血管外膜损伤对静脉移植物影响的研究进展

自 1969年Favaloro[1] 首先报道自体大隐静脉用于冠状动脉旁路术 (CABG)以来 ,大隐静脉已成为自体静脉移植物的首选 ,是目前应用最为广泛的移植物。但无论是CABG还是下肢动脉旁路术 ,其闭塞率均较高 ,1年内 15 %～ 3 0 %的移植物发生闭塞 ,10年内约 5 0 %的移植物发生闭塞。现已明确血管损伤是静脉移植物闭塞的主要原因 ,而血管外膜的损伤对静脉移植物的影响日益受到重视 ,“无创外科技术”获取静脉移植物也有了较大发展。一、静脉移植物闭塞的病理生理大隐静脉移植后 1个月内的早期失败率达 18%以上 ,1年内达 3 0 %以上 ,之后每年闭塞…     

血管外支架预防猪大隐静脉移植血管再狭窄的实验研究

目的以猪大隐静脉-颈总动脉旁路移植动物模型为基础,观察涤纶血管外支架支持预防静脉移植血管内、中膜增生的作用。方法将10只25~30kg普通长白猪行双侧大隐静脉-颈总动脉旁路移植术(端侧吻合),一侧静脉移植血管放置涤纶外支架(实验组),另一侧作为对照(对照组)。术后35d取出移植血管进行组织学和免疫组织化学检测。结果对照组静脉移植血管内膜增生较实验组明显增加(0.4872±0.0706mm vs.0.2259±0.0553mm,P<0.01);对照组中膜增生亦较实验组增加(0.6246±0.0859mm vs.0.4201±0.0615mm,P<0.01);对照组内膜面积是实验组的2倍,中膜面积是实验组的近1.5倍。实验组内膜及中膜内侧区域增殖细胞核抗原(PCNA)、血小板源性生长因子(PDGF)阳性细胞显著减少,PCNA从7.98%±4.06%减少至3.35%±0.95%(P<0.01),PDGF从9.47%±5.35%减少至2.67%±0.97%(P<0.01)。结论非限制性涤纶血管外支架可以显著抑制大隐静脉移植血管新内膜及中膜增生,可能预防大隐静脉移植血管的再狭窄。     

羧甲基壳聚糖通过抑制线粒体途径保护氧化损伤诱导雪旺细胞凋亡

[目的]探讨线粒体途径在羧甲基壳聚糖(carboxymethylated chitosan,CMCS)保护过氧化氢(H_2O_2)诱导雪旺细胞(Schwann cells,SCs)凋亡中的作用及机制。[方法]体外培养SCs,S-100免疫荧光染色鉴定。将SCs分为空白对照组、H_2O_2诱导组、H_2O_2加CMCS处理组。流式细胞仪检测细胞凋亡比率,罗丹明(Rhodamine123)荧光染色检测细胞线粒体膜电位水平,Western blot检测SCs内细胞色素C(Cytochrome C)表达水平。[结果]本实验培养细胞经S-100荧光染色鉴定阳性率达95%以上,H_2O_2诱导SCs凋亡,降低线粒体膜电位,增加细胞色素C释放;而在加入CMCS后SCs凋亡比例降低,线粒体膜电位增加,细胞色素C释放减少。[结论]CMCS通过抑制线粒体细胞凋亡途径保护H_2O_2诱导SCs凋亡。     

异丙酚对过氧化氢所致的心肌线粒体损伤的影响

本研究拟通过差速分级离心法分离线粒体，用H2O2模拟心肌线粒体的氧化应激，测定心肌线粒体膜渗透性转换(MPT)和线粒体跨膜电位(△ψm)对不同浓度异丙酚对线粒体的保护作用。     

血管移植物在腹部静脉修复重建中的应用

随着腹部外科的发展,牵涉到腹部静脉修复重建的手术日益增多,血管移植物的应用也越来越多。包括自体血管、同种异体血管、异种血管、人工血管等,其中最常用的是自体血管和人工血管,但应用自体血管会增加手术创伤和手术时间,而人工血管的生物相容性和顺应性较差,有待于进一步改进现有的或寻找新的血管移植物。就各种血管移植物的分类、优缺点及在腹部静脉修复重建中的应用作一综述。     

移植损伤对移植静脉影响的实验研究

目的探讨移植静脉再狭窄的机制,明确移植损伤对移植静脉的影响。方法健康新西兰大白兔36只,随机选取一侧将股静脉翻转后移植于同侧股动脉缺损(静-动组),另一侧将同等长度股静脉截取后行原位缝合(静-静组),另取正常股静脉作为对照组(取自静-动组移植前静脉的一部分)。均于术后4周取移植静脉段,行HE染色、弹力纤维的维多利亚蓝染色观察移植静脉管壁组织学变化;增殖细胞核抗原(proliferatingcellnuclearantigen,PCNA)免疫组织化学染色观察管壁细胞增殖情况;电镜观察管壁细胞超微结构改变。结果静-静组血管壁中膜平滑肌细胞增殖,但内膜(3.50±0.41μm)、中膜(12.23±1.59μm)厚度无明显变化;静-动组内膜、中膜细胞均增殖,内膜(25.60±3.21μm)、中膜(21.30±2.47μm)厚度较对照组、静-静组均增加,差异有统计学意义(P<0.01)。对照组未见PCNA阳性细胞,静-静组内膜(5.9%±1.3%)、中膜(23.4%±3.4%)PCNA阳性细胞百分比均小于静-动组内膜(16.4%±1.9%)、中膜(36.5%±3.7%),差异有统计学意义(P<0.01)。静-静组透射电镜下可见内皮细胞扁平,游离端有绒毛样突起,细胞排列紧密,中膜平滑肌细胞增殖;静-动组透射电镜下可见内皮细胞增殖明显,增殖的内皮细胞形态不规则,细胞间隙增宽,内膜中可见大量平滑肌细胞,基底膜不完整,中膜平滑肌细胞明显增殖;对照组内皮细胞形态及排列与静-静组相似,只是中膜平滑肌细胞未见增殖。结论静脉移植后可导致血管管壁细胞增殖,如合并血流动力学变化则会发生更严重的细胞增殖和迁移,导致管腔狭窄;减少移植损伤,改善移植静脉的微循环,成为预防移植静脉再狭窄的理论基础之一;静-静移植的动物模型,有助于探寻静脉移植后再狭窄的机制。     

软骨细胞线粒体氧化应激在骨关节炎发病机制中的研究进展

骨关节炎（OA）是老年人最常见的关节疾病之一,同时也是导致残疾的重要因素。软骨细胞是成熟软骨中唯一的细胞,软骨细胞的稳定和正常功能的维持对延缓OA进展有重要作用。近年来的研究发现,软骨细胞线粒体氧化应激与OA关系密切。本文综述了软骨细胞线粒体氧化应激在OA发病过程中的相关机制,为OA的相关研究提供一定参考。     

脓毒症心肌损伤的线粒体机制

背景 脓毒症是机体对感染的反应失调而导致危及生命的多器官功能障碍.虽然目前针对脓毒症有一些治疗措施,但脓毒症和脓毒症休克仍是导致危重症患者死亡的首要原因.心肌损伤是脓毒症的常见并发症,会导致左室和右室泵功能衰竭.参与脓毒症心肌损伤的物质和机制很多,包括毒素、细胞因子、一氧化氮、补体激活、凋亡和能量代谢紊乱等.然而,关于脓毒症心肌损伤的潜在分子机制尚未完全清楚.目的 讨论可能导致脓毒症心肌损伤线粒体功能异常的机制.内容 关于脓毒症心肌损伤研究比较多的是线粒体功能异常,目前研究认为线粒体功能损伤涉及许多机制,导致线粒体能量耗竭,最终导致心肌损伤.而对于线粒体功能的损伤和修复机制仍存在争议.趋向 关于脓毒症的研究不断升温,新的研究工具的出现为将来有效的特异性治疗方法的出现奠定了基础.     

浅静脉移植修复周围血管损伤患者的护理

我院显微外科1997年6月至1999年12月采用浅静脉游离移植治疗四肢血管损伤16例,均获成功。1　临床资料1.1　一般资料　16例中男10例、女6例,年龄11～56岁,平均28.0岁。动脉损伤9例,肱动脉4例,股动、静脉3例;血管完全断裂并缺损>2cm7例,部分断裂合并大段挫伤5例,单纯挫伤血栓形成4例。交通事故11例,高处坠落伤1例,机器挤伤2例,爆炸伤2例。16例中有12例合并骨折,3例膝关节脱位,1例合并膀胱破裂。1.2　手术方法手术根据损伤部位选择持续硬膜外或臂丛神经麻醉,清理血管周围组织及血管残端,彻底清除后更换清创器械。选择适当的内固定器械固定骨…     

间皮细胞种植人造血管静脉移植的研究

采用腹膜间皮细胞,种植涤纶人造血管,行狗股浅静脉移植。结果表明,间皮细胞种植的人造血管内壁能形成一层完整的、具有抗血栓形成的活性生物内膜,提高了人造血管通畅率。腹膜间皮细胞来源容易,取材方便,操作简单,整个种植过程能在一期手术中完成,临床实用价值较大。     

脓毒症病人氧化应激状态的临床研究

目的研究脓毒症病人氧化应激状态,为脓毒症治疗探索新方法。方法前瞻性研究2004年12月至2005年2月,中山大学附属第一医院31例外科重症监护病房(SICU)危重病人的血清丙二醛(malondialde-hyde,MDA)浓度变化,比较脓毒症组和非脓毒症组病人入SICU后第1、3天的MDA浓度差异,同时记录出现功能障碍器官的数目,分析MDA浓度与器官功能障碍的关系。结果脓毒症组病人MDA浓度高于非脓毒症组[(11·97±2·02)μmol/L vs(6·58±1·69)μmol/L,P<0·01],MDA浓度与器官功能障碍数量相关(r=0·850,P<0·01)。结论脓毒症病人体内存在严重氧化应激而导致病人器官功能损害。应用抗氧化剂可以成为脓毒症治疗的新策略。     

Markers of oxidative stress after renal transplantation

Abstract An increased degree of oxidative stress (OS) in chronic renal failure (CRF) and a possible role of free radicals in CRF have already been described. However, data on OS after renal transplantation are scarce. The aim of the present study was to estimate the degree of OS in renal transplant patients. The study included four groups: 1) 15 haemodialysis patients (HD group), 2) 11 renal transplant patients with stable function (SF group), 3) 12 renal transplant patients with chronic biopsy-proven rejection (CR group), and 4) 10 healthy controls (C group). Markers of OS (malondialdehyde and thiol group levels) and antioxidant activity (glutathione peroxidase and Cu, Zn-su-peroxide dismutase) were determined in plasma and in red blood cells of all examined individuals. After successful renal transplantation a significant improvement, but not normalization, of antioxidant enzyme activities accompanied by significantly reduced lipid peroxidation were found. In the CR group the degree of OS was increased, and our results suggest that OS may be a relevant pathophysiological factor for CR development.     

Combination of sodium butyrate and probiotics ameliorates severe burn-induced intestinal injury by inhibiting oxidative stress and inflammatory response

Burns are a common traumatic injuries with considerable morbidity and mortality rates. Post-burn intestinal injuries are closely related to oxidative stress and inflammatory response. The aim of the current study was to investigate the combined effect of sodium butyrate (NaB) and probiotics (PROB) on severe burn-induced oxidative stress and inflammatory response and the underlying mechanism of action. Sprague-Dawley rats with severe burns were treated with NaB with or without PROB. Pathomorphology of skin and small intestine tissue was observed using hematoxylin and eosin staining and severe burn-induced apoptosis in small intestine tissue was examined via terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. The release of factors related to inflammation was quantified using ELISA kits and qRT-PCR and levels of oxidative stress markers were evaluated using biochemical assays. Furthermore, mitochondrial morphological changes in small intestinal epithelial cells were observed using transmission electron microscopy. In addition, the underlying mechanism associated with the combined effect of NaB and PROB on severe burn-induced oxidative stress and inflammatory response was investigated using western blotting. The combination of NaB and PROB exerted protective effects against severe burn-induced intestinal barrier injury by reducing the levels of diamine oxidase and intestinal fatty acid binding protein. Combined NaB and PROB treatment inhibited severe burn-induced oxidative stress by increasing superoxide dismutase levels and decreasing those of malondialdehyde and myeloperoxidase levels. Severe burn-induced inflammation was suppressed by combined NaB and PROB administration, as demonstrated by the decreased mRNA expression of tumor necrosis factor-α, interleukin-6, interleukin-1β, and high mobility group box-1 in the small intestine. In addition, this study showed that combined NaB and PROB administration increased nuclear factor-erythroid 2-related factor 2 (Nrf2) protein expression and decreased the phosphorylation of nuclear factor (NF)-κB and extracellular signal-regulated kinase 1/2 (ERK 1/2). In conclusion, our findings indicate that combined NaB and PROB treatment may inhibit severe burn-induced inflammation and oxidative stress in the small intestine by regulating HMGB1/NF-κB and ERK1/2/Nrf2 signaling, thereby providing a new therapeutic strategy for intestinal injury induced by severe burn.     

慢性细菌性前列腺炎与氧化应激加剧和氧化损伤的关系

目的探讨慢性细菌性前列腺炎(CBP)与氧化应激加剧和氧化损伤的关系。方法采用病例对照设计和分光光度比色法,对随机纳入的70例CBP患者(CBPPs)和70例健康成人志愿者(HAVs)血浆一氧化氮(NO)、维生素C(VC)、维生素E(VE)、β-胡萝卜素(β-CAR)和红细胞丙二醛(MDA)水平,以及红细胞超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化氢酶(GPX)活性进行测定。结果CBPPs组NO和MDA均值分别为(426±31)nmol/L和(34.7±4.7)nmol/g·Hb,比HAVs组((378±33)nmol/L和(28.6±4.4)nmol/g·Hb)显著升高(P<0.001)。CBPPs组VC、VE、β-CAR、SOD、CAT和GPX均值分别为(47.4±11.6)μmol/L、(18.1±4.8)μmol/L、(1.4±0.4)μmol/L、(1912±221)U/g·Hb、(254±67)K/g·Hb和(25.0±5.0)U/g·Hb,比HAVs组((55.1±13.4)μmol/L、(25.7±4.5)μmol/L、(1.7±0.5)μmol/L、(2081±222)U/g·Hb、(294±77)K/g·Hb和(28.8±5.1)U/g·Hb)显著降低(P<0.001)。70例CBPPs的病程与上述各生化参数在校准年龄时的偏相关性分析提示,随着病程延长,NO和MDA值逐渐升高(rNO=0.4801,rMDA=0.4364,P<0.001),VC、VE、β-CAR、SOD、CAT和GPX值逐渐降低(rVC=-0.3437,rVE=-0.3712,rβ-CAR=-0.3192,rSOD=-0.3490,rCAT=-0.2805,rGPX=-0.2868,P<0.05~0.001)。70例CBPPs的病程和上述生化参数的逐步回归提示,逐步回归模型为Y=-13.2077 0.1894MDA 0.0415NO-0.1999GPX,F=18.2047,P<0.001,r=0.6729,P<0.001。结论CBP患者体内存在着由CBP引起的氧化应激加剧和氧化损伤,且该现象与患者的病程密切相关。     

p66Shc-mediated oxidative stress is involved in gestational diabetes mellitus

BACKGROUNDGestational diabetes mellitus (GDM) is associated with a heightened level of oxidative stress, which is characterized by the overproduction of reactive oxygen species (ROS) from mitochondria. Previous studies showed that mitochondrial dysfunction is regulated by dynamin-related protein 1 (Drp1) and p66Shc in GDM.AIMThe aim was to investigate the expression of Drp1 and p66Shc and their possible mechanisms in the pathogenesis of GDM.METHODSA total of 30 pregnant women, 15 with GDM and 15 without GDM, were enrolled. Peripheral blood mononuclear cells and placental tissue were collected. The human JEG3 trophoblast cell line was cultivated in 5.5 mmol/L or 30 mmol/L glucose and transfected with wild-type (wt)-p66Shc and p66Shc siRNA. P66Shc and Drp1 mRNA levels were detected by quantitative real-time polymerase chain reaction. The expression of p66Shc and Drp1 was assayed by immunohistochemistry and western blotting. ROS was assayed by dihydroethidium staining.RESULTSThe p66Shc mRNA level was increased in the serum (P < 0.01) and placentas (P < 0.01) of women with GDM, and the expression of Drp1 mRNA and protein were also increased in placentas (P < 0.05). In JEG3 cells treated with 30 mmol/L glucose, the mRNA and protein expression of p66Shc and Drp1 were increased at 24 h (both P < 0.05), 48 h (both P < 0.01) and 72 h (both P < 0.001). ROS expression was also increased. High levels of Drp1 and ROS expression were detected in JEG3 cells transfected with wt-p66Shc (P < 0.01), and low levels were detected in JEG3 cells transfected with p66Shc siRNA (P < 0.05).CONCLUSIONThe upregulated expression of Drp1 and p66shc may contribute to the occurrence and development of GDM. Regulation of the mitochondrial fusion-fission balance could be a novel strategy for GDM treatment.     

Daily treatment with sildenafil reverses endothelial dysfunction and oxidative stress in an animal model of insulin resistance

OBJECTIVES: Patients with insulin resistance exhibit endothelial dysfunction with decreased nitric oxide (NO) production and increased oxidative stress. We postulated that daily sildenafil improved endothelial function in fructose-fed rats. METHODS AND RESULTS: Wistar rats were fed a standard or fructose-enriched diet (FFR) for 9 wk. From weeks 6-8, sildenafil was administered twice daily (sc, 20 m g/kg), followed by a 1-wk washout. Concentration-response curves (CRCs) to endothelium-dependent (acetylcholine [Ach] and A23187) and -independent (sodium nitroprusside [SNP]) relaxing agents were performed on isolated precontracted aortas and superior mesenteric arteries (SMAs). Vascular cyclic guanosine monophosphate (cGMP) content, urinary excretion of nitrates/nitrites (NOx) and 8-isoprostanes (IPT), and plasma levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were evaluated. Relaxations to ACh were significantly reduced in aortas and SMAs of FFR. Sildenafil restored ACh-induced relaxations in aortas and provoked a significant leftward shift of the CRC to ACh in SMAs, whereas it did not modify the enhanced relaxations to SNP in FFR. IL-6, TNF-alpha, vascular cGMP, and urinary NOx levels were not modified by the fructose or sildenafil treatment. Urinary IPT levels were significantly elevated in FFR and normalized by sildenafil. CONCLUSIONS: Endothelial dysfunction and oxidative stress associated with insulin resistance can be reversed by daily sildenafil, even 1 wk after treatment cessation.     

银杏叶提取物经门静脉预处理对肝脏手术中氧化应激的影响

目的探讨银杏叶提取物经门静脉预处理对肝脏手术中氧化应激的影响。方法选择需肝门阻断行肝部分切除手术的患者60例,男38例,女22例,年龄28~67岁,ASAⅠ或Ⅱ级,心功能I或II级,肝功能Child-Pugh A级。随机分为三组:门静脉注射组(P组)、颈内静脉注射组(J组)和对照组(C组),每组20例。P组在游离出门静脉后经门静脉缓慢注射银杏叶提取物注射液5ml,J组游离出门静脉后经颈内静脉缓慢注射银杏叶提取物注射液5ml,C组游离出门静脉后经颈内静脉缓慢注射生理盐水5ml。分别于肝门阻断前10 min(T_0)、肝门开放后1h(T_1)、6h(T_2)、24h(T_3)经颈内静脉采血检测血清ALT、AST、TNF-α、丙二醛(MDA)浓度和超氧化物歧化酶(SOD)活性。结果与T_0时比较,T_1~T_3时三组血清ALT、AST、TNF-α和MDA浓度明显升高,SOD活性明显降低(P0.05)。与C组比较,T_1~T_3时J组、P组血清ALT、AST、TNF-α和MDA浓度明显下降,SOD活性明显升高(P0.05)。与J组比较,T_1~T_3时P组血清ALT、AST、TNF-α和MDA浓度明显下降,SOD活性明显升高(P0.05)。结论银杏叶提取物经门静脉预处理通过升高SOD活性,抑制库普弗细胞(Kupffer cells,KC)活化,减少TNF-α释放,增强体内抗氧化应激能力,有助于减轻肝脏缺血-再灌注损伤。     

右美托咪定经门静脉预处理对肝部分切除术患者术中炎症反应和氧化应激的影响

目的探讨右美托咪定经门静脉预处理对肝部分切除术患者术中肝脏缺血-再灌注损伤中炎症反应和氧化应激的影响。方法拟在全麻下行肝部分切除术患者60例,男34例,女26例,年龄25~64岁,体重55~70 kg,ASAⅡ级,肝功能Child-Pugh A级。采用随机数字表法将患者分为三组,每组20例。DP组在游离出门静脉后经门静脉输注右美托咪定1.0μg/kg,DJ组在游离出门静脉后经颈内静脉输注右美托咪定1.0μg/kg,C组给予等容量生理盐水。分别于肝门阻断前10 min、肝门开放后1、6、12、24 h经颈内静脉采血检测血清ALT、AST、TNF-α、IL-33、高迁移率族蛋白1(HMGB1)、血红素氧合酶-1(HO-1)浓度和超氧化物歧化酶(SOD)活性。结果与肝门阻断前10 min比较,肝门开放后1、6、12、24 h三组血清ALT、AST、TNF-α、IL-33、HMGB1和HO-1浓度明显升高,SOD活性明显降低(P<0.05)。与C组比较,肝门开放后1、6、12、24 h DP组和DJ组血清ALT、AST、TNF-α、IL-33、HMGB1浓度明显降低,HO-1浓度和SOD活性明显升高(P<0.05)。与DJ组比较,肝门开放后1、6、12、24 h DP组血清ALT、AST、TNF-α、IL-33、HMGB1浓度明显降低,HO-1浓度和SOD活性明显升高(P<0.05)。结论经门静脉输注右美托咪定能更有效抑制炎症反应和氧化应激,增强机体抗炎抗氧化能力,减轻肝部分切除术患者肝缺血-再灌注损伤。     

Evaluation of oxidative stress in laparoscopic cholecystectomy

Purpose: We conducted a prospective study to evaluate the effect of CO₂ pneumoperitoneum and increased intra-abdominal pressure on arterial blood gases, end-tidal CO₂ (ETCO₂), nitric oxide (NO), blood and tissue malondialdehyde (MDA), and total antioxidant (TAOx) levels during laparoscopic cholecystectomy. Methods: Fifty selected patients with cholelithiasis were randomized to undergo either laparoscopic or open surgery. Blood samples were taken pre-, mid-, and postinsufflation, and 24 h postoperatively. To determine the tissue MDA level, tissue samples were taken from the gallbladder just after removal. Results: The increased levels of ETCO₂ and PCO₂, caused by CO₂ pneumoperitoneum resulted in a minimal decrease in blood pH during the laparoscopic surgery. Although low levels of blood MDA were seen 30 min after the start of laparoscopy, due to less oxidative stress response and tissue trauma, increased levels of tissue MDA levels indicated that the gallbladder was more traumatized during laparoscopic dissection and handling. NO levels were slightly lower in the laparoscopic cholecystectomy (LC) group, but there were no significant differences compared with the open cholecystectomy group (OC). TAOx levels were similar in both groups 30 min after the start the procedure, but were much lower in the LC group 24 h postoperatively. Conclusions: These findings suggest that the antioxidant defense system is stimulated less with less oxidative stress, providing further evidence to support the opinion that LC is a safe technique. Received: June 13, 2001 / Accepted: March 5, 2002     

氧化应激与骨质疏松症的研究进展

骨质疏松症是一种以骨量低下、骨微结构破坏为特征,骨脆性增加、易发生骨折等的代谢性疾病。其发病病因多样,分子机制复杂,已成为影响人们生活质量的流行病之一。人体生活在一个充满氧气的环境,在其代谢过程中不可避免的不断产生活性氧（ ROS）,当人体因为衰老、疾病等原因产生ROS与消除ROS之间的平衡被打破时,机体便产生氧化应激。越来越多的研究发现ROS诱导的氧化应激在骨质疏松症中发挥重要作用,过多的ROS通过对多种细胞因子、酶活性的激活或抑制和上调或下调受体配体的表达调控多条信号通路,最终影响细胞核内基因表达,促进骨形成相关细胞如骨髓间充质干细胞（BMSCs）、成骨细胞、骨细胞的凋亡和破骨细胞的增殖及分化,使得骨形成速率相对骨吸收速率滞后,打破以破骨细胞吸收骨组织和成骨细胞形成骨组织相协调的动态平衡过程,从而促使骨质疏松症的产生。本文从ROS诱导的氧化应激对骨形成相关细胞、破骨细胞和骨基质的影响展开综述,为骨质疏松症的进一步研究提供依据。