Effects of Carvedilol on Cardiomyocyte Apoptosis and Gene Expression In Vivo after Ischemia-Reperfusion in Rats

The effects of carvedilol on cardiomyocyte apoptosis and expression of bcl-2, bax genesfollowing ischemia (0.5 h) and reperfusion (48 h) in vivo and the possible biological mechanism ofcarvedilol inhibiting cardiomyocyte apoptosis were studied. The left anterior descending artery inWistar rats were ligated to establish ischemia-reperfusion (I/R) models. The model animals were di-vided into two groups: I/R group, the model rats not subject to other treatments except ischemia-reperfusion (n=8); carvedilol-treated group (n=8), I/R model rats treated with carvedilol. Eightrats in the sham-operated group were subjected to only experimental open operation. The number ofapoptotic cardiomyocyte was determined by TUNEL staining. Immunohistochemistry and in situ hy-bridization histochemistry (ISHH) were used to detect the expression of bcl-2 and bax genes. Imageprocessing system was used to quantitatively dispose the positive metric substances of both immuno-histochemistry and ISHH through the average optical den     

Study on the effects of losartan on cardiomyocyte apoptosis and gene expression after ischemia and reperfusion in vivo in rats

Along with the thrombolysis therapy, PTCAand the coronary artery bypass graft are used inthe treatment of acute myocardial infarction(AMI), these method played the important rolesfor restoring the myocardial perfusion, rescuingagonal cardiomyocyte or reducing the extension ofthe myocardial infarctlon and protecting the cardiacfunction, but ischemia/reperfusion can cause themyocardial injury. Therefore the study of the myocardial ischemia and reperfusion injury become theclinical hotspot. It …     

卡维地洛对大鼠急性心肌梗死后心肌细胞凋亡和bcl-2/bax基因表达的干预作用

目的评价新一代β受体阻断剂卡维地洛对大鼠急性心肌梗死(AM I)后心肌细胞凋亡及其相关基因表达的干预作用。方法将冠状动脉结扎术后24 h存活的雌性SD大鼠(83只)分为AM I对照(M I组,43只)和卡维地洛(10 mg.kg-1.d-1)治疗组(C组,40只),另设假手术组(S组,27只)。各组再按观察时点分为48 h和4周两个亚组。C组于术后24 h直接灌胃法给药。用TUNEL法和DNA凝胶电泳检测心肌细胞凋亡。用免疫组化方法和W estern印迹法检测“抑制凋亡复合基因”bc l-2/bax的表达。结果(1)M I组梗死/瘢痕区、梗死边缘区和非梗死区的心肌细胞凋亡指数(48 h 21.2%±15.6%、19.8%±12.0%和6.3%±4.5%;4周23.5%±13.0%、8.0%±4.4%和3.2%±1.6%)高于假手术组(48 h 1.3%±1.1%,4周1.2%±0.3%,均P<0.05);凋亡促进基因bax的表达M I48 h组明显高于假手术组,但“凋亡抑制基因”bc l-2仅在M I48 h组梗死区心肌细胞中表达增加;bc l-2/bax的比值M I48 h组(1.06)低于假手术组(1.87)。(2)C48 h组3个区域的心肌细胞凋亡指数与M I组比较,差异无统计学意义(均P>0.05),但梗死区及边缘区bc l-2的表达均增加;C4周组梗死/瘢痕区及边缘区的心肌细胞凋亡指数(4.0%±2.0%,2.9%±1.6%)均低于M I组(23.5%±13.0%,8.0%±4.4%,均P<0.05),且瘢痕区心肌细胞中bax的表达亦明显降低,但bc l-2的表达均无明显变化;C组大鼠48 h和4周时的心肌细胞bc l-2/bax的比值(1.72,2.23)高于M I组(1.06,1.8),与假手术组(1.87,2.25)相当。结论大鼠出现AM I后,长时间(4周)用卡维地洛治疗能有效防止梗死/瘢痕区及其边缘区心肌细胞凋亡的发生,并使bc l-2/bax的比值增加。     

β受体阻滞剂阿替洛尔和酒石酸美托洛尔对大鼠急性心肌梗死后心肌细胞凋亡及凋亡相关基因表达的作用

目的比较阿替洛尔和酒石酸美托洛尔对大鼠急性心肌梗死(AMI)后心肌细胞凋亡及凋亡相关基因表达的作用。方法251只雌性SD大鼠结扎左冠状动脉建立AMI模型,术后24h存活的124只随机分为AMI对照(MI组,n=43)、阿替洛尔(A组,10mg·kg-1·d-1,n=39)和酒石酸美托洛尔(B组,20mg·kg-1·d-1,n=42)治疗组;另设假手术组(S组,n=27)。各组再按观察时点随机分为48h和4周两亚组。术后24h以直接灌胃法给药。末端脱氧核苷酸转移酶介导的dUTP切口末端标记技术(TUNEL)和DNA凝胶电泳检测心肌细胞凋亡。免疫组织化学方法和Western blot检测“凋亡抑制基因”bcl-2、“凋亡促进基因”bax和“凋亡执行因子”caspase-3基因的表达。结果与AMI对照组相比,AMI后48h,A、B两组梗死区、边缘区和非梗死区的心肌细胞凋亡指数,除B组梗死区显著降低(P<0·01)外,其他指标差异均无显著性(均P>0·05);心肌细胞中bcl-2的表达除A组的非梗死区外均增加(免疫组织化学染色),bax和caspase-3的表达均无明显降低。AMI4周时,A、B两组瘢痕区及其边缘区和非梗死区的心肌细胞凋亡指数均显著降低(P<0·05,P<0·01);bcl-2、bax和caspase-3的表达均无明显变化,仅A4周组非梗死区bax的表达明显降低。Western blot显示,与AMI对照组相比,A、B两组心肌细胞中caspase-3、bcl-2和bax的表达差异均无显著性,但bcl-2/bax的比值显著增加(P<0·05),并与假手术组相当。结论阿替洛尔和酒石酸美托洛尔均能减少AMI梗死/瘢痕区、边缘区和非梗死区的心肌细胞凋亡,作用相当,此作用主要是通过增加bcl-2的表达和bcl-2/bax的比值而实现。     

加强师资队伍建设是高校实施素质教育的重要保证

随着中国改革开放的不断发展和深入，特别是中国正式加入WTO之后，人才的需求量加大，人才的竞争更加激烈。     

缺血预处理第二保护窗对缺血再灌注心肌细胞凋亡和bcl-2的影响

目的 :探讨缺血预处理 (ischemicpreconditioning ,IP)第二保护窗对大鼠缺血再灌注 (ischemia/reperfu sion ,I/R)心肌细胞死亡和凋亡抑制基因bcl 2蛋白和mRNA表达的影响。方法 :采用末端脱氧核苷酸转移酶介导的带萤光的dUTP缺口末端标记 (TUNEL)法以及免疫组织化学和原位杂交方法。结果 :(1)IP组TUNEL法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于I/R组 (P <0 0 5 ) ;(2 )IP组表达bcl 2蛋白 (mRNA)阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显高于I/R组 (P <0 0 1)。结论 :(1)IP第二窗能够显著减少大鼠I/R心肌细胞死亡 ;(2 )IP通过上调凋亡抑制基因bcl 2的基因表达可能是其减少大鼠I/R心肌细胞死亡的机制之一     

灯盏花素对大鼠缺血-再灌注心肌细胞凋亡和bcl-2表达的影响

目的 :探讨灯盏花素 (breviscapine,BRE)对大鼠缺血 -再灌注 (ischemia/reperfusion ,I/R)心肌细胞凋亡和凋亡抑制基因bcl 2表达的影响。方法 :采用TUNEL法、免疫组化和原位杂交方法 ,观察I/R心肌细胞死亡和凋亡抑制基因的bcl 2表达。结果 :(1)灯盏花素组凋亡心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于I/R组 (P <0 0 5 ) ;(2 )灯盏花素组bcl 2蛋白 (mRNA)表达阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显高于I/R组 (P <0 0 1)。结论 :(1)灯盏花素能够显著减少大鼠I/R心肌细胞凋亡 ;(2 )灯盏花素通过上调凋亡抑制基因bcl 2的表达可能是其减少大鼠I/R心肌细胞凋亡的机制之一。     

Chronic intermittent hypoxia aggravates cardiomyocyte apoptosis in rat ovariectomized model

Background  The prevalence of obstructive sleep apnea (OSA) increases after menopause in women, but remains under diagnosed because of social or lifestyle factors. It is important to evaluate the hazards of OSA on cardiovascular disease in menopausal women. We tested the hypothesis that chronic intermittent hypoxia (CIH) may aggravate cardiomyocyte apoptosis in ovariectomized (OVX) Sprague Dawley (SD) rats; the changes of anti-oxidation ability in cardiac muscles may be one of the reasons for cardiomyocyte apoptosis.

Methods  Forty-eight 60-day old female SD rats were randomly divided into a CIH group, OVX group, OVX+CIH (OC) group, and handled control (HC) group, and the rats were exposed either to CIH (nadir O₂ 6%) or handled normoxic controls. The changes of body weight and whole heart weight were measured. Super oxide dismutase (SOD) and malonaldehyde (MDA) were used to evaluate the level of oxidative stress. TdT-mediated dUTP nick end labeling (TUNEL) was used to measure apoptosis in each rat. Western blotting was used to measure apoptosis associated proteins in cardiac muscle samples from each rat.

Results  When compared with the HC and CIH groups, the levels of oxidative stress in the OC and OVX groups were significantly higher. The levels of SOD in the HC, CIH, OC, and OVX groups were (47.99±4.89), (53.60±4.47), (20.99±2.72), and (30.64±3.79) mmol/mg protein; significantly increased in the CIH group (P <0.05) and significantly decreased in the OC (P <0.01) and OVX (P <0.05) groups. The levels of MDA in the HC, CIH, OVX, and OC groups were (1.63±0.20), (1.93±0.77), (3.30±0.39), and (1.95±0.20) mmol/mg protein; it significantly increased in the CIH (P <0.05), OC (P <0.01), and OVX (P <0.05) groups compared with the HC group. Bax protein expression was significantly increased and bcl-2 protein expression was significantly reduced after CIH compared with HC rats (P <0.05). The protein expression of bax and bcl-2 in the OC group was not significantly different from the CIH group, but the ratio of bax/bcl-2 was significantly increased in the OC group (P <0.05); this was associated with severe cardiomycyte apoptosis in the OC group. TUNEL confirmed this observation.

Conclusions  This study found that CIH may induce oxidative stress in OVX rats but not in CIH rats, and cause more severe cardiomyocyte apoptosis in OVX rats compared with CIH rats. This means that OVX rats exposed to CIH suffered more severe cardiac injury compared with CIH rats due to reduced antioxidation. These findings may partly explain the reason why OSA has a worse cardiovascular impact on menopausal women, and emphasize the importance of detection and early treatment of OSA in menopausal patients.

     

Study on apoptosis and expression of P53, Bcl-2, bax in cardiac myocytys of congestive heart failure induced by ventricular pacing

A characteristic feature of heart failure is theprogressive worsening of ventricular function overmonths or years despite the absence of clinically ap-parent intercurrent advance events.The mechanismresponsible for this hemodynamic deterioration arenot known.Recently,study of electrograph showsloss of myocytes exist in failure heart of human anddogs[1] .Another study revealed thatlossof myocyteswas thoughtto be apoptotic[2— 5] .In this study,we used Td T- mediatedbi-otinylated- d UTP nick e…     

Effect of Ginsenoside Re on Cardiomyocyte Apoptosis and Expression of Bcl—2／Bax Gene after Ischemia and Reperfusion in Rats

Development of thrombolysis and interven-tional therapy has minimized the degree of ischemicnecrosis by dredging occluded blood vessel andrestoring blood flow of infarct area in the earlierperiod. It has been proved that cardiomyocyteapoptosis plays a key role in ischemic reperfusioninjury[1] .The studies concerning control of coro-nary heart disease has been focusing on the inhibi-tion of cardiomyocyte apoptosis induced by is-chemia- reperfusion,reduction of cardiomyocyteloss and protection o…     

苯乙酸对胶质瘤C6细胞凋亡的影响及其机制

目的：观察苯乙酸(PA)对胶质瘤C6细胞凋亡的影响及机制,为其临床应用提供理论基础。方法：体外培养胶质瘤C6细胞经PA诱导分化后,TUNEL检测细胞凋亡,免疫细胞化学检测bcl-2、bax和caspase-3蛋白表达。结果： PA 0(对照)、2.5和5.0 mmol•L^-1分别作用C6细胞24 h后,细胞凋亡率(%)分别为2.5±0.2、10.3±0.5和20.6±1.1;作用72 h后,细胞凋亡率(%)分别为2.7±0.3、24.9±0.7和42.0±1.7,随PA浓度和作用时间的增加,细胞凋亡率增加,不同浓度和不同作用时间细胞凋亡率组间比较差异均有显著性（P<0.05）。在C6细胞中,bcl-2、bax和caspase-3的表达水平分别为0.275±0.022、0.21±0.019和0.149±0.004,PA 5.0 mmol•L^-1作用72 h后表达水平分别为0.244±0.024、0.399±0.030和0.206±0.033。PA作用前后bcl-2表达水平比较差异无显著性（P>0.05）,bax和caspase-3表达水平差异均有显著性（P<0.01）。结论：PA对胶质瘤C6细胞具有诱导凋亡作用,并呈时间及剂量依赖性;PA诱导凋亡的机制与bax和caspase-3表达上调有关。     

Synergistic Protection of Danhong Injection (丹红注射液) and Ischemic Postconditioning on Myocardial Reperfusion Injury in Minipigs

Objective: To explore the synergistic protection of Danhong Injection (丹红注射液,DHI) and ischemic postconditioning on myocardial reperfusion injury in minipigs.Methods: Acute myocardial infarction model was made by balloon occlusion in left anterior descending coronary artery (LAD) of minipigs,and then postconditioning was simulated through inflation/deflation of the angioplasty balloon.Minipigs were divided into four groups: the sham operation group (SH group),the ischemia/reperfusion group (I/R group),the ischemic postconditioning group (POC group) and DHI combined with ischemic postconditioning group (PAD group,DHI 20 mL through ear vein),six in each group.After 24-h continuous observation,myocardial infarction size was assessed by triphenyltetrazolium staining (TTC).Morphological changes of ischemic myocardium were observed by light microscopy,and cardiomyocyte ultrastructure was studied with electron microscopy.The superoxide dismutase (SOD) and malondialdehyde (MDA) activity in heart homogenates were measured by a biochemical method.Results: The myocardial infarction size was smaller in the POC group than in the I/R group (0.26±0.02 vs.0.37±0.09,P0.05),and the PAD group (0.14±0.08) displayed a significantly reduced infarction size relative to the I/R group (P0.01) and POC group (P0.05).The damage of myocardial tissue was severe in the I/R group shown by light and electron microscopy: myocardial fibers disorder,sarcoplasmic dissolution,myofilament fracture,mitochondria swelling and even vacuolization formation and a large number of inflammatory cell infiltrations.Compared with the I/R group,reduction of reperfusion injury in the PAD group included more orderly arranged myocardial fibers,less infiltration of inflammatory cells and maintenance of mitochondrial integrity.Compared with the I/R group,the damage of myocardial tissue in the POC group was improved,but not as significant as that in the PAD group.SOD levels in the POC group and the PAD group were significantly higher than those in the I/R group (96.96±13.43,112.25±22.75 vs.76.32±10.63,P0.05),and MDA was significantly lower in the POC group and the PAD group compared to the I/R group (1.27±0.19,1.09±0.21 vs.1.47±0.16,P0.05).Conclusion: DHI and ischemic postconditioning show a synergistic cardioprotection on myocardial reperfusion injury in minipigs.     

Effects of L-Tetrahydropalmatine on the Expressions of bcl-2 and bax in Rat after Acute Global Cerebral Ischemia and Reperfusion

Polygenesregulateapoptosis .bcl 2isananti apoptosisgene ,whilebaxisapro apoptosisgene .L Tetrahydropalmatine (L THP) ,akindofalkaloidextractedfromtraditionalChinesemedicineRhizomacorydalis,possessesanalgesic ,sedativeandhypnoticeffects.Recently ,ithasbeen…     

NAC对大鼠I/R心肌细胞凋亡及bad、bak、bax的影响

采用末端脱氧核苷酸转移酶介导的带荧光的ｄＵＴＰ缺口末端标记（ＴＵＥＮＬ）法和免疫组化方法对Ｎ－Ｌ酰基－Ｌ－半胱氨酸（ＮＡＣ）对大鼠心肌缺血４５ｍｉｎ再灌注２４ｈ心肌细胞凋亡的影响及其对凋亡促进基因ｂａｄ、ｂａｋ和ｂａｘ蛋白表达的调节进行研究。结果：（１）ＮＡＣ加ＩＲ组ＴＵＮＥＬ法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞的百分比均明显少于ＩＲ组（Ｐ〈０．０５）；（２）ＮＡＣ加ＩＲ组表达ｂａｄ、     

bcl-2/bax表达在左向右分流型肺动脉高压肺血管重构中的作用

目的 研究bel-2、bax蛋白表达与左向右分流型肺动脉高压肺血管重构的关系.方法 建立左向右分流肺动脉高压大鼠模型.比较肺血管重构指标,原位杂交和Western blot检测bel-2和bax分布及表达,TUNEL法检测肺血管细胞的凋亡.结果 分流12周和16周组大鼠的平均肺动脉压力(mPAP)、右室肥大指数(RVHI)、肺小动脉中膜厚度百分比(MT%)明显高于正常大鼠(P<0.05),肺小动脉新生内膜比率显著增加(P<0.01).bci-2蛋白表达在分流12周后明显增强,分流至16周时表达最高峰(P<0.01),而bax蛋白表达显著降低(P<0.01).bcl-2/bax呈上升趋势.结论 bcl-2和bax在肺动脉上均有表达,随着bcl-2和bax比值的上调,肺血管发生重构,bcl-2/bax比值失衡可能是大鼠左向右分流PAH形成的机制之一.     

NAD+在心脏缺血及再灌注损伤中的作用

目的 通过建立大鼠心肌缺血再灌注(ischemia/ reperfusion, I/R)模型,探索药物烟酰胺腺嘌呤二核苷酸(NAD⁺)在大鼠心肌缺血再灌注损伤中的保护作用。方法 采用手术结扎前降支建立大鼠心肌I/R模型,20只Sprague-Dawley ( SD)大鼠随机分入I/R+NAD⁺组(n=10)和I/R+NS组(n=10),通过血清肌钙蛋白(cTn-I),TTC染色检测心肌损伤程度, TUNEL染色用于检测缺血区域凋亡信号。结果 成功建立大鼠I/R模型,I/R+NAD⁺组大鼠血清cTn-I水平显著低于I/R+NS组[(10.01±3.26)ng/ml vs. (57.17±14.83)ng/ml, P＜0.01]。TTC染色结果显示: I/R+NAD⁺组大鼠心脏梗死体积显著低于I/R+NS组[(68.06±16.04)mm³ vs. (11.42±9.65)mm³, p=0.02]。TUNEL染色结果显示: I/R+NAD⁺组大鼠心脏梗死区域凋亡信号显著低于I/R+NS组。结论 NAD⁺在大鼠心肌缺血再灌注损伤具有显著保护作用,而其具体保护机制需进一步研究。     

缬草提取物预处理对大鼠心肌细胞缺血再灌注损伤的保护作用

目的:观察缬草提取物(VOL)预处理对大鼠离体心脏缺血再灌注(I/R)损伤和相关生化指标以及细胞内游离钙的影响,探讨VOL抗I/R损伤的机制.方法:利用Langendorff建立大鼠离体心脏I/R模型,观察左心室发展压(LVDP)恢复和再灌注痉挛度.用生化技术检测冠脉流出液中乳酸脱氢酶(LDH)、磷酸肌酸激酶(CK)的活性以及心肌细胞线粒体超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPx)、ATP酶(ATPase)活性和丙二醛(MDA)含量,并用激光扫描共聚焦显微镜,借用Fluo-3/AM荧光染色技术观察心肌细胞内Ca2+强度.结果:①VOL预处理对心肌I/R损伤具有明显保护作用,并随浓度增加,对心脏保护作用逐渐增强,再灌注痉挛度明显减弱,心脏从缺血后恢复跳动更迅速,心律失常的发生越来越少,与I/R组相比,100 mg/L VOL使LVDP的恢复从(20.35±2.81)％增加到(91.87±6.52)％(P＜0.01),再灌注痉挛度从(89.27±9.31) mmHg减轻为(12.23±3.51)mmHg(P＜0.01).②VOL预处理明显降低LDH、CK活性和MDA含量,显著增加SOD、GSHPx、ATPase的活性,且随VOL浓度增高,上述作用更加明显,100 mg/L VOL预处理组各项生化指标与对照组无明显差异.③VOL使I/R损伤后心室肌细胞内Ca2+荧光强度明显减少,随着VOL浓度增高,减少细胞内Ca2+的作用更加强烈.与I/R组相比,100 mg/L的VOL使心肌细胞内Ca2+荧光强度从144.85±16.41减少到了51.83±11.61(P＜0.01).结论:VOL预处理能明显抵抗I/R损伤,可能机制与VOL减少心脏I/R时心肌细胞内游离钙浓度的增加和抗脂质过氧化有密切关系.     

Effect of Ginsenoside—Rb1 on Cardiomyocyte Apoptosis after Ischemia and Reperfusion in Rats

Summary The effect of ginsenoside Rb₁ on cardiomyocyte apotosis after ischemia (30 min) and reperfusion (6 h) in rats was observed. The ischemia/reperfusion heart model was established by ligating left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were examined under transmission electron microscopy and counted byin situ nick end labeling (TUNEL) method and light microscopy. Results showed that (1) The apoptotic cardiomyocytes were found in ischemic regions in the ischemia/reperfusion group, but not in the sham-operating group under transmission electron microscopy; (2) The number of apoptotic cells were 134.45±45.61/field in the ischemia/reperfusion group, 0/field in the sham-operating group and 51.65±13.71/field in the ginsenoside Rb₁-treated group. The differences were significant among the three groups (P<0.01). It was concluded that myocardial ischemia-reperfusion could induce cardiomyocyte apoptosis, and ginsenoside Rb₁ could significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats, indicating that ginsenoside Rb₁ could inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion, thus alleviating ischemia-reperfusion injury. GUAN Li, female, born in 1967, Doctor in Charge This project was supported by a grant from the Natural Science Foundation of Hubei Province (Serial No. 2000J050).     

纳米磁性靶向药囊对人肝癌裸鼠移植瘤bcl-2/bax蛋白表达的影响

目的观察纳米磁性5-Fu药囊靶向治疗人肝癌裸鼠移植瘤对肿瘤细胞凋亡bcl-2及bax蛋白表达的影响。方法透射电镜观察各组移植瘤形态学特征，免疫组化SABC法测定bcl-2和bax蛋白表达水平。结果电镜观察可见B组（5-Fu）和D组（纳米磁性5-Fu药囊加内磁场）肿瘤组织大量癌细胞凋亡。B和D组bcl-2蛋白表达水平低于A组（生理盐水对照）、C组（纳米磁性5-Fu药囊）和E组（纳米磁小体加内磁场）（P〈0．01），D组bcl-2蛋白表达水平低于B组（P〈0．01）；B组和D组bax蛋白表达水平高于其他三组（P〈0．01），D组bax蛋白表达水平高于B组（P〈0．01）。结论纳米磁性5-Fu药囊靶向治疗能够降低bcl-2蛋白表达，增加bax蛋白表达，促进人肝癌裸鼠移植瘤细胞凋亡，提高5-Fu抗肿瘤作用。     

子宫肉瘤和子宫肌瘤中bcl-2和bax蛋白的表达及意义

目的：研究凋亡调节蛋白bcl-2及bax在子宫肉瘤和子宫肌瘤中的表达及意义。方法：用免疫组织化学ABC法检测34份子宫平滑肌肉瘤标本（Ⅰ期18例,Ⅱ期1例,Ⅲ期8例,Ⅳ期7例）和34份子宫平滑肌瘤以及34份正常子宫肌层标本中的bcl-2及bax蛋白的表达。结果：子宫肌瘤中bcl-2表达强于子宫肉瘤和正常子宫肌层（P<0.01）,肉瘤中的表达强于正常子宫肌层（P<0.05）。正常子宫肌层中bax的表达强于子宫肌瘤和子宫肉瘤（P<0.01）,但bax在肌瘤和肉瘤之间的表达无显著性差异（P>0.05）。Ⅰ,Ⅱ期子宫肉瘤中bcl-2和bax蛋白表达均高于Ⅲ,Ⅳ期者（P<0.01）。bcl-2表达阳性的子宫肉瘤的预后好于bcl-2表达阴性者。结论：bcl-2和bax的表达失调在子宫肌瘤和子宫肉瘤的发病机制中起一定作用。bcl-2和bax主要在子宫肉瘤发生的早期起作用,bcl-2与肉瘤预后相关。