谷胱甘肽对香烟烟雾作用大鼠淋巴细胞氧化应激的影响

谷胱甘肽是由谷氨酸、半胱氨酸和甘氨酸组成的三肽类巯基物质,以2种形式存在:还原型(GSH)和氧化型(GSSG)。GSH与许多重要的生物学现象,如基因表达调控DNA生物合成、酶活力和代谢调节、免疫功能调节代谢等密切相关,作为细胞内重要的抗氧化剂和解毒剂,对保护细胞、延缓衰老有重要     

香烟烟雾溶液作用下大鼠淋巴细胞的氧化应激反应

目的　以细胞内活性氧自由基 (ROS)水平、DNA损伤、脂质过氧化物 (LPO)水平以及超氧化物歧化酶 (SOD)活力为指标 ,研究细胞在香烟烟雾溶液作用下产生的氧化应激反应。方法　以PBS作吸收液 ,用大包氏管收集香烟主流烟雾 ,将香烟烟雾溶液 (CSS)分别以 0、1× 10 - 3、2× 10 - 3、4× 10 - 3、8× 10 - 3、12× 10 - 3、16× 10 - 3支 ml的浓度作用于大鼠淋巴细胞。用 2′ ,7′ 二乙酰二氯荧光素 (DCFH DA)测定细胞内ROS水平 ,用彗星试验检测细胞DNA损伤 ,同时检测细胞内SOD活力和LPO水平。结果　 2× 10 - 3支 ml以上剂量组二氯荧光素 (DCF)荧光强度、彗星尾长以及LPO水平均显著高于对照组 ,且随剂量增加而增加。 16× 10 - 3支 ml组SOD活力显著低于对照组。与对照组相比 ,1× 10 - 3支 ml组LPO水平显著降低、SOD活力则显著增高。结论　CSS达到一定剂量时使细胞内ROS水平增高 ,引起细胞DNA损伤和脂质过氧化 ,高剂量时SOD活力降低 ,而低剂量时能够诱导SOD活力     

黄芩苷对香烟烟雾提取物诱导的细胞损伤保护作用研究

目的研究黄芩苷对香烟烟雾提取物（cigarette smoke extract,CSE）诱导的人肺泡上皮细胞损伤的影响,并初步探讨其机制。方法制备CSE,用不同浓度黄芩苷对人肺泡上皮细胞A549进行预处理,再用CSE刺激细胞。用MTT法检测细胞存活率,流式细胞术测定细胞凋亡率,彗星实验观察DNA损伤情况,荧光法测定细胞内活性氧（reactive oxygen species,ROS）含量。结果随着CSE浓度的增加和作用时间的延长,细胞存活率下降,各组之间有统计学差异（P〈0.05）;黄芩苷能减少CSE诱导的细胞存活率下降,抑制CSE诱导的细胞内ROS的产生,并有剂量依赖关系（P〈0.05或P〈0.01）;黄芩苷＋CSE组细胞的彗星尾长、尾部DNA含量、尾距、Olive尾距均小于CSE组（P〈0.05）,并且黄芩苷可以减少CSE导致的细胞凋亡。结论黄芩苷可以拮抗CSE对细胞的损伤,提高细胞的存活率,降低凋亡率,其原因可能与黄芩苷能降低细胞ROS含量,减少DNA损伤有关。     

香烟烟雾对家兔的毒害作用

通过对家兔被动吸烟及静脉注射香烟烟雾溶液的毒害作用试验,推算出主动吸烟的人香烟中毒量;并通过对其病理解剖及组织观察,见到香烟烟雾能引起如下变化:使细胞的脂质膜溶掉,切断体内细胞的生物氧化链,血红蛋白变性,心肌疏离,心肌内血管收缩,以及使肺、肝等器官产生较多的癌变前期的细胞。     

盐酸氨溴索注射液对重型颅脑损伤患者的临床分析

目的 分析盐酸氨溴索注射液对重型颅脑损伤患者的临床作用.方法 统计分析我院自2001年7月到2011年5月期间收治的严重颅脑损伤合并多发伤患者213例的临床资料,其中治疗组有患者98例,对照组有患者115例,对照组采用经典的颅脑损伤治疗方案,治疗组在经典治疗的基础上加用盐酸氨溴索注射液(沐舒坦注射液)30mg+100mL.生理盐水静脉注射,每日3次.观察患者的临床症状、体征及实验室检查结果.结果 治疗组的ICU住院时间,总住院时间及28 d死亡率明显低于对照组(P＜0.05).结论 盐酸氨溴索注射液能预防重型颅脑损伤患者的肺部并发症,降低病死率,减少住院时间,提高重型颅脑损伤患者的疗效,临床效果明显,值得应用.     

香烟烟雾提取物致小鼠生殖细胞的遗传学损伤及其机制

吸烟与许多疾病有关，但其对遗传或生殖损害研究报道尚少。香烟烟雾提取物可致小鼠生殖细胞染色体损伤，但该作用是否可能遗传给后代或影响生殖细胞的功能尚未见报道。香烟烟雾中含有许多自由基，而自由基可致DNA损伤。我们给雄性小鼠腹腔注射不同剂量香烟烟雾提取物，观察生殖细胞染色体     

香烟烟雾水溶性提取物对肝细胞线粒体的损伤

目的 探讨香烟烟雾水溶性提取物(CSW)对L-02肝细胞线粒体结构与功能的影响.方法 采用噻唑蓝(MTT)检测CSW处理L-02肝细胞24 h后的生存率,以确定后续试验CSW染毒浓度为0、8×10-3、16×10-3、32×10-3、64×10-3支/ml培养基.CSW染毒处理L-02肝细胞24 h后用MTF法检测线粒体总酶活力抑制率,荧光分光光度法检测线粒体膜通透性转运孔(PTP)开放度与细胞线粒体膜电位(△ψm)的变化,透射电子显微镜观察细胞线粒体形态学变化.结果 8×10-3、16×10-3、32×10-3、64×10-3支/ml 4个不同浓度处理组CSW对L-02肝细胞具有一定的细胞毒性,其细胞生存率随CSW处理浓度的增高而降低,且二者呈明显负相关(相关系数r=-0.957);线粒体PTP开放程度则随CSW浓度的增高而增加,32 ×10-3支/ml及其以上CSW浓度组开放度与对照组比较,差异有统计学意义(P＜0.05);线粒体总酶活力与细胞线粒体膜电位(△ψm)随CSW浓度的增加而下降,二者分别在8×10-3、16×10-3支/ml及其以上CSW浓度组与对照组比较,差异均有统计学意义(P＜0.05).透射电子显微镜观察线粒体形态发生显著改变即表现为肿胀、空泡变性、膜和嵴破损.结论 香烟烟雾水溶性提取物可对L-02肝细胞线粒体的结构与功能造成一定程度损伤.     

盐酸氨溴索对小儿体外循环肺损伤的保护作用

目的:探讨盐酸氨溴索在小儿体外循环(CPB)手术中对肺的保护作用。方法:选择40例行房、室间隔缺损修补术的4～9岁的患儿,随机分为盐酸氨溴索组(M组)20例和对照组(C组)组20例。M组于麻醉后切皮前匀速静脉滴注盐酸氨溴索4.5mg/kg溶于50mL平衡液中,C组用等容量平衡盐溶液静脉注射,分别于麻醉后(T1)、给药后10min(T2)、停体外循环后5min(T3)、入ICU后1h(T4)、入ICU后2h(T5)、拔管前(T6),根据麻醉机及呼吸机记录气道峰压(PIP)和平台压(Plat)、气道阻力(R)及肺顺应性(CL)。采集静脉血液测定术前、术中、术后血白细胞(WBC)。结果:2组R处理因素与时间效应差异均有统计学意义(均P<0.01),2组在T5、T6时差异有统计学意义(P<0.01),2组均在T4时点达到最高值,以后呈下降趋势。2组患者CL在T1和T5时点差异均无统计学意义(P>0.05)。2组患者WBC组间和时间效应差异均有统计学意义(均P<0.01),处理因素与时间效应间存在交互作用(P<0.01)。2组PIP和Plat处理效应与时间效应差异均有统计学意义(均P<0.001);处理效应与时间效应存在交互作用(均P<0.01)。结论:在体外循环前使用盐酸氨溴索对肺有一定的保护作用。     

HPLC法测定盐酸氨溴索分散片中盐酸氨溴索的含量

目的采用高效液相色谱法测定盐酸氨溴索分散片中盐酸氨溴索的含量。方法使用C18柱(大连依利特Hypersil ODS25μm,4.6mm×200mm),柱温:室温,流动相:以0.025mol.L-1磷酸二氢钾溶液(用磷酸调节pH值为3.0)∶乙腈(75∶25);流速1.0mL.min-1;检测波长244nm。结果采用高效液相色谱法测定盐酸氨溴索分散片中盐酸氨溴索的含量,线性范围为24.528～36.792μg.mL-1,r=0.9998;平均回收率分别为100.9%(RSD=0.5%)。结论用高效液相色谱法测定盐酸氨溴索分散片中盐酸氨溴索的含量,方法简便快速准确,能更好地控制产品质量。     

氨溴索对慢性阻塞性肺疾病患者氧化应激的影响

目的：研究氨溴索针剂对慢性阻塞性肺疾病（COPD）急性加重期患者氧化与抗氧化能力的影响。方法：COPD急性加重期患者,采用氨溴索针剂治疗,检测患者血清丙二醛（MDA）、超氧化物歧化酶活性（SOD）水平。并比较两组患者总有效率。结果：氨溴索治疗显著降低患者血清MDA含量,显著增加SOD水平,总有效率提高。结论：氨溴索能减轻COPD急性加重期患者氧化应激程度,提高患者抗氧化能力,对COPD患者有一定辅助治疗价值。     

Diphenyl diselenide prevents oxidative damage induced by cigarette smoke exposure in lung of rat pups

The effect of cigarette smoke exposure on lungs of rat pups was evaluated. Animals were exposed to passive cigarette smoke during 3 weeks and a number of toxicological parameters in lung of pups were examined, such as lipid peroxidation, δ-aminolevulic acid dehydratase (δ-ALA-D) activity, components of the enzymatic antioxidant defenses (superoxide dismutase (SOD) and catalase activities) and non-enzymatic antioxidant defenses (Vitamin C and non-protein thiol (NPSH) levels). Furthermore, a possible protective effect of diphenyl diselenide, (PhSe)₂, was studied. The results demonstrated an increase in lipid peroxidation, an inhibition of δ-ALA-D activity, a reduction of Vitamin C and NPSH levels induced by cigarette smoke exposure, indicating damage in lungs of rat pups. Oral administration of (PhSe)₂ (0.5 mg/kg) restored TBARS levels, non-enzymatic antioxidant defenses and activity of δ-ALA-D. These results indicated that exposure to cigarette smoke enhanced oxidative stress, thereby disturbing the tissue defense system. (PhSe)₂ protected against oxidative damage induced by cigarette smoke exposure in lung of rat pups.     

Aryl hydrocarbon receptor protects lung adenocarcinoma cells against cigarette sidestream smoke particulates-induced oxidative stress

Environmental cigarette smoke has been suggested to promote lung adenocarcinoma progression through aryl hydrocarbon receptor (AhR)-signaled metabolism. However, whether AhR facilitates metabolic activation or detoxification in exposed adenocarcinoma cells remains ambiguous. To address this question, we have modified the expression level of AhR in two human lung adenocarcinoma cell lines and examined their response to an extract of cigarette sidestream smoke particulates (CSSP). We found that overexpression of AhR in the CL1-5 cell line reduced CSSP-induced ROS production and oxidative DNA damage, whereas knockdown of AhR expression increased ROS level in CSSP-exposed H1355 cells. Oxidative stress sensor Nrf2 and its target gene NQO1 were insensitive to AhR expression level and CSSP treatment in human lung adenocarcinoma cells. In contrast, induction of AhR expression concurrently increased mRNA expression of xenobiotic-metabolizing genes CYP1B1, UGT1A8, and UGT1A10 in a ligand-independent manner. It appeared that AhR accelerated xenobiotic clearing and diminished associated oxidative stress by coordinate regulation of a set of phase I and II metabolizing genes. However, the AhR-signaled protection could not shield cells from constant oxidative stress. Prolonged exposure to high concentrations of CSSP induced G0/G1 cell cycle arrest via the p53-p21-Rb1 signaling pathway. Despite no effect on DNA repair rate, AhR facilitated the recovery of cells from growth arrest when CSSP exposure ended. AhR-overexpressing lung adenocarcinoma cells exhibited an increased anchorage-dependent and independent proliferation when recovery from exposure. In summary, our data demonstrated that AhR protected lung adenocarcinoma cells against CSSP-induced oxidative stress and promoted post-exposure clonogenicity.     

Separate effects of cigarette smoke yield and smoke taste on smoking behavior

The purpose of this experiment was to compare independently the influence of different cigarette smoke taste categories and different machine standard smoke yield values on cigarette smoking behavior and related subjective measures. In six separate sessions 15 regular smokers were presented with a medium and a low smoke yield cigarette of each of the three taste categories, mentholated, dark (Gauloises) and blond (Muratti) tobacco. Each session, included a natural and a forced smoking procedure of one cigarette type only. Forced smoking consisted of smoking 30 puffs whereby a new half-length cigarette was presented after every third puff. During the seventh session, habitual brand cigarettes were smoked as a reference. The sessions followed in weekly intervals, and the subjects became familiar with the test cigarettes during the last 5 days preceding each test session. Although general acceptability of the cigarettes, smoking satisfaction and pleasantness of taste were clearly lower for all test cigarettes as opposed to the habitual brand reference, cigarettes, these measures remained unaffected by taste or smoke yield of the test cigarettes. Harshness of smoke was higher in the dark tobacco category and generally decreased with the lower smoke yield cigarettes. Independent effects of taste and smoke yield were obtained for total puff volume, inhalation time and CO absorption, suggesting a compensatory intensification of smoking behavior for low yield cigarettes and an independent increase of smoking intensity from mentholated to dark tobacco to blond tobacco. The results suggest therefore that factors which affect cigarette smoke taste have effects on smoking behavior which are separate from those obtained by comparing smoke yields.     

芹菜素对烟草烟雾提取物诱导血管内皮细胞损伤的作用

目的探讨芹菜素改善烟草烟雾提取物诱导的血管内皮细胞损伤的机制。方法培养人脐静脉内皮细胞株,给予烟雾提取物(CSE)模拟吸烟环境和不同浓度芹菜素。实验分为正常对照组、CSE组、芹菜素组,检测细胞存活率、凋亡率、细胞内活性氧ROS水平,以及细胞上清液中IL-6、TGF-β、INF-γ各因子的表达。结果芹菜素在24 h和48 h均能显著缓解不同浓度CSE诱导的内皮细胞存活率的降低,降低不同浓度CSE诱导的内皮细胞的凋亡率,同时芹菜素可抑制CSE诱导的细胞内ROS水平,以及上清液中炎性因子IL-6、TGF-β、INF-γ的升高,差异均有统计学意义(P<0.05,P<0.01)。结论芹菜素以血管内皮细胞凋亡和炎性反应为标靶,抑制吸烟引起的血管内皮细胞损伤,为临床治疗提供理论依据。     

氨溴索联合阿奇霉素对稳定期慢性阻塞性肺病患者氧化应激的影响

目的探讨氨溴索联合阿奇霉素对稳定期慢性阻塞性肺疾病（COPD）患者氧化应激的影响。方法选取稳定期COPD患者90例,随机分为氨溴索组、阿奇霉素组、联用组各30例,均按需予长效茶碱片和／或沙丁胺醇雾化吸入治疗,氨溴索组加服氨溴索片,阿奇霉素组加服阿奇霉素片,联用组两药联用,疗程6个月。比较3组患者治疗前后血清超氧化物歧化酶（SOD）、丙二醛（NDA）含量及24h痰量、肺功能的变化。结果联用组治疗后外周血SOD增加,MDA降低,24h痰量减少,肺功能得到改善,且较氨溴索组和阿奇霉素组变化更明显（P〈0．05）。结论氨溴索联合阿奇霉素能使COPD稳定期患者痰液减少,肺功能改善,可能与提高机体的抗氧化能力有关。     

同型半胱氨酸诱导人血管平滑肌细胞氧化损伤的研究

目的探讨同型半胱氨酸（Hcy）对人脐静脉血管平滑肌细胞（VSMCs）氧化损伤的作用及机制。方法用含不同剂量Hcy（50～1000μmol/L）的培养基培养VSMCs24h后,以分光光度比色法分别测定细胞内丙二醛（MDA）含量和超氧化物酶（SOD）、过氧化氢酶（CAT）活力的改变。结果随Hcy浓度增加,VSMCs内MDA的含量明显增加,SOD和CAT的活力也显著升高。Hcy明显促进了VSMCs的氧化。结论Hcy可直接诱导VSMCs的氧化损伤。     

肥胖者吸烟对动脉僵硬度与氧化应激的影响

目的观察肥胖者吸烟对动脉僵硬度及氧化应激的影响。方法选取大学在校男生85人,按照BMI或腰围大小分为2组,对照组41人,实验组44人,实验组进行吸烟干预25d,对照组无任何干预,测定对照组及实验组吸烟前、后每位受试者动脉僵硬度、血浆谷胱甘肽、丙二醛、尿酸含量并进行对比。结果实验组吸烟前与对照组比较,动脉僵硬度（1．78±0．26VS1．97±0．38,P〈0．05）及血浆丙二醛[（3．88±1．13）μmol／LVS（4．32±1．56）μmol／L,P〈0．05]、尿酸含量[（295±43）μmol／LVS（361±57）μmol／L,P〈0．05]显著增高;实验组吸烟后与对照组及实验组吸烟前比较,动脉顺应性显著下降[（1．54±0．32）ml／mmHgVS（1．97±0．38）ml／mmHg,P〈0．01;（1．54±0．32）ml／mmHgVS（1．78±0．26）ml／mmHg,P〈0．05],与对照组比较,实验组吸烟前后丙二醛尿酸含量则显著上升[丙二醛：（4．32±1．56）vs（3．88±1．13）,（4．77±1．07）vs（3．88±1．13）;尿酸：（361±57）VS（295±43）,（472±39）μmol／L vs（295±43）μmol／L,P〈0．01或P〈0．05]。结论氧化应激反应产物丙二醛、尿酸含量的增高,说明机体氧化．抗氧化机制失衡有助于动脉僵硬度和动脉顺应性发生改变,增加心血管疾病的患病风险,而肥胖者吸烟更具有患病的高危性。     

氨溴索对高浓度氧和通气机联合所致大鼠急性肺损伤的防护作用

目的:研究氨溴索对高浓度氧和通气机联合所致大鼠急性肺损伤的防护作用。方法:将36只雄性SD大鼠随机分为3组。A组实施空气大潮气量通气,B组实施高氧大潮气量通气,C组为氨溴索干预组。测定左肺W/D值,BALF中性粒细胞计数、TNF-α、IL-1β、MIP-2含量以及肺组织MDA、SOD水平。结果:C组大鼠左肺W/D值、BALF中性粒细胞计数、TNF-α、IL-1β、MIP-2含量、肺组织MDA水平较B组显著下降,而SOD水平较B组显著增加。结论:氨溴索对高浓度氧和通气机联合所致大鼠急性肺损伤有较明显的防护作用。