were used for studying the effects of amylin at different concentrations on insulin secretion, and DNA content and insulin contents in the cells. RESULTS: Insulin secretion was significantly inhibited when amylin concentration was higher than 10 micromol/L (P < 0.01). After incubation with 10 micromol/L amylin for 2 h, insulin secretion of islet cells was dose-dependently inhibited by to 16.7 mmol/L glucose stimulation (P < 0.01). The DNA and insulin contents in the cells rose significantly when amylin concentration was higher than 10 micromol/L as compared with the control group (P < 0.01). CONCLUSION: Amylin at concentrations higher than 10 micromol/L can remarkably inhibit insulin secretion and release induced by 16.7 mmol/L glucose stimulation.     

Effects of mature Sertoli cells on allogeneic islets cocultured in vitro

INTRODUCTIONNowadays 180 million people suffer from dia-betes mellitus in world. An exogenous insulininjection has been the gold standard treatment fortype I diabetic patients, which is complicated andcould never completely correct the underlying loss ofislet cells and the resulting unregulated glucose lev-els. Islet transplantation seems to be an almost idealtherapy for insulin-dependent patients [1]. However,in isolate islet transplants the early clinical islet graftloss in 1 month is a…     

miR-221对糖尿病肾病小鼠胰岛β细胞功能的保护作用及其机制

目的：研究miR-221对糖尿病肾病（DN）小鼠胰岛β细胞功能的影响,阐明miR-221在DN中的保护作用机制。方法：8周龄野生型雄性C57BL/6J小鼠20只随机分成对照组和DN组,每组10只,对照组小鼠给予正常饮食,DN组小鼠给予高脂饮食,并注射100 mg·kg^-1链脲佐菌素（STZ）诱导部分胰岛素缺陷,对照组小鼠注射同体积柠檬酸缓冲液。之后DN组继续给予高脂饮食,对照组给予正常饮食,饲养10周后收集小鼠血液和尿液,检测血糖、血肌酐、血尿素氮浓度和24 h尿白蛋白排泄率等生理参数。在DN组小鼠中分离得到胰岛细胞。利用Real-time PCR检测胰岛细胞中SOCS3 mRNA表达水平,采用MTT法检测胰岛细胞增殖情况,ELISA法检测胰岛细胞中胰岛素含量和胰岛素的释放水平,荧光素酶报告基因法检测SOCS3活性荧光酶素报告基因活性。结果：成功构建DN小鼠模型。DN组小鼠的血糖、血肌酐、血尿素氮浓度和24h尿白蛋白排泄率均高于对照组（P<0.05）。过表达miR-221后,DN组小鼠胰岛细胞中SOCS3 mRNA表达水平低于正常胰岛细胞（P<0.05）,过表达miR-221后胰岛细胞的增殖能力低于正常胰岛细胞（P<0.05）,荧光素酶报告基因法确定SOCS3为miR-221下游靶基因。过表达miR-221后,胰岛细胞中胰岛素质量分数和胰岛素释放水平均高于正常胰岛细胞（P<0.05）。结论：miR-221通过下调SOCS3水平促进胰岛细胞合成和分泌胰岛素的功能,改善DN小鼠中胰岛细胞的功能障碍。     

高脂饮食肥胖大鼠胰岛细胞胰岛素抵抗机理的探讨

目的探讨高脂饮食诱导的肥胖大鼠在具有外周胰岛素抵抗(IR)的情况下,胰岛胰岛素、胰高血糖素的分泌和合成功能,高糖刺激下胰高血糖素和胰岛素的分泌以及胰岛内胰岛素信号转导分子的改变。方法30只雄性Wistar大鼠随机分为高脂饲料喂养的肥胖组和普通饲料喂养的对照组,每组各15只,共喂养20周。采用胰腺组织匀浆,检测胰岛素和胰高血糖素的含量;胰岛细胞表面灌注检测高糖状态胰岛素和胰高血糖素的动态分泌变化;免疫组织化学染色及图像分析检测胰岛素受体(IRc)及胰岛素受体底物1、2(IRS1、IRS2)在两组大鼠胰岛的表达。结果(1)肥胖组胰岛素敏感指数(ISI)明显低于对照组,肥胖组血胰高血糖素水平和胰岛内的胰高血糖素水平均显著高于对照组(362pg/ml±58pg/mlvs291pg/ml±35pg/ml,P<0.05;442pg/ml±56pg/mlvs287pg/ml±48pg/ml,均P<0.05)。(2)肥胖组葡萄糖刺激的胰岛素分泌(GSIS)受损,16.7mmol/L葡萄糖可显著抑制对照组胰岛α细胞胰高血糖素的分泌,而在肥胖组这种抑制作用消失。(3)胰岛存在IRc、IRS1和IRS2的表达。肥胖组胰岛IRc、IRS2的表达较对照组胰岛分别低28%和22%(均P<0.01)。结论高脂饮食诱导的肥胖大鼠胰岛细胞的胰岛素信号转导通路受损,即在有外周IR的同时也具有胰岛内的IR,这可能是肥胖状态下胰岛细胞功能障碍的内在机制之一。     

胰岛素信号通路在高游离脂肪酸所致的β细胞功能紊乱中的作用及机制

目的:观察血浆游离脂肪酸(FFA)水平升高对β细胞胰岛素分泌功能的影响,探讨β细胞胰岛素信号通路在其中所起的作用及其机制. 方法: 将8周龄雄性SD大鼠随机分为脂肪乳输注组(FFA组,13只)和生理盐水输注组(NS组,12只).分别输注48 h,检测以下指标:(1)采血检测胰岛素, FFA水平;(2)正常血糖高胰岛素钳夹实验,评价外周组织胰岛素抵抗程度;(3)静脉葡萄糖耐量实验,评价活体胰岛β细胞分泌功能;(4)胰岛细胞表面灌注实验,评价离体胰岛β细胞动态分泌功能;(5)采用实时荧光定量PCR方法检测肌肉中胰岛素受体底物-1(IRS-1)、胰岛素受体底物-2(IRS-2)mRNA表达的变化;(6)用实时荧光定量PCR方法检测胰岛细胞IRS-1,IRS-2和葡萄糖转运子-2(Glut-2)mRNA表达的变化.结果:(1)FFA组血中胰岛素水平比NS组增高[(24.44±1.25) mIU/L vs (18.09±1.37) mIU/L,P＜0.05],FFA水平也显著高于NS组[(1.39±0.18) mmol/L vs (0.64±0.10) mmol/L,P＜0.001];(2)FFA刺激后,离体和活体的胰岛β细胞分泌功能均增强;(3)FFA组葡萄糖输注率(GIR)较NS组明显降低(P＜0.05),提示存在明显的外周胰岛素抵抗;(4)FFA组肌肉IRS-1 mRNA表达比NS组降低87.7%,IRS-2表达降低50.7%(P＜0.05);(5) FFA组胰岛细胞IRS-1 mRNA表达增加29.3%(P＜0.05),IRS-2及Glut-2分别增加345.1%和536.4%(P＜0.01).结论:血浆FFA水平短期升高,造成外周胰岛素抵抗的同时,对β细胞胰岛素分泌有刺激作用,此时胰岛细胞胰岛素信号通路分子基因表达增加.     

Relationship between islet beta cell dysfunction and gene expression of uncoupling protein-2 and possible mechanism thereof

OBJECTIVE: To study the effects of high fat diet on the functions of islet beta cells and the role of uncoupling protein-2 (UCP2) therein and possible mechanism. METHODS: Forty SD rats were randomly divided into two equal groups: high-fat-(HF) diet group, fed with HF diet for 20 weeks, and normal diet control (NC) group, fed with normal diet. At the end of the twentieth week blood samples were collected from the heart to determine the serum fasting blood glucose (FBG) and fasting insulin (FINS), and plasma nitrotyrosine, malondialdehyde (MDA), and glutamylcysteinylglycine (GSH), indicators of oxidative stress. Glucose infusion rate (GIR) was measured using euglycemic hyperinsulinemic clamp test to evaluate the peripheral insulin resistance. Pancreatic islets were isolated and collected. Islet perfusion was conducted to evaluate the insulin secretion in the islet beta cells. Real-time PCR was used to detect the expression of insulin receptor substrate-1 (IRS-1), IRS-2, and uncoupling protein 2 (UCP2) genes in the islet. Immunohistochemistry was used to detect the protein expression of IRS-1 and IRS-2. RESULTS: (1) The concentrations of plasma nitrotyrosine and MDA of the HF group were both significantly higher than those of the NC group (both P < 0.05). However, the plasma GSH of the HF group was significantly lower than that of the NC group (P < 0.01). (2) The blood glucose of both groups became stable since 60 min after the experiment and the GIR of the HF group was (5.25 +/- 1.2) mg x min(-1) x kg(-1), significantly lower r than that of the NC group [(13.6 +/- 1l.7) mg x min(-1) x kg(-1), P < 0.01). (3) The peak of glucose-stimulated insulin secretion (GSIS) of the HF group was significantly lower than that of the NC group; and the GSIS peak increase In comparison with the NC group. (4) In comparison with the NC group, the mRNA expression levels of IRS-1 and IRS-2 genes of the HF group were significantly lower, by 42.3% and 28.1% respectively (both P < 0.05), and the expression of UCP2 was significantly higher, by 32.5% (P < 0.05). (5) Compared with the NC group, the protein expression levels of IRS-1 and IRS-2 in the islets of the HF group were lower, by 26.3% and 11.2% respectively, however not significantly (both P > 0.05). (6) There was a significantly negative correlation between the UCP2 and IRS-1/IRS-2 gene expression in islet beta cells in the HF group (r = -0.621 and r = -0.436, both P < 0.05). CONCLUSION: High-fat-diet impairs the expression of insulin signal transduction molecules and the function of islet beta cells that may be correlated with overexpression of UCP2. The basic insulin secretion of HF group was significantly higher than that of the NC group; but the glucose-stimulated insulin secretion (GSIS) peak decreased in comparison with the NC group. Compared with the NC group, the protein expression levels of IRS-1 and IRS-2 in the islets of the HF group were lower, by 26.3% (P < 0.05) and 11.2% (P > 0.05) respectively.     

Apelin对葡萄糖的毒性作用及对胰岛细胞PDX-1表达的影响

目的 探讨Apelin对葡萄糖毒性作用及对胰岛细胞胰十二指肠同源盒蛋白-1(PDX-1)表达的影响.方法 在不同葡萄糖浓度下(正糖组5.6 mmol/L,高糖组16.7 mmol/L,极高糖组33.3 mmol/L),+/-Apelin-36培养胰岛β细胞株NIT-1细胞3d,然后测定基础和葡萄糖刺激后胰岛细胞胰岛素分泌量,测定细胞内胰岛素含量和PDX-1蛋白及mRNA表达.结果 与正糖组比较,高糖组和极高糖组的基础和葡萄糖刺激后胰岛素分泌、细胞内胰岛素均明显减少,PDX-1蛋白表达下降(P＜0.05);与未加Apelin组比较,加Apelin高糖组和极高糖组的基础和葡萄糖刺激后胰岛素分泌、细胞内胰岛素明显减少,PDX-1蛋白表达下降(P＜0.05);6组胰岛细胞的胰岛素水平与PDX-1蛋白表达呈正相关,与PDX-1 mRNA表达无关.结论 Apelin可能通过降低PDX-1蛋白表达参与葡萄糖毒性作用,引起胰岛素分泌减少,从而在糖尿病的发病机制中发挥作用.     

Protection of human islets from induction of apoptosis and improved islet function with HO-1 gene transduction

Background Islet transplantation represents an ideal therapeutic approach for treatment of type 1 diabetes but islet function and regeneration may be influenced by necrosis or apoptosis induced by oxidative stress and other insults. Heme oxygenase-1 (HO-1) is the rate-limiting enzyme in the catabolism of heme into biliverdin, releasing free iron and carbon monoxide. It has also been reported to be an antioxidant enzyme which can improve the function of grafted islets by cytoprotection via free radical scavenging and apoptosis prevention. In the present study, we investigated whether transduction of HO-1 genes into human islets with an adenovirus vector has cytoprotective action on islets cultured in vitro and discuss this method of gene therapy for clinical islet transplantation.Methods Cadaveric pancreatic islets were isolated and purified in vitro. Transduction efficiency of islets was determined by infecting islets with adenovirus vector containing the enhanced green fluorescent protein gene (Ad-EGFP) at multiplicities of infection (MOI) of 2, 5, 10, or 20. Newly isolated islets were divided into three groups: EGFP group, islets transduced with Ad-EGFP using MOI＝20; HO-1 group, transduced with adenovirus vectors containing the human HO-1 gene using MOI＝20; and control group, mock transduced islets. Insulin release after glucose stimulation of the cell lines was determined by a radioimmunoassay kit and the stimulation index was calculated. Flow cytometry was used to detect apoptotic cells in the HO-1 group and in the control group after induction by recombinant human tumor necrosis factor-α (rTNFα) and cycloheximide (CHX) for 48 hours.Results Adenovirus vectors have a high efficiency of gene transduction into adult islet cells. Transduction of islets with the Ad-EGFP was most successful at MOI 20, at which MOI fluorescence was very intense on day 7 after transduction and EGFP was expressed in cultured islet cells for more than four weeks in vitro. The insulin release in the control group was (182.36±58.96) mIU/L after stimulation by high glucose media (16.7 mmol/L), while insulin release from the HO-1 group and the EGFP group were (270.09±89.37) mIU/L and (175.95±75.05) mIU/L respectively. Compared to the control group and the EGFP group, insulin release in the HO-1 group increased significantly (P＜0.05). After treatment with rTNFα and CHX the apoptotic ratio of islet cells was (63.09±10.86)% in the HO-1 group, significantly lower than (90.86±11.25)% in the control group (P&lt;0.05).Conclusions Transduction of human islets with Ad-HO-1 can protect against TNF-α and CHX mediated cytotoxicity. The HO-1 gene also appears to facilitate insulin release from human islets. Transduction of donor islets with the adenovirus vector containing an HO-1 gene might have potential value in clinical islet transplantation.