中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2012年
19期
3529-3534
,共6页
牛广华%高玉洁%都静%郭鹤%王柏山%高明利
牛廣華%高玉潔%都靜%郭鶴%王柏山%高明利
우엄화%고옥길%도정%곽학%왕백산%고명리
基质金属蛋白酶%脐血干细胞%细胞移植%类风湿关节炎%甲氨蝶呤
基質金屬蛋白酶%臍血榦細胞%細胞移植%類風濕關節炎%甲氨蝶呤
기질금속단백매%제혈간세포%세포이식%류풍습관절염%갑안접령
背景:基质金属蛋白酶对细胞外基质的降解是类风湿关节炎患者关节破坏的必要环节,基质金属蛋白酶2,9可以作为类风湿关节炎病情评估及有无关节进行性破坏的预测指标.目的:观察异种异基因脐血干细胞移植对Ⅱ型胶原性关节炎小鼠脾组织基质金属蛋白酶2,9表达的影响.方法:无菌取胎儿脐血,分离脐血干细胞.将C57BL/6(H-2b)小鼠分为5组,每组10只.除正常对照组外,氟氏完全佐剂+Ⅱ型胶原诱导小鼠建立胶原性关节炎模型.甲氨喋呤组以甲氨蝶呤混悬液0.017 5 g/kg灌胃,每5 d 1 次.其余各组均采用尾静脉注射,模型组、正常对照组注射生理盐水,单、双份脐血干细胞移植组注射来源于一个或两个母体的2×106/kg的脐血干细胞.注射后第42天处死动物取踝关节进行病理组织学检测,取脾组织采用反转录-聚合酶链反应法检测基质金属蛋白酶2,9 mRNA的表达.结果与结论:双份脐血干细胞移植能显著抑制Ⅱ型胶原性关节炎小鼠关节滑膜组织中炎性细胞浸润,修复损伤的软骨组织,修复效果优于甲氨蝶呤组及单份脐血干细胞移植组.双份脐血干细胞移植组脾组织中基质金属蛋白酶2,9 mRNA的表达水平明显低于单份移植组(P < 0.01),提示异种异基因双份脐血干细胞移植可以通过调控基质金属蛋白酶2,9 mRNA表达,参与类风湿关节炎软骨的病理变化过程及软骨细胞外基质的合成,有效治疗类风湿关节炎.
揹景:基質金屬蛋白酶對細胞外基質的降解是類風濕關節炎患者關節破壞的必要環節,基質金屬蛋白酶2,9可以作為類風濕關節炎病情評估及有無關節進行性破壞的預測指標.目的:觀察異種異基因臍血榦細胞移植對Ⅱ型膠原性關節炎小鼠脾組織基質金屬蛋白酶2,9錶達的影響.方法:無菌取胎兒臍血,分離臍血榦細胞.將C57BL/6(H-2b)小鼠分為5組,每組10隻.除正常對照組外,氟氏完全佐劑+Ⅱ型膠原誘導小鼠建立膠原性關節炎模型.甲氨喋呤組以甲氨蝶呤混懸液0.017 5 g/kg灌胃,每5 d 1 次.其餘各組均採用尾靜脈註射,模型組、正常對照組註射生理鹽水,單、雙份臍血榦細胞移植組註射來源于一箇或兩箇母體的2×106/kg的臍血榦細胞.註射後第42天處死動物取踝關節進行病理組織學檢測,取脾組織採用反轉錄-聚閤酶鏈反應法檢測基質金屬蛋白酶2,9 mRNA的錶達.結果與結論:雙份臍血榦細胞移植能顯著抑製Ⅱ型膠原性關節炎小鼠關節滑膜組織中炎性細胞浸潤,脩複損傷的軟骨組織,脩複效果優于甲氨蝶呤組及單份臍血榦細胞移植組.雙份臍血榦細胞移植組脾組織中基質金屬蛋白酶2,9 mRNA的錶達水平明顯低于單份移植組(P < 0.01),提示異種異基因雙份臍血榦細胞移植可以通過調控基質金屬蛋白酶2,9 mRNA錶達,參與類風濕關節炎軟骨的病理變化過程及軟骨細胞外基質的閤成,有效治療類風濕關節炎.
배경:기질금속단백매대세포외기질적강해시류풍습관절염환자관절파배적필요배절,기질금속단백매2,9가이작위류풍습관절염병정평고급유무관절진행성파배적예측지표.목적:관찰이충이기인제혈간세포이식대Ⅱ형효원성관절염소서비조직기질금속단백매2,9표체적영향.방법:무균취태인제혈,분리제혈간세포.장C57BL/6(H-2b)소서분위5조,매조10지.제정상대조조외,불씨완전좌제+Ⅱ형효원유도소서건립효원성관절염모형.갑안첩령조이갑안접령혼현액0.017 5 g/kg관위,매5 d 1 차.기여각조균채용미정맥주사,모형조、정상대조조주사생리염수,단、쌍빈제혈간세포이식조주사래원우일개혹량개모체적2×106/kg적제혈간세포.주사후제42천처사동물취과관절진행병리조직학검측,취비조직채용반전록-취합매련반응법검측기질금속단백매2,9 mRNA적표체.결과여결론:쌍빈제혈간세포이식능현저억제Ⅱ형효원성관절염소서관절활막조직중염성세포침윤,수복손상적연골조직,수복효과우우갑안접령조급단빈제혈간세포이식조.쌍빈제혈간세포이식조비조직중기질금속단백매2,9 mRNA적표체수평명현저우단빈이식조(P < 0.01),제시이충이기인쌍빈제혈간세포이식가이통과조공기질금속단백매2,9 mRNA표체,삼여류풍습관절염연골적병리변화과정급연골세포외기질적합성,유효치료류풍습관절염.
BACKGROUND: Matrix metalloproteinase (MMP) degrades extracellular matrix, which is a necessity of joint destruction in rheumatoid arthritis patients. MMP-2 and MMP-9 can evaluate rheumatoid arthritis and serve as an index to predict progressive destruction of the joint. OBJECTIVE: To observe heterogenous allogeneic umbilical cord blood stem cell (UBSC) transplantation on MMP-2 and MMP-9 expression in the spleen of mice with type Ⅱ collagen-induced arthritis. METHODS: Fetus cord blood was sterilely obtained and cord blood stem cells were separated. The C57BL/6(H-2b) mice were assigned to five groups (n=10). Except normal control group, models of collagen-induced arthritis were established using complete Freund's adjuvant + type Ⅱ collagen. Mice from the methopterin group were intragastrically administered methopterin suspension 0.017 5 g/kg, once every 5 days. Other groups used caudal vein injection. Mice from the model and normal control groups were injected with saline. Mice from the mono-UBSCs group and double-UBSCs group were injected with 2×106/kg UBSCs from one and two parents. At 42 days following injection, animals were sacrificed and the ankle joint was obtained for histopathological detection. MMP-2 and MMP-9 mRNA expression in the spleen was examined using reverse transcription-polymerase chain reaction. RESULTS AND CONCLUSION: Double-UBSC transplantation could significantly inhibit inflammatory cell infiltration in synovial tissue of mice with type Ⅱ collagen-induced arthritis, repaired impaired cartilage tissue. The repair effect was better than that in methopterin group and mono-UBSCs group. MMP-2 and MMP-9 mRNA expression in the spleen was significantly lower in the double-UBSCs group than the mono-UBSCs group (P < 0.01). These suggest that heterogenous allogeneic double-UBSCs transplantation participated in pathological changes in rheumatoid arthritis cartilage and in synthesis of cartilage extracellular matrix and effectively treated rheumatoid arthritis by regulating MMP-2 and MMP-9 mRNA expression.