血管内皮细胞生长因子和c-Fos在单基因遗传自然发病型糖尿病小鼠颌下腺中的表达

目的:观察血管内皮细胞生长因子和c-Fos蛋白在db/db自发性糖尿病小鼠颌下腺的表达,及其与糖尿病病程和颌下腺形态学改变的关系。方法:实验于2004-05在承德医学院中心实验室和承德医学院附属医院病理科完成。取3,4,6,8,10月龄db/db(单基因遗传自然发病型)糖尿病小鼠颌下腺(实验组)及相应月龄的db/ m正常小鼠颌下腺(对照组),采用SP免疫组化染色,观察颌下腺血管内皮细胞生长因子、c-Fos阳性表达的变化。结果:①颌下腺血管内皮细胞生长因子阳性细胞数目:实验组3,4,6,8,10月龄高于相应对照组[(11.8±3.35),(17.4±2.61),(20.6±1.92),(26.8±4.85),(28.0±4.22)个/视野;(6.6±0.89),(11.8±1.64),(16.2±3.27),(16.4±3.97),(17.6±1.82)个/视野,P<0.05,0.01],且呈逐渐增加趋势。②颌下腺c-Fos阳性细胞数目:实验组3,4,6月龄低于相应对照组[(6.4±0.65),(7.8±0.84),(7.9±0.65)个/视野;(12.2±0.84),(11.4±0.55),(10.8±0.84)个/视野,P<0.01]。③糖尿病病程的延长,实验组下颌下腺的实质细胞有明显形态学改变,其中腺泡萎缩明显,细胞排列紊乱。结论:①血管内皮细胞生长因子表达在db/db糖尿病小鼠颌下腺中随病程延长表达增加,与糖尿病病程呈正相关。②db/db糖尿病状态下颌下腺实质发生萎缩性形态学变化,颌下腺细胞表达c-Fos蛋白明显降低,可能与其密切相关。     

糖尿病大鼠颌下腺肥大细胞数量及转化生长因子β1的表达

背景：研究表明,持续高血糖可导致大鼠颌下腺的细胞出现退行性改变,表现为细胞因子表达增加,糖原代谢改变,分泌功能减弱。关于肥大细胞及转化生长因子β1与糖尿病颌下腺组织病变的关系研究较少。目的：观察糖尿病状态下颌下腺组织中肥大细胞数量与形态变化和转化生长因子β1的表达。方法：雄性SD大鼠32只,随机分为实验组和对照组,实验组注射四氧嘧啶成模后的4,8,12周测量体质量和血糖,并与对照组大鼠-同取下颌下腺组织做苏木精-伊红染色和甲苯胺蓝染色观察并计数肥大细胞,SP免疫组织化学染色方法检测转化生长因子β1棕黄色阳性细胞数量。结果与结论：①肥大细胞在正常鼠及糖尿病鼠颌下腺组织中均有表达,实验组与对照组比较肥大细胞数随病程延长而增多,实验组不同时期明显多于对照组（P〈0．01）。②转化生长因子β1阳性细胞数在正常大鼠及糖尿病大鼠颌下腺的腺泡细胞、颗粒曲管及纹状管细胞中均有表达,阳性颗粒位于胞浆内,糖尿病时,随病程延长而增多,实验组不同时期明显多于对照组（P〈0．01）。结果可见糖尿病大鼠颌下腺中肥大细胞与转化生长因子β1表达增强与糖尿病病程呈正相关。     

小鼠下颌下腺发育中转化生长因子β受体的表达

背景：小鼠的下颌下腺是研究唾液腺的发育的良好模型,转化生长因子β是器官发育和疾病中重要的生长因子,但是在下颌下腺中转化生长因子β受体的表达以及作用机制至今并不明确。目的：观察胚胎小鼠下颌下腺发育过程中转化生长因子βⅠ型受体和Ⅱ型受体以及p-ERK1／2的表达,揭示转化生长因子β在小鼠涎腺发育中的作用。方法：取C57BL／6J小鼠胚胎期第14.5天的标本,使用转化生长因子βⅠ型受体和Ⅱ型受体以及p-ERK1／2抗体,对小鼠的下颌下腺进行免疫组化染色。取新生小鼠标本,大体观察下颌下腺,并且使用苏木精-伊红染色观察其形态。结果与结论：①小鼠出生时,下颌下腺位于下颌骨下方;苏木精-伊红染色发现小鼠下颌下腺的腺泡、导管和闰管细胞也已经分化完成。②在胚胎期第14．5天,转化生长因子βⅠ型和Ⅱ型受体在腺泡上皮和导管上皮内高表达,而腺体上皮细胞外的间充质没有表达。③p-ERK1／2主要也是表达在下颌下腺的上皮细胞中,与转化生长因子βⅠ型受体和Ⅱ型受体在下颌下腺中的表达基本一致。说明在小鼠下颌下腺的发育过程中,转化生长因子β蛋白可能通过与上皮细胞表面的受体结合,激活ERK信号通路来调节涎腺腺泡和导管的发育。     

血管内皮生长因子反义寡核苷酸对小鼠在体肺癌细胞的抑制作用

目的:探讨血管内皮生长因子反义寡核苷酸基因治疗方法对模型小鼠在体肺癌细胞的抑制作用。方法:于2001-05/2002-01在哈尔滨医科大学第一临床医学院实验动物中心制作C57BL/6小鼠皮下肺癌模型30只,分为血管内皮生长因子反义寡核苷酸治疗组、血管内皮生长因子正义寡核苷酸治疗组及对照组。接种Lewis肺癌细胞后24h内,用反义寡核苷酸及正义寡核苷酸皮下注射进行治疗,对照组只注射生理盐水,观察小鼠肿瘤的生长情况。用免疫组化方法检测血管内皮生长因子蛋白表达,强阳性为,弱阳性为+。通过反转录多聚酶链反应检测血管内皮生长因子mRNA的表达,计算血管内皮生长因子与β-actin比值作为血管内皮生长因子表达水平参数。结果:30只模型鼠均进入结果分析。①平均瘤质量:对照组、血管内皮生长因子反义寡核苷酸治疗组、血管内皮生长因子正义寡核苷酸治疗组分别为(7.83±0.78),(4.49±0.43)和(7.73±0.69)g。②血管内皮生长因子在癌周表达强度高于癌内,在对照组及血管内皮生长因子正义寡核苷酸组多呈强阳性,而血管内皮生长因子反义寡核苷酸组多呈弱阳性。③血管内皮生长因子120/β-actin:血管内皮生长因子反义寡核苷酸组(0.1594±0.025)低于对照组[(0.4020±0.032),P<0.01],低于血管内皮生长因子正义寡核苷酸组[(0.3805±0.030),P<0.01]。④血管内皮生长因子164/β-actin:血管内皮生长因子反义寡核苷酸组(0.3073±0.021)低于对照组[(0.8780±0.029),P<0.01],低于血管内皮生长因子正义寡核苷酸组[(0.8481±0.020),P<0.01]。结论:血管内皮生长因子反义寡核苷酸与肿瘤血管的生成密切相关。原位注射血管内皮生长因子反义寡核苷酸能抑制小鼠在体肺癌细胞的生长。     

血管内皮细胞相关生长因子在高血压不同阶段心肌细胞和血管内皮细胞中的分布特征

目的:观察血管内皮细胞生长因子、碱性成纤维生长因子在高血压不同阶段心肌细胞和血管内皮细胞的分布变化。方法:实验于2001-10/2002-06在承德医学院附属医院中心实验室完成。选用遗传性盐敏感型高血压大鼠(DahlS)和遗传性盐抵抗型高血压大鼠(DahlR),在5周龄投与8%食盐饲料,分别在10,11,12周时取材,制作心肌组织切片。应用免疫组织化学方法观察血管内皮细胞生长因子和碱性成纤维生长因子在心肌组织中的表达变化情况,计算单位面积心肌组织血管内皮细胞生长因子和碱性成纤维生长因子的阳性细胞数和血管内皮细胞的阳性表达。结果:血管内皮细胞生长因子和碱性成纤维生长因子免疫细胞在DahlS和DahlR组大鼠的心肌细胞及血管内皮细胞中均有表达,DahlS组血管内皮细胞生长因子和碱性成纤维生长因子阳性细胞数均较同时期DahlR组增多(P<0.01)。DahlS组自10周起至12周心肌细胞血管内皮细胞生长因子和碱性成纤维生长因子阳性细胞数逐渐增多(P<0.01)。DahlR组在高血压不同时期血管内皮细胞生长因子和碱性成纤维生长因子无显著性变化(P>0.05)。心肌组织的血管内皮细胞的表达强度,DahlS组血管内皮细胞生长因子和碱性成纤维生长因子均由(+)到(),且均可见组织内毛细血管增多。DahlR组无变化。结论:血管内皮细胞生长因子和     

血管内皮生长因子在大鼠静脉窦血栓模型水肿脑组织中的表达与影像学评估指标的关系

目的:分析血管内皮生长因子在静脉窦血栓的血管源性水肿中的作用。方法:实验于2004-10/2005-5在解放军沈阳军区总医院放射诊断科完成。Wistar大鼠14只,随机选取7只结扎上矢状窦,定为实验组。另外7只不结扎上矢状窦,定为正常对照组。24h后行大鼠脑组织磁共振检查弥散加权成像,计算表观弥散系数值。并将脑组织标本分别进行苏木精-伊红染色和免疫组织化学染色,观察血管内皮生长因子的表达,分析表观弥散系数值与血管内皮生长因子的关系。结果:血管内皮生长因子表达与血管源性水肿相关,在表观弥散系数图上表现为高信号犤实验组血管源性水肿区域血管内皮生长因子免疫阳性细胞数为(21.00±2.23)个/高倍视野,表观弥散系数值(0.81±0.05)×10-3mm2/s。正常对照组血管内皮生长因子免疫阳性细胞数为(3.34±1.05)个/高倍视野,表观弥散系数值(0.75±0.03)×10-3mm2/s犦。结论:血管内皮生长因子表达在急性期静脉窦血栓的血管源性水肿脑组织中明显增强,并与影像学指标变化一致。     

转化生长因子β1联合血管内皮细胞生长因子体外诱导胚胎干细胞向血管内皮细胞分化

目的:观察胚胎干细胞在转化生长因子β1和血管内皮细胞生长因子体外诱导分化血管内皮细胞的能力,探讨提高诱导效率的方法。方法:实验于2004/2006在南昌大学医学院第二附属医院血液病研究所进行。实验材料:成年昆明小鼠由南昌大学医学院动物科学部提供(机构许可证号:96021),经自然交配怀孕。小鼠胚胎干细胞129×1/SvJ细胞系,购于ATCC公司。实验方法:取孕12.5～14.5d的胎鼠,制作小鼠胚胎成纤维细胞饲养层。在小鼠胚胎成纤维细胞饲养层上培养扩增胚胎干细胞。将饲养层上扩增后生长状态好的胚胎干细胞以0.25%胰酶消化,小心吹打成单个细胞悬液,以差速贴壁法将饲养层细胞去掉,按1×104L-1胚胎干细胞悬液悬滴在细胞培养皿的盖上,每滴10～20μL,不换液,3d后形成拟胚体,培养液为不含白血病抑制因子的胚胎干细胞培养液。挑选状态好的拟胚体分3组:转化生长因子β1诱导组、血管内皮细胞生长因子诱导组、转化生长因子β1 血管内皮细胞生长因子诱导组。采用RT-PCR和免疫组织化学方法证实诱导的细胞是否为内皮细胞。结果:①胚胎干细胞体外诱导生长观察:3组中拟胚体贴壁后第2天,胚体均略摊开,周围有上皮样细胞出现,第3,4天有许多卵石样细胞产生,至第6天开始出现由卵石样细胞构成的管状结构,自胚体向周围呈辐射状生长,渐呈网状,诱导时间约2周。转化生长因子β1 血管内皮细胞生长因子诱导组中产生的管样结构的拟胚体数较转化生长因子β1诱导组、血管内皮细胞生长因子诱导组多(44.67±3.88,28.17±6.08,33.00±2.68,P<0.05)。②RT-PCR法检测基因mRNA水平:3组基因表达的扩增片断分别为1086,733,265bp,与DNAmark相比较,条带位置相符。③扩增细胞的免疫组织化学染色:Ⅷ因子抗体反应显示阳性。结论:转化生长因子β1与血管内皮细胞生长因子均能诱导胚胎干细胞为内皮细胞,两者合用有可能提高诱导效率。     

多种细胞因子对绒癌细胞系JEG-3表达转化生长因子-β3及血管内皮生长因子影响

目的:观察白细胞介素等多种细胞因子对绒癌细胞系表达转化生长因子-β3及血管内皮生长因子的影响.方法:将JEG-3细胞分别予12.5 ng/mL白细胞介素-2、10 ng/mL白细胞介素-3、50 u/mL白细胞介素-6、5 ng/mL白细胞介素-8、10 ng/mL白细胞介素-10、10 ng/mL白细胞介素-15、10 ng/mL表皮生长因子、10 ng/mL粒-巨噬细胞集落刺激因子、10 ng/mL巨噬细胞集落刺激因子处理24 h后,采用RT-PCR方法检测JEG-3绒癌细胞系中转化生长因子-β3及血管内皮生长因子的转录表达.结果:白细胞介素-2、白细胞介素-3、白细胞介素-6、白细胞介素-8、巨噬细胞集落刺激因子对转化生长因子-β3和血管内皮生长因子均表现出诱导表达的作用,表皮生长因子、粒-巨噬细胞集落刺激因子仅诱导转化生长因子-β3的表达,白细胞介素-10则仅诱导血管内皮生长因子的表达,而白细胞介素-15则对JEG-3细胞表达转化生长因子-β3和血管内皮生长因子均无显著影响.结论:在调节滋养层细胞侵入的复杂细胞因子网络中,各种细胞因子之间存在相互影响.     

不同月龄大鼠椎间盘纤维环退行性变与血管内皮生长因子表达的关系

目的:观察大鼠不同月龄椎间盘纤维环的形态学变化并检测其中血管内皮生长因子的表达,探讨血管内皮生长因子与椎间盘纤维环退行性变的关系。方法:实验于2004-12/2005-01在中国医科大学基础医学院组织工程第三实验室完成。取Wistar大鼠50只,以大鼠1,3,6,12,18个月龄不同分为5组。采用免疫组织化学方法观察椎间盘纤维环中血管内皮生长因子的表达情况,并测定部分视野的平均吸光度值,以平均吸光度值的高与低显示血管内皮生长因子表达的强与弱;采用苏木精-伊红染色观察软骨细胞、成纤维细胞及胶原纤维的形态学变化。结果:进入结果分析实验大鼠50只。①随着大鼠月龄的增长,其椎间盘纤维环中血管内皮生长因子的表达发生变化,低月龄组(1,3个月龄)血管内皮生长因子表达强烈(平均吸光度值41.70±11.19,36.42±11.98),成龄组(12个月龄)表达较弱(平均吸光度值6.67±4.44),两组差异意义显著(P<0.01)。②大鼠椎间盘纤维环的组织结构也随大鼠月龄增长发生变化,软骨细胞数量减少,胶原纤维增生、粗大,走行紊乱。结论:大鼠椎间盘纤维环结构随月龄增长发生退行性变,纤维环中血管内皮生长因子表达强烈,则纤维环退行性变进程快,对椎间盘退行性变有不良影响。     

血管内皮细胞生长因子和转化生长因子β1在骨关节炎滑膜组织中的表达及相关性

背景:血管内皮细胞生长因子和转化生长因子β1都是与骨关节炎关系比较密切的合成及分解类细胞因子家族,在骨关节炎组织中表达情况的报道多限于软骨细胞及基质方面,且报道结果并不完全一致,对滑膜组织研究尚不深入.目的:进一步了解虹管内皮细胞生长因子和转化生长因子β1在骨关节炎滑膜组织中的表达及相关性.设计、时间及地点:细胞分子生物学体外实验,2003-01/2004-09在滨州医学院附属淄博市中心医院分子生物学实验室完成.对象:选取符合骨关节炎诊断标准并经辅检证实的患者的滑膜病理标本30例;非正常死亡及创伤性截肢的健康国人滑膜标本8例为正常对照.方法:所有滑膜标本进行免疫组织化学染色,常规脱蜡至水,先后加入过氧化酶阻断溶液及正常羊血清孵育,并依次加一抗、生物素标记二抗、链亲和素-过氧化物酶溶液及DAB溶液,其间均充分水洗,苏木精复染封固观察.对照实验采用替代实验,用PBS替代一抗,余步骤同上述实验方法.主要观察指标:血管内皮细胞生长因子和转化生长因子β1在滑膜组织中的表达情况及其相关性.结果:血管内皮细胞生长因子和转化生长因子β1的阳性表达率分别为86.7%和13.3%,与正常组织比较,转化生长因子β1 表达率降低(P<0.05),血管内皮细胞生长因子表达率增高(P<0.05).血管内皮细胞生长因子和转化生长因子β1表达的相关性有显著性意义(rs=0.373,0.01相似文献   

Recombinant basic fibroblast growth factor stimulates wound healing in healing-impaired db/db mice

The stimulatory effect of recombinant basic fibroblast growth factor (bFGF) on wound healing was assessed using healing-impaired (db/db) mice. Full-thickness wounds were made in female diabetic C57BL/KsJ db/db mice, and their normal (db/+) littermates with a punch biopsy instrument. Recombinant bFGF was applied locally to the open wound once a day. The mice were later killed and histological sections of the wounds were prepared. The degree of wound healing was evaluated using several histological parameters such as degree of reepithelialization, granulation tissue thickness, matrix density, number of infiltrated cells, and number of capillaries. Wounds from normal mice displayed good reepithelialization rates and granulation tissue formation, while wounds from db/db mice had poor responses, especially in the dermal parameters. Although the application of bFGF to wounds in the normal (db/+) mice had little effect, application of bFGF to wounds in db/db mice induced significant responses in all of the dermal parameters compared with nontreated db/db mice (p less than 0.001). In the presence of bFGF, these parameters approximated those observed in nontreated littermates. A minimum of 0.5 microgram bFGF in either single or multiple applications was required for a significant effect. bFGF that was either boiled or pretreated with neutralizing antibody had little stimulatory effect. Time-course experiments indicated that the granulation response in bFGF-treated mice peaked between 8 and 12 d, and decreased after 12 d, while matrix density continued to increase until the 18th day (p less than 0.05). The breaking strength of healed linear wounds in db/db mice was also decreased when compared with heterozygous littermates. This parameter was also improved by the administration of bFGF to the wounds (p less than 0.05).     

厄贝沙坦对db/db糖尿病小鼠血糖的影响

目的:观察厄贝沙坦治疗能否对db/db糖尿病小鼠的高血糖状态具有改善作用。方法:4周龄的db/db小鼠分为对照组(生理盐水)和厄贝沙坦[10mg/(kg·d)]治疗组。于每周监测各组小鼠的体重及随机血糖,并于第8周末行腹腔糖耐量试验(IPGTT),分别测定各组小鼠0、30、60及120min血糖及血浆胰岛素水平。结果:在厄贝沙坦治疗8周后治疗组与对照组相比,体重无明显差异,随机血糖无明显改善,IPGTT试验结果与对照组差异无统计学意义。结论:厄贝沙坦对改善db/db糖尿病小鼠糖代谢疗效不明显,同时不能明显改善db/db小鼠的糖耐量。     

MicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice

Inflammation and its consequent fibrosis are two main features of diabetic nephropathy (DN), but target therapy on these processes for DN remains yet ineffective. We report here that miR-29b is a novel therapeutic agent capable of inhibiting progressive renal inflammation and fibrosis in type 2 diabetes in db/db mice. Under diabetic conditions, miR-29b was largely downregulated in response to advanced glycation end (AGE) product, which was associated with upregulation of collagen matrix in mesangial cells via the transforming growth factor-β (TGF-β)/Smad3-dependent mechanism. These pathological changes were reversed by overexpressing miR-29b, but enhanced by knocking-down miR-29b. Similarly, loss of renal miR-29b was associated with progressive diabetic kidney injury, including microalbuminuria, renal fibrosis, and inflammation. Restored renal miR-29b by the ultrasound-based gene therapy was capable of attenuating diabetic kidney disease. Further studies revealed that inhibition of Sp1 expression, TGF-β/Smad3-dependent renal fibrosis, NF-κB–driven renal inflammation, and T-bet/Th1-mediated immune response may be mechanisms associated with miR-29b treatment in db/db mice. In conclusion, miR-29b may play a protective role in diabetic kidney disease and may have therapeutic potential for diabetic kidney complication.     

Antihyperglycemic and antioxidant properties of caffeic acid in db/db mice

This study investigated the blood glucose-lowering effect and antioxidant capacity of caffeic acid in C57BL/KsJ-db/db mice. Caffeic acid induced a significant reduction of the blood glucose and glycosylated hemoglobin levels than the control group. The plasma insulin, C-peptide, and leptin levels in caffeic acid group were significantly higher than those of the control group, whereas the plasma glucagon level was lower. Increased plasma insulin by caffeic acid was attributable to an antidegenerative effect on the islets. Caffeic acid also markedly increased glucokinase activity and its mRNA expression and glycogen content and simultaneously lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities and their respective mRNA expressions, accompanied by a reduction in the glucose transporter 2 expression in the liver. In contrast to the hepatic glucose transporter 2, adipocyte glucose transporter 4 expression was greater than the control group. In addition, caffeic acid significantly increased superoxide dismutase, catalase, and glutathione peroxidase activities and their respective mRNA levels, while lowering the hydrogen peroxide and thiobarbituric acid reactive substances levels in the erythrocyte and liver of db/db mice. These results indicate that caffeic acid exhibits a significant potential as an antidiabetic agent by suppressing a progression of type 2 diabetic states that is suggested by an attenuation of hepatic glucose output and enhancement of adipocyte glucose uptake, insulin secretion, and antioxidant capacity.     

依布硒啉对db/db小鼠蛋白尿作用及其机制

目的探讨依布硒啉（ebselen）对db/db小鼠蛋白尿的作用及其可能机制。方法 16只8周龄db/db小鼠随机分为依布硒啉组8只（Ebs组）和糖尿病肾病组8只（DN组）,分别给予依布硒啉50mg/kg和生理盐水灌胃,2次/d;8只8周龄db/m小鼠为非糖尿病对照组（对照组）,给予生理盐水灌胃,2次/d;每周监测各组体质量、空腹血糖。8周后检测24h尿白蛋白、尿8-羟基脱氧鸟苷酸、肾脏组织丙二醛含量、超氧化物歧化酶和谷胱甘肽过氧化物酶活性。结果治疗8周后,DN组空腹血糖（（31.9±2.4）mmol/L）、24h尿白蛋白（（240.7±26.3）μg/24h）、尿8-羟基脱氧鸟苷酸（183.5±26.7）ng/24h）、肾组织匀浆丙二醛含量（（11.5±2.2）nmol/mg）明显高于对照组（（6.7±0.8）mmol/L、（16.4±1.1）μg/24h、（74.8±13.5）ng/24h、（3.6±0.9）nmol/mg）和Ebs组（（21.3±1.1）mmol/L、（76.3±14.7）μg/24h、（86.9±16.5）ng/24h、（7.7±1.6）nmol/mg）,肾脏组织超氧化物歧化酶和谷胱甘肽过氧化物酶活性（（312.4±16.9）、（167.2±14.8）u/mg）明显低于对照组（（358.2±13.4）、（217.4±15.7）u/mg）和Ebs组（（366.5±24.7）、（191.2±16.5）u/mg）（P〈0.01）;Ebs组空腹血糖、24h尿白蛋白和肾组织丙二醛含量高于对照组（P〈0.01）,尿8-羟基脱氧鸟苷酸水平、超氧化物歧化酶和谷胱甘肽过氧化物酶活性与对照组比较差异无统计学意义（P〉0.05）。结论依布硒啉能降低蛋白尿,其机制可能与减轻db/db小鼠肾脏组织氧化应激有关。     

富含半胱氨酸的酸性分泌蛋白在db/db鼠肝脏组织中的表达及意义

目的 观察富含半胱氨酸的酸性分泌蛋白(secreted protein acidic rich in cysteine,SPARC)在具有2型糖尿病表型的db/db鼠(10周龄)肝脏组织中的表达情况.方法 选择10周龄的db/db鼠(C57BL/KSJ)与其同窝野生对照型各6只,采用反转录-聚合酶链反应(RT-PCR)方法检测肝脏组织中SPARC mRNA的表达水平,免疫荧光染色方法检测肝脏组织中SPARC蛋白的表达水平.结果 SPARC在db/db鼠肝脏组织中呈现高表达(36.91±1.91vs 15.31±0.31)(P＜0.01).结论 SPARC在db/db鼠肝脏组织中呈现高表达,其可能与糖尿病有关的脂肪肝病变有关.     

Sustained release of human growth hormone (hGH) from collagen film and evaluation of effect on wound healing in db/db mice.

Collagen films containing human growth hormone (hGH) were prepared and the release of hGH from these films and their effect on healing of full-thickness wounds in db/db mice were evaluated. The release profiles of hGH from the collagen films varied with composition and preparation conditions. The film prepared by air-drying of the mixture of hGH and collagen solution released hGH continuously over 3 days both in vitro and in vivo. By application of collagen film containing 3 mg of hGH twice at an interval of 6 days to wounds, area of wounds on day 21 was significantly reduced compared with that of non-treated wounds. Application of hGH alone at the same dose had no significant effect on wound healing. The maximum serum hGH concentration after single administration of the hGH collagen film was lower than that with hGH alone, and hGH persisted in serum over 3 days. These results suggest that hGH collagen film may be a useful topical formulation for the treatment of wounds.