CAJ | 학술논문

背景:有报道1型糖尿病可导致骨再生与修复障碍,局部注射成纤维细胞因子2可明显促进骨折愈合,但其对2型糖尿病的影响尚不十分清楚.目的:观察重组人成纤维细胞生长因子2和可溶性肿瘤坏死因子Ⅰ型受体蛋白联合治疗2型糖尿病引起的骨再生及其修复障碍的作用.设计:随机对照实验.单位:中南大学湘雅三医院骨科.材料:选择雄性Zucker糖尿病大鼠(ZDF/Gmi-fa/fa)20只,10周龄,购自美国查尔斯河实验室.重组人成纤维细胞生长因子2购自美国Orquest公司,可溶性肿瘤坏死因子Ⅰ型受体蛋白购自美国Amgen公司.方法:实验于2006-09/11在中南大学湘雅三医院中心实验室完成.①实验分组:将20只大鼠随机分为对照组和治疗组,每组10只.②实验方法:检测大鼠体质量,血糖、尿糖和尿酮.1周后,接受左胫骨中上段低能截骨,安置外延长固定架.第2天起开始胫骨延长0.2 mm/次,2次/d,共14 d.期间治疗组大鼠接受截骨处血肿内重组人成纤维细胞生长因子225 μg/kg注射1次,可溶性肿瘤坏死因子Ⅰ型受体蛋白8 mg/kg皮下注射隔日1次,共14 d;对照组仅接受载体和生理盐水注射.③实验评估:测定血液生化指标、胫骨延长间隙中新生骨量及增殖细胞数量.主要观察指标:两组血液生化指标、胫骨延长间隙中新生骨量及增殖细胞数量比较.结果:纳入大鼠20只,全部进入结果分析.①两组血糖、尿糖、尿酮、血清胰岛素和骨钙素比较,差异不明显(P＞0.05).②治疗组大鼠左胫骨延长间隙内新生骨的面积、密度和骨内膜成骨、骨膜成骨均明显高于对照组(P＜0.05～0.01).治疗组大鼠的胫骨牵引间隙中的纤维间区和初始骨基质前沿增殖细胞核抗原阳性细胞及百分比均明显多于对照组(P＜0.05～0.01).结论:2型糖尿病可引起骨再生与修复障碍,重组人成纤维细胞生长因子2和可溶性肿瘤坏死因子Ⅰ型受体蛋白联合治疗可促进成骨细胞增殖,加快牵引成骨速率,有利于2型糖尿病合并骨折的愈合障碍. 揹景:有報道1型糖尿病可導緻骨再生與脩複障礙,跼部註射成纖維細胞因子2可明顯促進骨摺愈閤,但其對2型糖尿病的影響尚不十分清楚.目的:觀察重組人成纖維細胞生長因子2和可溶性腫瘤壞死因子Ⅰ型受體蛋白聯閤治療2型糖尿病引起的骨再生及其脩複障礙的作用.設計:隨機對照實驗.單位:中南大學湘雅三醫院骨科.材料:選擇雄性Zucker糖尿病大鼠(ZDF/Gmi-fa/fa)20隻,10週齡,購自美國查爾斯河實驗室.重組人成纖維細胞生長因子2購自美國Orquest公司,可溶性腫瘤壞死因子Ⅰ型受體蛋白購自美國Amgen公司.方法:實驗于2006-09/11在中南大學湘雅三醫院中心實驗室完成.①實驗分組:將20隻大鼠隨機分為對照組和治療組,每組10隻.②實驗方法:檢測大鼠體質量,血糖、尿糖和尿酮.1週後,接受左脛骨中上段低能截骨,安置外延長固定架.第2天起開始脛骨延長0.2 mm/次,2次/d,共14 d.期間治療組大鼠接受截骨處血腫內重組人成纖維細胞生長因子225 μg/kg註射1次,可溶性腫瘤壞死因子Ⅰ型受體蛋白8 mg/kg皮下註射隔日1次,共14 d;對照組僅接受載體和生理鹽水註射.③實驗評估:測定血液生化指標、脛骨延長間隙中新生骨量及增殖細胞數量.主要觀察指標:兩組血液生化指標、脛骨延長間隙中新生骨量及增殖細胞數量比較.結果:納入大鼠20隻,全部進入結果分析.①兩組血糖、尿糖、尿酮、血清胰島素和骨鈣素比較,差異不明顯(P＞0.05).②治療組大鼠左脛骨延長間隙內新生骨的麵積、密度和骨內膜成骨、骨膜成骨均明顯高于對照組(P＜0.05～0.01).治療組大鼠的脛骨牽引間隙中的纖維間區和初始骨基質前沿增殖細胞覈抗原暘性細胞及百分比均明顯多于對照組(P＜0.05～0.01).結論:2型糖尿病可引起骨再生與脩複障礙,重組人成纖維細胞生長因子2和可溶性腫瘤壞死因子Ⅰ型受體蛋白聯閤治療可促進成骨細胞增殖,加快牽引成骨速率,有利于2型糖尿病閤併骨摺的愈閤障礙.
배경:유보도1형당뇨병가도치골재생여수복장애,국부주사성섬유세포인자2가명현촉진골절유합,단기대2형당뇨병적영향상불십분청초.목적:관찰중조인성섬유세포생장인자2화가용성종류배사인자Ⅰ형수체단백연합치료2형당뇨병인기적골재생급기수복장애적작용.설계:수궤대조실험.단위:중남대학상아삼의원골과.재료:선택웅성Zucker당뇨병대서(ZDF/Gmi-fa/fa)20지,10주령,구자미국사이사하실험실.중조인성섬유세포생장인자2구자미국Orquest공사,가용성종류배사인자Ⅰ형수체단백구자미국Amgen공사.방법:실험우2006-09/11재중남대학상아삼의원중심실험실완성.①실험분조:장20지대서수궤분위대조조화치료조,매조10지.②실험방법:검측대서체질량,혈당、뇨당화뇨동.1주후,접수좌경골중상단저능절골,안치외연장고정가.제2천기개시경골연장0.2 mm/차,2차/d,공14 d.기간치료조대서접수절골처혈종내중조인성섬유세포생장인자225 μg/kg주사1차,가용성종류배사인자Ⅰ형수체단백8 mg/kg피하주사격일1차,공14 d;대조조부접수재체화생리염수주사.③실험평고:측정혈액생화지표、경골연장간극중신생골량급증식세포수량.주요관찰지표:량조혈액생화지표、경골연장간극중신생골량급증식세포수량비교.결과:납입대서20지,전부진입결과분석.①량조혈당、뇨당、뇨동、혈청이도소화골개소비교,차이불명현(P＞0.05).②치료조대서좌경골연장간극내신생골적면적、밀도화골내막성골、골막성골균명현고우대조조(P＜0.05～0.01).치료조대서적경골견인간극중적섬유간구화초시골기질전연증식세포핵항원양성세포급백분비균명현다우대조조(P＜0.05～0.01).결론:2형당뇨병가인기골재생여수복장애,중조인성섬유세포생장인자2화가용성종류배사인자Ⅰ형수체단백연합치료가촉진성골세포증식,가쾌견인성골속솔,유리우2형당뇨병합병골절적유합장애.
BACKGROUND: It has been reported that type 1 diabetes mellitus can result in impairments of bone regeneration and repair, and local injection of fibroblastic growth factor-2 (FGF-2) can obviously promote fracture healing, but its effect on type 2 diabetes mellitus is still unclear.OBJECTIVE: To observe the effects of recombinant human fibroblastic growth factor-2 (rhFGF-2) combined with soluble tumor necrosis factor receptor-1 (sTNF-R1) on impaired bone regeneration and repair in type 2 diabetes mellitus.DESTGN: A randomized controlled trial.SETTING: Department of Orthopaedics, the Third Xiangya Hospital of Central South University.MATERIALS: Twenty male Zucker diabetic fatty rats (ZDF/Gemi-fa/fa), 10 weeks of age, were purchased from Charles River Laboratory. rhFGF-2 was obtained from Orquest Incorporation; sTNF-R1 protein (PEG-r-metHu-sTNF-R1) was provided by Amgen Incorporation.METHODS: This experiment was finished in the central lab of the Third Xiangya Hospital of Central South University from September to November in 2006. ①Grouping: The 20 rats were randomly assigned into treated group (n =10)and control group (n =10). ② Experimental methods: All rats were examined for body mass, blood glucose, glycosuria and glycosemia. One week later, all the rats underwent the standard DO protocol, including placement of the external fixators and osteotomies to the left tibia. Distraction was initiated in the following morning (one day latency) at 0.2 mm b.I.d. (0.4 mm per day) and continued for 14 days. During surgery, all the rats received an injection of either rhFGF-2(25 mg/kg) for the treated group, or physiological saline (25 mg/kg) for the control group, into the hematoma of the osteotomic gap. The sTNF-R1 (8 mg/kg) or the same. Amount of saline was subcutaneously injected into the treated and control rats respectively every other day for 14 days. Evaluation: The serum biochemical indexes, amount of bone formation and number of proliferative cells in the distraction gaps were determined.MAIN OUTCOME MEASURES: Biochemical indexes, amount of bone formation and number of proliferative cells in the distraction gaps.RESULTS: All the 20 rats were involved in the final analysis of results. ①The blood glucose, glucosuria, ketonuria,serum levels of insulin and osteocalcin were not obviously different between the treated group and control group (P ＞0.05). ② The area and density of mineralization of the distraction gaps, and the endosteal and peristeal new bone formation in the treated group were all obviously higher than those in the control group (P ＜ 0.05-0.01). The number and percentage of the positive cells of proliferating cell nuclear antigen (PCNA) in the distraction gaps were obviously higher in the treated group than in the control group (P ＜ 0.05-0.01).CONCLUSION: The local application of rhFGF-2 combined with sTNF-R1 can enhance bone formation by increasing the proliferation during distraction osteogenesis in ZDF rats. The combination of rhFGF-2 and sTNF-R1 may be an effective treatment for type 2 diabetic patients with fracture healing problem.