血小板反应蛋白1在纤维化模型大鼠肾组织中的表达

BACKGROUND:Thrombospondin-1 is an important endogenous activator of transforming growth factor beta 1 in this experimental inflammatory kidney disease model. Transforming growth factor beta 1 is considered the major cytokine that causes tissue fibrosis in many different inflammatory disease processes, in particular in renal disease. OBJECTIVE:To investigate the expression of thrombospondin-1 on renal fibrosis in rats. METHODS:Healthy male Sprague-Dawley rats were randomly divided into sham surgery group and model group. In the model group, right ureters of rats were ligated to construct models of renal fibrosis. 3 weeks after surgery, blood and urine were obtained weekly. Enzyme linked immunosorbent assay and Bradford method were used to detect the contents of serum creatinine, blood urea nitrogen and urinary protein. After rats were sacrificed, kidneys were fixed. Western blot assay was utilized to identify the expression of vascular endothelial growth factor, transforming growth factor beta 1 and thrombospondin-1 protein. Hematoxylin-eosin staining was applied to detect the changes in pathological structure of the kidney after surgery. RESULTS AND CONCLUSION: (1) One week after model induction, urinary protein, serum creatinine and urea nitrogen levels were significantly higher in the model group than in the sham surgery group (P < 0.05). Three weeks later, the difference in each index was significant (P < 0.01), which showed that the injury of the kidney was aggravated. (2) Transforming growth factor beta 1 protein and thrombospondin-1 expression was significantly higher in the model group than in the sham surgery group, but vascular endothelial growth factor protein expression was significantly lower in the model group than in the sham surgery group. (3) Hematoxylin-eosin staining results demonstrated that severe pathological changes of renal tissue in rats were detected after ligation of renal tubule. (4) These results confirmed that thrombospondin-1 expression increased in renal tissue, and its expression was strongly associated with vascular endothelial growth factor protein and transforming growth factor beta 1, which may play an important role in the renal fibrosis.     

骨髓间充质干细胞移植对糖尿病模型大鼠肾脏的保护作用

BACKGROUND:So far numerous theoretical studies have shown the treatment effect of stem cell transplantation for chronic complications of diabetes, while its treatment effects on diabetic nephropathy have not yet been confirmed in animal models. OBJECTIVE:To investigate the protective effect of bone marrow mesenchymal stem cell transplantation on the kidney in rat models of diabetes. METHODS:Rats were fed with high-sugar and high-fat diet for 4 weeks, and then were given injection of streptozotocin to establish type 2 diabetic rat models. At 2 days after modeling, bone marrow mesenchymal stem cells were injected via the tail vein (stem cell transplantation group). In the meanwhile, control and diabetes groups were established. At 21 days after cell transplantation, levels of glucose, triglyceride and insulin in the tail vein were detected. Additionally, morphological observations of kidney and pancreatic tissues were performed. RESULTS AND CONCLUSION:The levels of blood sugar, insulin and triglycerides in the diabetes group were significantly higher than those of the control group (P < 0.05). Blood glucose and insulin levels in the stem cell transplantation group were significantly lower than those of the diabetes group (P < 0.05). In addition, mesangial area and glomerular volume in the stem cell transplantation group were significantly lower compared with the diabetes group (P < 0.05). These results confirm that bone marrow mesenchymal stem cell transplantation can reduce levels of blood glucose and serum insulin, contributing to the repair of damaged pancreas and kidney.     

The inhibitory effect of siRNAs on the high glucose-induced overexpression of TGF-beta1 in mesangial cells

Diabetic nephropathy is characterized by an expansion of the glomerular mesangium, caused by mesangial cell proliferation and an excessive accumulation of extracellar matrix (ECM) proteins, which eventually leading to glomerulosclerosis. TGF-beta1 was found to play an important role in the accumulation of ECM in the kidney. In this study, TGF-beta1 RNA interference was used as an effective therapeutic strategy. The inhibitory effect of TGF-beta1 small interfering RNAs (siRNAs) on the high glucose-induced overexpression of TGF-beta1 in rat mesangial ceys (RMCs). A high levels of glucose induces TGF-beta1 mRNA and protein, and TGF-beta1 siRNAs reduce the ability of high glucose to stimulate their expression. We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. In conclusion, the present study demonstrates that TGF-beta1 siRNAs effectively inhibits TGF-beta1 mRNA and protein expression in RMCs. These suggest that TGF-beta1 siRNAs through RNAi may be a useful tool for developing new therapeutic applications for the treatment of diabetic nephropathy.     

bcl—2癌基因反义硫代磷酸寡脱氧核苷酸诱导HL60细胞凋亡

目的 不同浓度ｂｃｌ－２癌基因反义硫代磷酸寡脱氧核苷酸９ＡＳ－ＰＳ－ＯＤＮ,ＡＳＰＯ）对ＨＬ６０细胞凋亡的诱导作用。方法 ＡＳＰＯ与ＨＬ６０细胞共培养后,用吖啶橙（ＡＯ）染色法,流式细胞仪ＤＮＡ倍体分析,电镜观察、ＤＮＡ片段电沪等方法进行观察。结果 ＡＳＰＯ组与正义组比较能特异诱导ＨＬ６０细胞的凋亡,且于培养２４５小时即可出现,此时ＡＳＰＯ５、１０、２０μｍｏｌ／Ｌ浓度各组的凋亡率分别为：（９．７     

脂质体转染细胞周期素B1反义脱氧寡核苷酸对HL60细胞增殖调控的影响

目的:探讨脂质体转染细胞周期素B1(cyclinB1)反义脱氧寡核苷酸(ASON)对HL60细胞增殖调控的作用。方法:用针对cyclinB1mRNA5’端编码区起始密码子(ATG/AUG)的ASON,通过脂质体导入HL60细胞共培养后,用流式细胞术(FCM)和RT-PCR分别检测cyclinB1蛋白和mRNA的表达水平,电镜和原位细胞凋亡检测法(POD)、FCM及DNA凝胶电泳法检测细胞凋亡。结果:CyclinB1ASON组与SON及空白对照组相比,ASON能特异地抑制cyclinB1蛋白及mRNA水平的表达,当ASON的浓度达到一定程度时,HL60细胞的增殖及集落形成率均明显受抑制,出现细胞凋亡,并且此作用随ASON浓度的升高而增强。结论:CyclinB1的特异ASON能封闭其蛋白及mRNA的表达水平,可剂量依赖性地抑制白血病细胞增殖,诱导细胞凋亡。     

磷酸胆碱聚合物MPC30-DEA70负载转化生长因子β1AS-ODN转染心肌细胞

背景：目前反义寡核苷酸的基因治疗已经拥有良好的应用前景,但是反义寡核苷酸的相对分子质量小却不容易入细胞并且易被核酸酶降解,能否有效地穿过细胞膜且不被核酸酶降解从而与目的基因结合发挥作用,因此人们一直致力于理想载体的选择、基因转移效率的增加和转移特异性等研究。目的：探讨新型阳离子磷酸胆碱聚合物MPC₃₀-DEA₇₀能否有效地负载转化生长因子β1反义寡核苷酸(AS-ODN)进入心肌细胞,并观察其对该基因胞内生物表达的影响。方法：按不同N/P电荷比值将载体MPC₃₀-DEA₇₀与转化生长因子β1 AS-ODN络合成形成基因复合物并且对其总电性进行表征;采用MTT法检测MPC₃₀-DEA₇₀与心肌细胞的生物相容性;共聚焦激光扫描显微镜观察MPC₃₀-DEA₇₀/TGF-β1AS-ODN在细胞内的分布和定位;应用流式细胞仪检测MPC₃₀-DEA₇₀/TGF- β1AS-ODN(FAM标记)的细胞转染效率和荧光强度;Western blot、RT-PCR法检测转化生长因子β1细胞内表达水平。结果与结论：MPC₃₀-DEA₇₀与心肌细胞具有较好的细胞相容性,在较高质量浓度(>20 mg/L)下才表现出一定的细胞毒性并呈剂量依赖;MPC₃₀-DEA₇₀/TGF-β1AS-ODN复合物对心肌细胞具有较高的转染效率,并且能够携带转化生长因子β1 AS-ODN进入细胞后下调转化生长因子β1 mRNA和蛋白的表达。新型阳离子磷酸胆碱基聚合物MPC₃₀-DEA₇₀可以有效负载和运输转化生长因子。中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

糖尿病大鼠模型的制备

目的探讨理想糖尿病大鼠模型的制备方法。方法采用单次腹腔注射65 mg/kg链脲佐菌素(STZ)的方法建立SD大鼠1型糖尿病的动物模型。结果建模3 d后测血糖均高于16.7 mmol/L。持续观察8周,血糖值始终在建模初期高血糖水平上波动,未见转复,并出现典型的"三多一少"症状,胰腺HE染色符合糖尿病动物的病理学变化。结论采用腹腔单次注射65 mg/kg链脲佐菌素的方法建立1型糖尿病大鼠模型,具有建模方法简便、用药量小,药物毒性低,胰岛B细胞损害特异性高等优点,可应用于糖尿病及其并发症研究的各个领域。     

Overexpression of USF increases TGF-beta1 protein levels, but G1 phase arrest was not induced in FRTL-5 cells

Transforming growth factor-beta1 (TGF-beta1) is a potent inhibitor of cellular growth and proliferation by G1 phase arrest or apoptosis. We investigated the association of TGF-beta1 with the anti-proliferative effect of upstream stimulatory factor (USF) in Fischer rat thyroid cell line (FRTL-5) cells. [methyl-(3)H] thymidine uptake was measured after treatment of FRTL-5 cells with TGF-beta1 to identify its anti-proliferative effect. USF-1 and USF-2 proteins were in vitro translated, and an electrophoretic mobility shift assay was performed to identify the interaction between USF and the TGF-beta1 promoter. FRTL-5 cells were transfected with USF cDNA, and then the expression of TGF-beta1 was examined with Northern and Western blotting. The cell cycle-regulating proteins associated with TGF-beta1 were also measured. TGF-beta1 significantly inhibited [methyl-(3)H] thymidine uptake in FRTL-5 cells. Two specific binding sites for USF were found in the TGF-beta1 promoter: -1,846 approximately -1,841 (CACATG) and -621 approximately -616 (CATGTG). Overexpression of USF increased both the mRNA levels and protein levels of TGF-beta1. However, the expression of cyclin D1, CDK4, cyclin E, and CDK2, and the phosphorylation of retinoblastoma protein remained unchanged. Overexpression of USF in FRTL-5 cells increased the expression of TGF-beta10 through specific binding to TGF-beta1 promoter. However, the USF-induced expression of TGF-beta1 did not cause G1 arrest.     

链脲佐菌素联合高脂饲养诱导2型糖尿病大鼠模型的稳定性及其眼病特点

背景：目前链脲佐菌素诱导糖尿病眼病动物模型的研究较为常见,但其病理改变较为局限且主要关注视网膜的改变,关于与临床上糖尿病眼病病理改变密切相关的动物疾病模型研究报道较少。 目的：探讨链脲佐菌素联合高脂饲养诱发大鼠2型糖尿病模型的长期稳定性及其眼病特点。 方法：将大鼠随机分为正常对照组及糖尿病组,正常对照组大鼠给予普通饲养,糖尿病组大鼠通过腹腔注射链脲佐菌素联合高脂饲养制作糖尿病动物模型。 结果与结论：与对照组比较,建模后1个月,糖尿病组大鼠空腹血糖水平增高,胰岛素敏感指数降低(P < 0.05);伊文思蓝染色显示,建模后3个月,糖尿病组大鼠视网膜各层细胞病变加重;建模后5个月,糖尿病组大鼠视网膜血管走行迂曲、紊乱,同时伴有渗漏,视网膜伊文思蓝含量随建模后时间延长呈递增趋势(P < 0.05)。透射电镜观察显示,糖尿病组5个月大鼠晶状体呈片絮状等典型白内障改变。结果证实,链脲佐菌素联合高脂饲养诱发大鼠糖尿病模型长期且稳定,其眼病改变符合糖尿病眼病的特点,是研究糖尿病眼病较为理想的动物模型。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

糖尿病牙周炎模型大鼠的牙槽骨丧失

背景：糖尿病牙周炎大鼠与单纯慢性牙周炎大鼠以及正常对照组大鼠在不同时间段内体质量、血糖、牙周组织的变化对牙槽骨丧失程度的影响不同。 目的：建立糖尿病牙周炎模型大鼠和慢性牙周炎模型大鼠,观察糖尿病加重牙周炎大鼠槽骨吸收的破坏程度。 方法：选用8周龄SPF级雄性SD大鼠52只,随机分为糖尿病牙周炎组、慢性牙周炎组以及正常对照组。糖尿病牙周炎组大鼠按采用注射链脲佐菌素+牙周结扎的方法建立糖尿病牙周炎模型大鼠。慢性牙周炎组大鼠采用牙周结扎并不断加压的方法建立慢性牙周炎大鼠模型;正常对照组大鼠正常喂养。各组大鼠分别于结扎后1,2,3,4周,观察各组大鼠牙周组织变化,取上颌骨牙槽骨标本,在体视显微镜下观察各组大鼠牙槽骨丧失值程度。 结果与结论：钢丝结扎后1,2,3,4周大鼠牙槽骨丧失程度：糖尿病牙周炎组>慢性牙周炎组>正常对照组(P < 0.05)。结果证实,实验成功建立糖尿病牙周炎和慢性牙周炎动物模型,糖尿病可加重牙周炎牙周组织破坏,牙槽骨丧失增加。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

硫代反义寡核苷酸在鸭体内外对鸭乙型肝炎病毒DNA复制的影响

目的：研究在转录起始区域设计硫代反义寡核苷酸抑制鸭乙型肝炎病毒DNA（DHBV DNA）复制的可行性。方法：设计合成分别基于DHBV PreS1、PreS2、S抗原启动基因的硫代反义寡核苷酸，应用Southern blot实验和cpm计数测定其对原代鸭肝细胞中及雏鸭中感染DHBV的DHBV DNA的作用。结果：在1.5μmol/L浓度下，体外抑制率分别是61．5％，69．3％和62．4％。选取PreS1抗原基因起始区段的硫代反义寡核苷酸进行整体动物实验。每只动物每天按10μg/g体重静脉注射一次，共给药6d。对动物肝脏进行取样分析表明，在此剂量下，对DHBV DNA的抑制率可达87.9%。结论：本实验所设计的针对转录起始区的硫代反义寡核苷酸在体内外对DHBV DNA复制均有明显抑制作用，说明了在这一区域设计硫代反义寡核苷酸的可行性。     

糖尿病在糖尿病大鼠心肌梗死后心力衰竭形成中的效应

目的： 评估糖尿病在链脲霉素（STZ）诱导的血糖不加控制的糖尿病大鼠急性心肌梗死（AMI）后心力衰竭(HF)形成中的效应。方法：所有SD大鼠随机分组,糖尿病组经腹腔内注射STZ（65mg/kg）诱导糖尿病,70 d后所有AMI组结扎冠状动脉左前降支建立AMI模型。确定AMI前后各时点观察大鼠的生存率,心肌超微结构的变化,进行血流动力学分析、心肌纤维化测定及左心肥厚的评估。结果：结扎左冠状动脉前降支后,糖尿病大鼠的左心功能恶化及左室重构的速度均较非糖尿病大鼠显著。在早期阶段,糖尿病与非糖尿病大鼠心肌纤维化相似,而1月后却出现显著差别。结论：糖尿病大鼠AMI后心力衰竭进展明显加速。     

玻璃体腔注射促红细胞生成素保护糖尿病视网膜病变模型大鼠的视神经作用

BACKGROUND: Diabetes can lead to many complications. Of them, retinopathy is a common type. To explore the effect of erythropoietin in diabetic retinopathy, it is necessary to establish an animal model of similar pathologic features and high reproducibility in clinical retinal neovascularization.     

1型糖尿病模型大鼠股骨骨代谢紊乱及唑来膦酸的影响

背景：糖尿病引起的骨质疏松作为常见的继发性骨质疏松,近年来越来越受到重视;唑来膦酸作为新型治疗骨质疏松的药物,其对体内成骨细胞的作用尚未完全清楚。目的：观察1型糖尿病大鼠股骨干骺端骨形态发生蛋白2与Noggin的表达变化,以及唑来膦酸的干预作用。方法：随机取130只Wistar大鼠腹腔注射链脲佐菌素建立1型糖尿病模型,3 d后连续3次血糖> 16.7 mmol/L鼠为造模成功鼠,共120只,随机等分为模型组、预防组和治疗组。后2组大鼠分别在造模后当天和2周后一次性静脉给予唑来膦酸(0.1 mg/kg)。另取40只大鼠注射柠檬酸缓冲液作为对照组。结果与结论：与对照组相比,模型组大鼠股骨骨密度、血清碱性磷酸酶水平、股骨骨形态发生蛋白2 mRNA表达水平明显降低(P < 0.05),Noggin mRNA表达水平显著升高(P < 0.05)。与模型组相比,预防组和治疗组大鼠骨密度和骨形态发生蛋白2 mRNA表达水平显著升高(P < 0.05),Noggin mRNA表达水平显著降低(P < 0.05),血清骨碱性磷酸酶水平也逐渐恢复。提示1型糖尿病大鼠骨代谢紊乱在病程早期即出现,而应用唑来膦酸可以促进骨形成,增加骨密度,改善骨代谢。中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

Prevention of tissue injury by ribbon antisense to TGF-beta1 in the kidney

Transforming growth factor-beta1 (TGF-beta1) is an important mediator of glomerulosclerosis and tubulointerstitial fibrosis in renal diseases. We designed ribbon-type antisense oligos of TGF-beta1, TGF-beta1 RiAS, and combined them with a short peptide of the nuclear localization signal to form a transfection complex of DNA/peptide/liposomes (DPL) for enhanced cellular uptake. When H4IIE cells were transfected with TGF-beta1 RiAS, the level of TGF-beta1 mRNA was reduced by >70%. We then examined the ratio of the kidney weight per body weight in rats. Whereas the weight ratio was 0.47% for the normal kidney, the ratio was 0.99% on day 5 after unilateral ureteric obstruction (UUO). The ratios were 0.95% with PBS injection, 1.07% with scrambled RiAS, and 0.68% with TGF-beta1 RiAS. When examined for TGF-beta1 expression in the tissue, the level of TGF-beta1 mRNA was also significantly reduced following treatment with TGF-beta1 RiAS. Further, physical changes such as diminished dilation, atrophy, as well as apoptosis caused by UUO were also found to be markedly reduced by TGF-beta1 RiAS. The results show that ribbon antisense to TGF-beta1 when combined with efficient uptake can effectively block TGF-beta1 expression and preserve tissue integrity in kidneys with UUO.     

链尿佐菌素制备糖尿病神经源性膀胱大鼠模型

目的对使用单次腹腔注射大剂量链尿佐菌素（STZ）制备糖尿病神经源性膀胱大鼠模型的方法进行探讨。方法使用随机分组的方法将30只SPF级健康雄性sD大鼠随机分成正常对照组（NC组）10只、糖尿病组（DM组）20只;给予糖尿病组大鼠单次腹腔注射链尿佐菌素（60mg／kg）,同时给予对照组大鼠相同剂量的柠檬酸钠缓冲液,3d后测空腹血糖,血糖≥16．7mmol／L大鼠入选为糖尿病组模型。后观察大鼠一般指标（精神、皮毛光泽度、血糖、体重、饮食量、饮水量等）,8周时取出膀胱测残尿量、膀胱湿重、行HE染色。结果3d后糖尿病组大鼠糖尿病成模率达到90％,8周后血糖值稳定,糖尿病组膀胱HE染色有明显病理改变。DM组中糖尿病大鼠模型的糖尿病神经源性膀胱大鼠模型成模率为100％。结论通过单次大剂量腹腔注射链尿佐菌素（60mg／kg）可快速制备稳定的糖尿病大鼠模型,且在此基础上诱导神经源性膀胱大鼠模型的成功率高,在8周时其成模率可达100％。是目前一种简便、快速获取稳定糖尿病神经源性性膀胱大鼠模型的方法。     

Effect of antisense oligodeoxynucleotides for ICAM-1 on renal ischaemia–reperfusion injury in the anaesthetised rat

An antisense oligodeoxynucleotide (As-ODN) to the 3' untranslated region of the mRNA sequence expressing the intracellular adhesion molecule-1 (ICAM-1) was employed to determine ICAM-1's role in renal ischaemia–reperfusion injury in the rat. Wistar-Kyoto rats receiving i.v. either lipofectin–As-ODN (As-ODN group), lipofectin–reverse ODN (Rv-ODN group) or lipofectin (ischaemia control group) 8 h prior to study were anaesthetized and subjected to 30 min of renal artery occlusion. Renal haemodynamic and excretory parameters were monitored before and after renal ischaemia. On termination of the study renal tissue was subjected to histological and Western blot analysis. Renal blood flow decreased in the 3 h post-ischaemia period in the ischaemia control and Rv-ODN groups, but was maintained in the As-ODN group. Glomerular filtration rate was depressed initially but gradually increased to 10% above basal levels in the ischaemia control and Rv-ODN groups, but was below basal levels (20%) in the As-ODN group. There was a three- to fourfold increase in sodium and water excretion following ischaemia in the ischaemia control and reverse-ODN groups but not in the As-ODN treated group. The As-ODN ameliorated the histological evidence of ischaemic damage and reduced ICAM-1 protein levels to a greater extent in the medulla than cortex. These observations suggested that in the post-ischaemic period afferent and efferent arteriolar tone was increased with a loss of reabsorptive capacity which was in part due to ICAM-1. The possibility arises that the action of ICAM-1 at vascular and tubular sites in the deeper regions of the kidney contributes to the ischaemia–reperfusion injury.     

白细胞介素10基因对未发病非肥胖型糖尿病小鼠肝脏胰-十二指肠同源盒1表达的影响

背景：研究发现肝脏细胞在给予转入胰-十二指肠同源盒1基因后可合成胰岛素,抗CD20单克隆抗体可抑制产胰岛素的肝脏细胞发生自身免疫反应,但机制尚不明确。 目的：了解腺病毒介导的小鼠白细胞介素10(Adenovirus vector-mediated murine interleukin,Ad-mIL-10)及抗CD20单克隆抗体联合干预未发病非肥胖糖尿病模型小鼠,对其肝脏细胞以及肝脏胰-十二指肠同源盒1表达的影响。 方法：3-5周龄雌性未发病非肥胖糖尿病模型小鼠40只,随机分为抗CD20单克隆抗体组、抗CD20单克隆抗体+白细胞介素10组、白细胞介素10组和对照组,分别于第1,8,15,21天尾静脉注射抗CD20单克隆抗体、抗CD20单克隆抗体+ Ad-mIL-10、Ad-mIL-10和生理盐水。  结果与结论：12周后,与对照组相比,经抗CD20单克隆抗体和/或白细胞介素10治疗的未发病非肥胖糖尿病模型小鼠血糖水平明显降低,而血清和肝脏中胰岛素、白细胞介素10和CD20表达明显增加,同时肝脏中胰-十二指肠同源盒1表达水平增加;且经抗CD20单克隆抗体和白细胞介素10联合对上述指标的影响高于单独应用;但无论是联合干预还是单独干预均对小鼠肝脏炎症病变无明显影响。证实CD20单抗及白细胞介素10基因联合干预为促使非肥胖糖尿病模型小鼠肝脏胰-十二指肠同源盒1表达机制之一。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

灯盏花素干预糖尿病模型大鼠睾丸组织增殖细胞核抗原和c-fos的表达

背景：有研究表明灯盏花素可影响2型糖尿病大鼠的生殖能力,但其作用机制少有报道。 目的：探讨灯盏花素对2型糖尿病大鼠睾丸增殖细胞核抗原和原癌基因c-fos表达的影响作用。 方法：选取36只健康雄性大鼠随机分为对照组、模型组和灯盏花素组各12只。模型组和灯盏花素组采用链脲佐菌素连续腹腔注射建立2型糖尿病大鼠模型,大鼠血糖监测达到16.7 mmol/L作为建模标准,对照组大鼠予以同等容积的柠檬酸缓冲液单次腹腔注射。灯盏花素组采用灯盏花素注射液10 mg/(kg•d)连续4周腹腔注射,其他2组在相同时间注入等量生理盐水。 结果与结论：干预4周后,血清睾酮检测、免疫组织化学染色和PCR检测结果显示,血清睾酮水平、增殖细胞核抗原、c-Fos蛋白及mRNA表达：对照组>灯盏花素组>模型组(P < 0.05);血糖水平：对照组<灯盏花素组<模型组(P < 0.05)。结果证实,灯盏花素可以通过增强增殖细胞核抗原和c-fos的表达,保护2型糖尿病大鼠的生殖功能。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

糖尿病大鼠心肌TGF-β1表达及细胞凋亡的实验研究

目的:研究糖尿病大鼠心肌转化生长因子β1(TGF-β₁)表达水平和细胞凋亡的变化，探讨糖尿病性心肌病的病理生理机制。方法：链脲菌素法复制不同病程的糖尿病模型。免疫组化方法测定TGF-β₁的表达。DNA断端末端标记法测定心肌细胞凋亡指数。结果：糖尿病大鼠心肌细胞TGF-β₁表达明显高于正常对照组（P<0.01）。TUNEL法测定心肌细胞的凋亡阳性细胞数量在糖尿病早期明显高于正常，晚期有所减少。结论：TGF-β₁在糖尿病的心肌中表达增加，且随病程发展而上升，可能是糖尿病心肌纤维化的重要促发因子。糖尿病心肌中细胞凋亡现象随病程延长而逐渐减弱，机制有待探讨。