中国骨质疏松杂志
中國骨質疏鬆雜誌
중국골질소송잡지
CHINESE JOURNAL OF OSTEOPOROSIS
2015年
1期
88-93
,共6页
刘禄林%王啸%李光飞%高超%俞晨%沈光思%张鹏%吴明霞%王爱东%XiHuang%徐又佳
劉祿林%王嘯%李光飛%高超%俞晨%瀋光思%張鵬%吳明霞%王愛東%XiHuang%徐又佳
류록림%왕소%리광비%고초%유신%침광사%장붕%오명하%왕애동%XiHuang%서우가
去铁胺%铁蓄积%雄性小鼠%骨量下降
去鐵胺%鐵蓄積%雄性小鼠%骨量下降
거철알%철축적%웅성소서%골량하강
Deferoxamine%Iron accumulation%Male mice%Osteopeia
目的：观察甲磺酸去铁胺（DFO）干预对铁蓄积导致的小鼠骨量下降骨代谢的治疗作用及其相关机制。方法32只2月龄雄性小鼠随机分为A、B、C、D 4组，每组8只，A组为对照组（生理盐水干预），B组、C组、D组均运用铁剂腹腔注射干预2月，2月后A、B组处死；C组和D组分别再用生理盐水、DFO干预1月后处死；检测血清铁、钙、磷水平，骨转换指标I型胶原C端肽（CTX）、抗酒石酸酸性磷酸酶（TRAP?5b）、骨钙素（BGP）含量，以及氧化应激指标超氧化物歧化酶（SOD）活性、丙二醛（MDA）水平；测定肝脏铁含量，肝脏铁Perls’染色；股骨远端松质骨micro?CT扫描分析和三维重建。结果①血清铁、肝脏铁含量测定及肝脏Perls’染色示B组铁指标显著高于A组，铁蓄积模型成功建立；DFO干预后D组铁指标显著下降。②血清骨转换指标示B组CTX、Trap?5b显著高于A组，BGP水平低于A组；D组CTX、Trap?5b水平均低于C组，BGP含量高于C组，提示DFO可以部分逆转铁蓄积导致的骨吸收增强和骨形成抑制。③血清氧化应激指标示B组MDA水平高于A组，SOD活性低于A组；D组较C组MDA水平显著降低、SOD升高。④micro?CT示B组较A组骨密度下降，各骨小梁参数减低；而降铁干预1月后D组较对照干预C组各骨参数指标均有改善。结论 DFO可部分逆转铁蓄积导致的骨吸收活性增强和骨形成抑制，从而提高骨密度、改善骨的微结构，其机理可能与降铁改善氧化应激水平有关。
目的：觀察甲磺痠去鐵胺（DFO）榦預對鐵蓄積導緻的小鼠骨量下降骨代謝的治療作用及其相關機製。方法32隻2月齡雄性小鼠隨機分為A、B、C、D 4組，每組8隻，A組為對照組（生理鹽水榦預），B組、C組、D組均運用鐵劑腹腔註射榦預2月，2月後A、B組處死；C組和D組分彆再用生理鹽水、DFO榦預1月後處死；檢測血清鐵、鈣、燐水平，骨轉換指標I型膠原C耑肽（CTX）、抗酒石痠痠性燐痠酶（TRAP?5b）、骨鈣素（BGP）含量，以及氧化應激指標超氧化物歧化酶（SOD）活性、丙二醛（MDA）水平；測定肝髒鐵含量，肝髒鐵Perls’染色；股骨遠耑鬆質骨micro?CT掃描分析和三維重建。結果①血清鐵、肝髒鐵含量測定及肝髒Perls’染色示B組鐵指標顯著高于A組，鐵蓄積模型成功建立；DFO榦預後D組鐵指標顯著下降。②血清骨轉換指標示B組CTX、Trap?5b顯著高于A組，BGP水平低于A組；D組CTX、Trap?5b水平均低于C組，BGP含量高于C組，提示DFO可以部分逆轉鐵蓄積導緻的骨吸收增彊和骨形成抑製。③血清氧化應激指標示B組MDA水平高于A組，SOD活性低于A組；D組較C組MDA水平顯著降低、SOD升高。④micro?CT示B組較A組骨密度下降，各骨小樑參數減低；而降鐵榦預1月後D組較對照榦預C組各骨參數指標均有改善。結論 DFO可部分逆轉鐵蓄積導緻的骨吸收活性增彊和骨形成抑製，從而提高骨密度、改善骨的微結構，其機理可能與降鐵改善氧化應激水平有關。
목적：관찰갑광산거철알（DFO）간예대철축적도치적소서골량하강골대사적치료작용급기상관궤제。방법32지2월령웅성소서수궤분위A、B、C、D 4조，매조8지，A조위대조조（생리염수간예），B조、C조、D조균운용철제복강주사간예2월，2월후A、B조처사；C조화D조분별재용생리염수、DFO간예1월후처사；검측혈청철、개、린수평，골전환지표I형효원C단태（CTX）、항주석산산성린산매（TRAP?5b）、골개소（BGP）함량，이급양화응격지표초양화물기화매（SOD）활성、병이철（MDA）수평；측정간장철함량，간장철Perls’염색；고골원단송질골micro?CT소묘분석화삼유중건。결과①혈청철、간장철함량측정급간장Perls’염색시B조철지표현저고우A조，철축적모형성공건립；DFO간예후D조철지표현저하강。②혈청골전환지표시B조CTX、Trap?5b현저고우A조，BGP수평저우A조；D조CTX、Trap?5b수평균저우C조，BGP함량고우C조，제시DFO가이부분역전철축적도치적골흡수증강화골형성억제。③혈청양화응격지표시B조MDA수평고우A조，SOD활성저우A조；D조교C조MDA수평현저강저、SOD승고。④micro?CT시B조교A조골밀도하강，각골소량삼수감저；이강철간예1월후D조교대조간예C조각골삼수지표균유개선。결론 DFO가부분역전철축적도치적골흡수활성증강화골형성억제，종이제고골밀도、개선골적미결구，기궤리가능여강철개선양화응격수평유관。
Objective To explore the therapeutic effect of deferoxamine on iron accumulation?induced osteopenia and to understanditsmechanismofaction.Methods Thirty?two2-month?oldmaleICRmicewererandomlydividedinto4groups(n=8, in each). Group A (control) received normal saline. Group B, C, and D received intraperitoneal ferric ammonium citrate (FAC) injection of for 2 months. After 2?month intervention, group A and B were sacrificed. Group C and D received intraperitoneal injection of normal saline or DFO for another month, and then sacrificed. Serum iron, calcium, phosphorus, type I collagen C?terminal peptide (CTX), tartrate?resistant acid phosphatase 5b (TRAP?5b), osteocalcin (BGP), superoxide dismutase (SOD), malondialdehyde( MDA) , liver iron content, and liver iron particle Peals’ staining were determined. The cancellous bone of the left femur scanned and analyzedusingmicro?CTand3Dreconstruction.Results (1)SerumandliverironcontentmeasurementaswellasliverPeals’ staining showed a significant increase in group B than in group A, indicating the success of the iron accumulation model. The iron related indices decreased significantly after DFO treatment in group D. (2) CTX and TRAP?5b in group B were significantly higher than in group A, but BGP was lower than in group A. CTX and TRAP-5b in group D was lower than in group C, but BGP was higher in group D than in group C, indicating DFO reversed partially the increase of bone resorption and inhibition of bone formation due to iron accumulation. (3) Serum oxidative stress makers MDA was higher in group B than in group A, but SOD was lower than in group A. MDA decreased but SOD increased in group D compared to group C. (4) Micro?CT demonstrated that compared with group A, group B showed decresed cancellous bone parameters. After one month intervention, bone parameters improved in group D comparing to group B. Conclusion The administration of DFO can reverse partially the increase of bone resorption and inhibition of bone formation due to iron accumulation, therefore increase BMD and improve bone microarchitecture. The mechanism may be associated with the modulateion of oxidative stress.
