体内IFN-γ基因转染巨噬细胞对化疗小鼠免疫功能的影响

采用磷酸钙-DNA共沉淀法,将IFN-γ真核表达质粒直接注射至经大剂量化疗后的小鼠腹腔内,可成功地转染腹腔巨噬细胞（MФ）,并表达基因产物。能刺激脾脏增生,促进淋巴细胞增殖,增加腹腔巨噬细胞数量,提高腹腔MФ的细胞毒活性,诱导腹腔MФ产生IL-1、TNF和NO。实验结果提示:IFN-γ基因转染MФ可增强化疗后受损机体的免疫功能。     

卡介苗对鼠源性巨噬细胞株释放一氧化氮和IFN-γ的影响

目的:观察卡介苗(BCG)对鼠源性巨噬细胞株RAW264释放的诱导型一氧化氮(NO)合成酶(iNOS)及γ干扰素(IFN-γ)表达的影响.方法:在鼠源性巨噬细胞株RAW264培养液中加入BCG,Griess检测法测定NO释放量,半定量RT-PCR法检测iNOS及IFN-γ的表达.结果:BCG添加后使巨噬细胞NO产生量增加,IFN-γ、iNOS的mRNA表达增强.结论:在巨噬细胞吞噬、杀灭结核分枝杆菌时IFN-γ具有活化巨噬细胞的作用.     

黑色素瘤抗原-1诱导特异性抗肝癌免疫应答

目的:探讨黑色素瘤抗原-1(MAGE-1)对特异性抗肝癌免疫应答反应的影响。方法:分别用转染pcD-NA3.1-MAGE-1(重组子)、pcDNA3.1(空质粒)以及未行转染的人肝癌细胞SMMC-7721冻融抗原致敏树突状细胞(DC),诱导T淋巴细胞增殖分化为细胞毒性T淋巴细胞(CTL)。乳酸脱氢酶释放法检测CTL对SMMC-7721细胞的杀伤活性。48只C57BL小鼠随机分为重组子组、空质粒组和PBS组,每组16只。用pcDNA3.1-MAGE-1预先免疫重组子组小鼠,1次/10d,第3次免疫后第5天ELISA法检测各组8只小鼠脾细胞培养液中IFN-γ和IL-2的含量,第6天各组8只小鼠接种鼠源性肝癌细胞H22,观察其生存时间。结果:未转染、空质粒和重组子组诱导的CTL对靶细胞的杀伤率以及各组小鼠股四头肌MAGE-1mRNA表达的比较差异有统计学意义(F=139.601和538.650,P﹤0.001),重组子组高于未转染和空质粒组。PBS组和空质粒组小鼠脾细胞培养液中IFN-γ和IL-2的含量为0,重组子组小鼠脾细胞培养液中IFN-γ含量为(372.33±10.08)ng/L,IL-2含量为(108.67±12.81)ng/L。3组小鼠荷瘤生存时间比较差异有统计学意义(F=31.837,P<0.001),重组子组小鼠生存时间明显延长。结论:MAGE-1可诱导特异性抗肿瘤免疫应答,从而显著延长荷瘤小鼠的生存时间。     

一种新型的表达PPE68蛋白的重组耻垢分枝杆菌载体疫苗的构建及鉴定

目的:构建一种新型的、含结核分枝杆菌(M.S)抗原PPE68的耻垢分枝杆菌载体疫苗.方法:以结核分枝杆菌标准株H37Rv的基因组为模板,PCR方法获得Rv3873基因,然后通过克隆构建获得真核表达质粒pVAX-1-Rv3873,最后通过电转化的方法将pVAX1-Rv3873真核表达质粒转化至耻垢分枝杆菌的感受态细胞中获...     

结核分枝杆菌异柠檬酸裂合酶对耻垢分枝杆菌胞内存活的影响及相关机制

目的 明确结核分枝杆菌(MTB)异柠檬酸裂合酶(ICL)对耻垢分枝杆菌(MS)在巨噬细胞内存活的影响,并初步探讨其可能的机制.方法 构建MTB-icl基因的穿梭表达质粒pUV15-icl,电转化法导入MS中后检测MTB-ICL在MS中的表达.分别用rMS-pUV15-icl和rMS-pUV15感染鼠巨噬细胞系RAW264.7细胞,于感染一定时间后测定细胞内存活的细菌数,评价MTB-ICL对MS在巨噬细胞内存活的影响.分别留取上述两组巨噬细胞的培养上清液,检测干扰素γ(IFN-γ)和一氧化氮(NO)的水平,同时采用原位TUNEL技术检测两组巨噬细胞的凋亡水平,探讨MTB-ICL对MS在巨噬细胞内存活影响的可能机制.结果 RT-PCR、Western印迹和荧光显微镜检测结果证实MTB-ICL可在MS中有效表达.与rMS-pUV15比较,rMS-pUV15-icl在巨噬细胞内的存活率明显高(P＜0.01),感染后24 h和48 h,其菌落数分别为(32.78±2.90)×103和(23.33 ±2.34)×103,而rMS-pUV15菌落数分别为(14.67±2.45)×103和(2.28 ±0.25)×103.MTB-ICL对巨噬细胞产生IFN-γ和NO没有明显影响.原位凋亡检测结果显示,与rMS-pUV15感染组比较,rMS-pUV15-icl感染组巨噬细胞的凋亡水平明显下降.结论 MTB-ICL可促进MS在巨噬细胞内的存活,其机制之一可能是抑制宿主巨噬细胞的凋亡.     

结核分枝杆菌Rv1246c和Rv1247c假想蛋白间的相互作用

目的 观察结核分枝杆菌Rv1246c和Rv1247c假想蛋白间的相互作用.方法 采用PCR技术克隆结核分枝杆菌Rv1246c和Rv1247c假想蛋白基因, 构建酵母双杂交载体质粒pGBKT7-Rv1247c和pGADT7-Rv1246c, 经酶切分析和DNA测序证实重组质粒构建成功后, 采用醋酸锂法顺序转染酵母菌AH109,检测β半乳糖苷酶活性.结果 共转染GBKT7-Rv1247c和pGADT7-Rv1246c的酵母菌AH109可以在SD/-Ade/-His/-Leu/-Trp营养缺陷培养基上生长,β半乳糖苷酶活性实验阳性.结论 利用酵母双杂交系统证实结核分枝杆菌Rv1246c与Rv1247c假想蛋白可以相互作用.     

巨噬细胞对转染粒细胞-巨噬细胞集落刺激因子的胰腺癌细胞株PC-3的杀伤作用

目的 研究巨噬细胞对转染粒细胞-巨噬细胞细胞集落刺激因子(GM-CSF)基因后的胰腺癌细胞系PC-3的杀伤作用。方法 巨噬细胞由小鼠腹腔注射ConA刺激后分离培养而获得。通过脂质体转染法,将含GM-CSF基因的质粒及空质粒转染至PC-3细胞。以上基因的表达由Western blot免疫印迹法鉴定。采用Cal-cein-AM释放法行巨噬细胞杀伤试验以评估GM-CSF对肿瘤免疫调节作用。结果 巨噬细胞对转染GM-CSF基因后的PC-3细胞杀伤率较空质粒组显著增高(P<0.001)。结论 GM-CSF能增强巨噬细胞杀伤PC-3细胞的能力,提示GM-CSF对于胰腺癌的免疫治疗有潜在价值。     

人γ-干扰素真核表达载体的构建及其体外抑制HBV的作用

目的 观察携带人γ干扰素(IFN-γ)基因的真核表达载体(pcDNA3.1-IFN-γ)体外转染hepG2.2.15细胞后抑制乙型肝炎病毒(HBV)的作用.方法 利用PCR技术和基因重组方法构建表达人IFN-γ的真核表达载体,体外转染hepG2.2.15细胞后收集细胞培养上清液,用ELISA法检测人IFN-γ蛋白的分泌量.并分别用荧光定量PCR和ELISA试剂盒检测细胞培养上清中病毒释放的HBV-DNA和HBeAg、HBsAg抗原含量.结果 转染pcDNA3.1-IFN-γ组细胞HBeAg含量比空载体阴性对照组和空白2.2.15细胞对照组下降了49%,而两个对照组间HBeAg含鼍无显著差异;HBsAg含量比宅载体阴性对照组下降了35%、比空白2.2.15细胞对照组下降了33%,两个对照组问HBsAg含量无显著差异.同时,转染pcDNA3.1-IFN-γ组细胞上清中HBVDNA含量比两个对照组均显著降低,而对照组间HBVDNA含量无显著差异.结论 成功构建了人IFN-γ真核表达载体并可以在体外有效抑制HBV复制,为将人IFN-γ应用于抗HBV的基因治疗奠定基础.     

结核分枝杆菌 Rv0757基因的原核表达及其编码蛋白对巨噬细胞功能的影响

目的构建结核杆菌Rv0757基因原核表达重组质粒pET28a-Rv0757,并研究表达的目标蛋白对小鼠骨髓巨噬细胞株ANA-1细胞的作用。方法将扩增出的Rv0757基因重组到原核表达质粒pET28a(+),并通过SDS-PAGE和Western blot鉴定诱导表达的目的蛋白。纯化目标蛋白后将目标蛋白PhoP作用于小鼠ANA-1细胞,检测活细胞数、乳酸脱氢酶(lactate dehydrogenase,LDH)、一氧化氮(NO)和细胞凋亡指标。结果成功构建出pET28a-Rv0757原核表达质粒,诱导表达的目标蛋白经SDS-PAGE和Western blot鉴定分析,其相对分子质量约为32×103。目的蛋白作用于小鼠ANA-1细胞后对活细胞数和细胞上清LDH活力无明显影响,但可以明显抑制细胞释放NO和细胞凋亡。结论本研究成功构建了原核表达载体pET28a-Rv0757,并成功表达出目标蛋白,该蛋白对小鼠ANA-1细胞没有毒性损伤,但可以抑制细胞释放NO和细胞的凋亡。     

iASPP真核表达载体构建及其功能鉴定

目的构建P53凋亡刺激蛋白(ASPP)家族的抑制成员iASPP的真核表达载体,并将其通过脂质体转染到结肠癌细胞株SW480及Lovo中,观察转染前后iASPP表达变化及其对细胞凋亡的影响。方法将解放军第十六医院检验科经测序鉴定的pMD19-T-iASPP质粒亚克隆至真核表达质粒pcDNA3.1(+),构建重组真核表达质粒pcDNA3.1(+)-iASPP,测序鉴定后用脂质体将重组质粒转染至结肠癌细胞株SW480及Lovo中,用逆转录聚合酶链反应(RT-PCR)检测iASPP的表达以及用流式细胞仪检测细胞凋亡的变化情况。结果重组表达质粒pcDNA3.1(+)-iASPP,经酶切测序与GenBank上记录的人iASPP cDNA序列(gi 60457962)完全一致。经pcDNA3.1(+)-iASPP质粒转染的结肠癌细胞株SW480及Lovo的iASPP mRNA表达增高,细胞凋亡率下降。结论成功构建了重组表达质粒pcDNA3.1(+)-iASPP,并成功在结肠癌细胞株SW480及Lovo中获得了表达,细胞株的凋亡率下降,提示抑制iASPP高表达有可能成为恢复P53抑癌功能的新策略。     

反复热性惊厥过程中γ-氨基丁酸B受体对一氧化氮/一氧化氮合酶体系的调节作用

目的:探讨γ-氨基丁酸B受体(γ-aminobutyric acid B receptor,GABABR)对热性惊厥(febrile seizure,FS)大鼠一氧化氮(nitric oxide,NO)/一氧化氮合酶(nitric oxide synthase,NOS)体系表达的影响.方法:将21 d龄SD大鼠随机分为对照组、FS组、FS+巴氯芬(baclofen)组和FS+法克罗芬(phaclofen)组.采用热水浴诱导大鼠FS,隔日诱导1次,共10次.采用分光光度计法测定大鼠血浆中NO含量;用原位杂交方法观察神经元型一氧化氮合酶(neuronal nitric oxide synthase,nNOS)mRNA表达情况;用免疫组化方法观察nNOS蛋白表达情况.结果:FS+baclofen组NO含量低于FS组[(19.02±9.31)μmol/L比(40.03±9.12)μmol/L],同时nNOS蛋白和mRNA表达也较FS组减弱;而FS+phaclofen组NO含量高于FS组[(66.46±8.15)μmol/L比(40.03±9.12)μmol/L],同时nNOS蛋白和mRNA表达也较FS组增强.结论:反复热性惊厥过程中,GABABR的改变可影响NO/NOS体系的表达.     

转染Livin基因对膀胱癌细胞凋亡的影响

目的 探讨凋亡抑制基因Livin对膀胱癌细胞凋亡的影响.方法 采用脂质体转染法将Livin基因转入膀胱癌T24细胞系,经G418筛选后获得稳定表达Livin的亚克隆细胞系T24/Livin+及仅转染载体的T24/pcDNA3.1(+).用丝裂霉素C(MMC)分别作用于转染前后的膀胱癌细胞系,应用四甲基偶氮唑盐(MTT)比色法检测转染前后细胞生长抑制率,应用流式细胞仪(FCM)及吖啶橙(AO)染色检测细胞凋亡.结果 成功建立了稳定表达Livin的亚克隆细胞系T24/Livin+;经MMC作用24 h后,T24/pcDNA3.1(+)细胞与T24的细胞凋亡率分别为(21.4±2.3)%和(19.6±2.3)%,而T24/Livin+的细胞凋亡率则为(8.7±1.5)%,差异有统计学意义(P＜0.01).结论 Livin基因提高了T24膀胱癌细胞的抗凋亡能力,特别是在膀胱癌化疗中显示出更强的抗凋亡能力.     

新型气体信号分子二氧化硫对自发性高血压大鼠主动脉平滑肌细胞增殖和凋亡的影响

OBJECTIVE: To explore the effects of sulfur dioxide (SO2) on the proliferation and apoptosis of aorta smooth muscle cells in hypertension rats and possible mechanism thereof. METHODS: Sixteen 4-week-old male spontaneously hypertensive rats (SHRs) were randomly divided into 2 equal groups: control and Na2SO3/NaHSO3 (a SO2 donor)-treated group. Eight 4-week-old male WKY (Wistar Kyoto) rats were assigned for normal control group. Five weeks later, the pressure was measured. The rat aortas were dyed with Hart's method. The morphometric parameters were calculated by Leica workstation. The plasma level of SO2 was determined by HPLC method. VSMC apoptosis was measured by TUNEL technique. The expression levels of proliferating cell nuclear antigen (PCNA), Bcl-2, Fas and caspase-3 were detected by immunohistochemical assay. RESULTS: (1) Compared with those of the WKY rats, the blood pressure, ratio of media to lumen radius, and proliferation index (PI) of the SHRs were increased [(172 +/- 10) mm Hg vs (112 +/- 9) mm Hg, 0.073 +/- 0.004 vs 0.057 +/- 0.004, 0.32 +/- 0.06 vs 0.05 +/- 0.03, respectively], but the plasma level of SO2 and the apoptosis index (AI) were decreased in the SHRs [(6.4 +/- 1.5) micromol/L vs (11.3 +/- 1.0) micromol/L, 0.16 +/- 0.07 vs 0.30 +/- 0.19, respectively]. The expression of Bcl-2 was increased (0.209 +/- 0.007 vs 0.202 +/- 0.006), and the expression levels of Fas and caspase-3 of SHRs were both lower than those of the WKY rats (0.205 +/- 0.006 vs 0.211 +/- 0.005, 0.229 +/- 0.005 vs 0.244 +/- 0.010, respectively). (2) Compared with the SHR control group, the systolic blood and the ratio of media to lumen radius were decreased [(128 +/- 7) mm Hg, 0.066 +/- 0.002, respectively], but the plasma level of SO2 was increased [(8.3 +/- 1) micromol/L] for the SHR + Na2SO3/NaHSO3 group. PI was lower (0.14 +/- 0.03) and AI was higher (0.40 +/- 0.11) in SHR + Na2SO3/NaHSO3 group than those in SHR control group. The expression of Bcl-2 of VSMCs was down-regulated (0.199 +/- 0.006), but the levels of Fas and caspase-3 were up-regulated (0.218 +/- 0.003 and 0.251 +/- 0.011 respectively) in the SHR + Na2SO3/NaHSO3 group. CONCLUSION: SO2 may attenuate the structural remodeling through reducing the proliferation and enhancing the apoptosis of smooth muscle cells in SHRs. SO2 may modulate the process of apoptosis possibly through the downward regulation of the level of Bcl-2 and enhance the expression of Fas and caspase-3.     

转染血管内皮生长因子基因对大鼠任意皮瓣成活的影响

OBJECTIVE: To investigate the effects of vascular endothelial growth factor (VEGF) gene transfection on survival of the random skin flap in rats. METHOD: Thirty SD rats were randomized equally into 3 groups: pcDNA3-VEGF165, pcDNA3 and control groups, with the former two groups transfected via liposome with pcDNA3-VEGF165 and pcDNA3 respectively 48 h before and during the operation. Ischemic random skin flaps ( 1 cmx7 cm) were constructed from the rats. Seven days later, the amount of viable tissue within the flap was measured by planimetry. After the animals were killed, and specimens from the random skin flaps were harvested for immunohistologic evidence of VEGF protein expression and for HE staining to examine the microvascular growth. RESULTS: The results of tissue survival planimetry of the skin flap of pcDNA3-VEGF165, pcDNA3 and control groups were 48.46% +/-3.35%, 30.20%+/-2.16%, and 31.35% +/-1.99%, which were highest in the VEGF- transfected group (P<0.05), in which immunohistochemical staining revealed increased deposition of VEGF in comparison with the other control groups P<0.05 . The VEGF group had also higher average vessel number as compared with the vector and control group (107.72+/-9.42 vs 91.35+/-7.28 and 89.85+/-7.66, P<0.05), and smaller average vessel lumen diameter (25.76+/-3.23 microm vs 32.12+/-1.58 microm and 33.49+/-2.29 microm, P<0.05). CONCLUSION: pcDNA3-VEGF165 transfection may enhance the survival of the ischemic skin flaps and achieve VEGF expression in the flaps in rats.     

绿色荧光蛋白GFP在转化细胞和肿瘤细胞中的表达

目的　在肿瘤基因治疗研究中建立一个用绿色荧光蛋白(green fluorescent protein,GFP)为标记基因的合适条件。方法　用带有GFP突变体的质粒转染到表达细胞,观察GFP瞬时表达的情况：1．直接测定GFP在COS-7细胞中的表达并观察表达的稳定性;2．比较不同启动子驱动的pcDNAa-EGFP和pSVKa-S65T两种质粒在不同肿瘤细胞中的转染效率;3．用LacZ基因与GFP基因共转染48h后,通过FACS分选测定两种基因在同一细胞中的表达情况。结果　在不同条件下的活细胞中有GFP基因表达,且表达具有稳定性,表达持续约2周左右;CMV启动子和SV40启动子调控的GFP对不同肿瘤细胞株的转染效率有差异。当两种基因共转染后用FACS分选,选出GFP细胞带有LacZ基因细胞在1：4时可达85％以上。结论　通过GFP表达可连续而直接地观察活细胞中的基因表达,利用GFP可快速地挑选带有靶基因的细胞。     

诱导型一氧化氮合酶基因在3T3细胞中的转染和鉴定

目的 :观察人诱导型一氧化氮合酶 (iNOS)基因转染 3T3成纤维细胞的可能性。　方法 :用阳性脂质体将含人iNOS基因的真核表达载体pcDNA3.0 iNOS转染至 3T3成纤维细胞 ,用G4 18筛选 ,通过RT PCR、免疫组化的方法鉴定。　结果 :pcDNA3.0 iNOS基因转染的 3T3细胞有人iNOS基因mRNA和iNOS蛋白的表达。　结论 :iNOS基因能在 3T3成纤维细胞得到稳定转染和表达 ,能为模拟体内一氧化氮 (NO)作用提供有力的工具。     

乙型肝炎病毒X蛋白羧基端氨基酸缺失对肝癌细胞生物学行为的影响

目的探讨乙肝病毒X蛋白(HBx)羧基端缺失了40个氨基酸的突变体(HBx3′-40)和野生型HBx对Huh7和SMMC-7721肝癌细胞的生物学行为的影响。方法脂质体和磷酸钙法介导pcDNA3HBx3′-40和pcDNA3HBx重组体转染HBV(-)的人肝癌细胞Huh7和SMMC-7721。Neo基因PCR及Western印迹方法检测质粒DNA片断插入和HBx蛋白质的表达。借助生长曲线、平板克隆形成、细胞周期、凋亡和裸鼠成瘤实验以及氯霉素乙酰转移酶(CAT)-ELISA法对转染细胞的生物学活性进行检测。结果pcDNA3HBx3′-40组细胞生长速度明显快于pcDNA3HBx和pcDNA3组;pcDNA3HBx3′-40组克隆形成率明显高于pcDNA3HBx和pcDNA3组(P<0·05);流式细胞仪检测结果显示pcDNA3HBx3′-40表达能加速Huh7细胞由G0/G1期→S期的进程;但细胞凋亡检测显示无血清诱导的SMMC-7721细胞HBx3′-40组能部分取消HBx的促凋亡效应,并且该组几乎丧失了HBx的反式激活作用;裸鼠成瘤实验显示,pcDNA3HBx3′-40组成瘤体积明显大于pcDNA3HBx组和pcDNA3组,瘤体重量间差异具有统计学意义(P<0·05)。表明HBx3′-40对肝癌细胞的生长具有明显促增殖作用。结论HBx碳端缺失了40个氨基酸的突变体转染细胞对比野生型HBx显示促增殖能力明显增强,推测HBx通过缺失突变修饰其生物学功能,取消了野生型HBx的反式激活功能和抗增殖效应。另一方面,HBx114~154个氨基酸位点的缺失可能导致p53无法发挥其抑癌作用。     

Mechanism of apoptotic effects induced by 5-fluorouracil on human liver carc inoma Bel7402 cell line

Objective To evaluate the effect of endogenous nitric oxide (NO) on the ability of 5-fluourouracil (5-FU) to induce apoptosis in the liver carcinoma Bel7402 cell line, and to observe the anti-tumor mechanism and effective adjuvant of 5-FU. Methods Cells were cultured under routine conditions with Dulbecco’s modified Eagle’s medium (DMEM) without L-arginine (L-Arg).We observed the expression of inducible nitric oxide synthase (iNOS) and apoptosis of cells induced by 5-FU with L-Arg added to the medium. The production of nitric oxide was determined by the cell expression of iNOS detected by immunohistochemical staining, and by the concentrations of nitrite and nitrate in the supernatant. Results 5-fluourouracil significantly increased the iNOS expression to 0.1687±0.01968 (P&lt;0.05, vs control group), and the concentration of nitric oxide to 213±30.2 μmol/L (P&lt;0.05, vs control group) The apoptotic cell rate increased significantly to 17.85±0.78%, while the necrotic cell rate decreased to 32.99±0.83% (P&lt;0.05, compared with the 5-FU group). Nω-nitro-L-Arginine methyl ester (L-NAME), the antagonist of L-Arg, can block the apoptotic effects of endogenous nitric oxide. Conclusions 5-FU had a synergistic effects with L-Arg by increasing the production of endogenous nitric oxide. Endogenous nitric oxide plays an important role in the process where 5-FU induces apoptosis in liver carcinoma cells. L-Arg may be a good adjuvant for chemotherapy with 5-FU.     

诱导型一氧化氮合酶基因在3T3成纤维细胞中的转染和意义

目的观察人诱导型一氧化氮合酶基因(iNOS)转染3T3成纤维细胞的可能性.方法用阳性脂质体将含人诱导型一氧化氮的真核表达载体pcDNA3.0-iNOS转染至3T3细胞,用G418筛选,通过RT-PCR、免疫组化的方法鉴定.结果 pcDNA3.0-iNOS基因转染的3T3细胞有人iNOS基因mRNA的表达,细胞中有iNOS蛋白的表达,空载体和对照组没有表达.结论人iNOS基因能够在3T3成纤维细胞得到稳定转染和表达.     

Effect of continuous positive airway pressure treatment on vascular endothelial function in patients with obstructive sleep apnea hypopnea syndrome and coronary artery disease

Background Continuous positive airway pressure (CPAP) treatment has been proven to be effective in improving the symptoms of coexisting coronary heart disease (CHD) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). However, it is still unclear whether such improvements are linked to changes in vascular endothelial function. This research was carried out to investigate the effects of CPAP treatment on vascular endothelial function in patients with OSAHS and CHD.Methods Thirty-six patients with moderate or severe OSAHS and CHD undergoing three months of CPAP treatment were recruited for this study. The changes in their morning plasma nitric oxide (NO) and endothelin (ET) levels, NO/ET ratio, total ischemic burden (TIB) of the myocardium, apnea hypopnea index (AHI), and minimal and mean pulse oxygen saturation (SpO2) were compared and analyzed before and during CPAP treatment. Results Compared with the plasma levels of ET ［(51.39±11.69) ng/L］ and NO ［(36.67±11.86) μmol/L］, NO/ET (0.71±0.14), AHI (32.4±7.9), minimal SpO2 ［(68.9±11.4)%］, and myocardial TIB ［(66.29±16.37) mm·min］ before treatment, there were significant decreases in ET ［(33.41±10.03) ng/L］ （P&lt;0.05）, increases in NO ［(59.89±10.26) μmol/L］ and NO/ET (1.79±0.38) （P&lt;0.01）, decreases in AHI (1.9±0.5), and increases in minimal SpO2 ［(90.6±1.8) %］ （all P&lt;0.01） and myocardial TIB ［(36.42±10.87) mm·min］ （P&lt;0.05） after three months of CPAP treatment.Conclusion CPAP treatment may play an important role in the improvement and protection of vascular endothelial dysfunction and myocardial ischemia in OSAHS patients with CHD.