全反式维甲酸对亚砷酸钠致人肝细胞损伤保护性作用的研究

目的 观察全反式维甲酸(ATRA)对亚砷酸钠致人肝细胞系(HHL)-5细胞损伤的保护性作用,探讨可能机制.方法 采用细胞培养方法,体外培养HHL-5细胞48 h后进行实验,实验分为4组:正常组、ATRA组、亚砷酸钠组、ATRA+亚砷酸钠组.用细胞增殖实验(WST)观察HHL-5细胞的活力;生物化学方法测定各组HHL-5细胞内超氧化物歧化酶(SOD)、谷胱甘肤过氧化物酶(GSH-Px)的活力及丙二醛(MDA)的含量和细胞培养液中谷草转氨酶(AST)的活力;透射电镜观察各组细胞超微结构的变化.结果 亚砷酸钠组HHL-5细胞活力(0.57±0.02)与正常组(0.70±0.01)比较,差异有统计学意义(P＜ 0.05);SOD、GSH-Px、MDA、AST [(153.84±2.35 )U/mg Prot、(0.08±0.02)U/mg Prot、(4.15±0.50)nmol/mg Prot、(265.43±4.62)×103 U/L]与正常组[(237.41±18.30) U/mg Prot、(0.93±0.02)U/mg Prot、(2.26±0.40)nmol/mg Prot、(177±9.85)×103 U/L]比较,差异有统计学意义(P均.＜0.05).ATRA+亚砷酸钠组HHL-5细胞活力(0.65±0.04)与亚砷酸钠组比较,差异有统计学意义(P＜0.05);SOD、GSH-Px、MDA、AST[(286.85±3.39)U/mg Prot、(0.56±0.09)U/mg Prot、(3.36±0.37)nmol/mg Prot、(220.02±1.07)×103 U/L]与亚砷酸钠组比较,差异有统计学意义(P均＜ 0.05).电镜结果显示,亚砷酸钠组同正常组及ATRA组比较,细胞表面微绒毛减少,双层核膜结构不清,胞质内可见空泡样变,肝糖原凝集;ATRA+亚砷酸钠组上述损伤程度减轻.结论 ATRA通过提高HHL-5细胞内抗氧化酶的活力,清除或者减少氧自由基对细胞的损伤,从而发挥保护作用.     

tBHQ对无机砷致HaCaT细胞细胞周期调节失控的拮抗作用

目的探讨叔丁基对苯二酚(tert-butylhydroquinone,tBHQ)对亚砷酸钠(sodium arsenite,NaAsO2)致人皮肤角质细胞系HaCaT细胞周期阻滞及其调控蛋白异常改变的拮抗作用。方法流式细胞仪法测定细胞周期;Western Blot检测细胞内Cyclin D1和CDK4的蛋白表达情况。结果 NaAsO2单独作用HaCaT细胞,G0/G1期细胞比例明显下降(P<0.01),S期和G2/M期细胞比例较对照组明显增加(P<0.01);tBHQ预处理后,tBHQ(50μmol/L)预处理的NaAsO2(25、50μmol/L)组细胞G0/G1期细胞比例有所上升(P<0.01);tBHQ(50μmol/L)预处理的NaAsO2(50μmol/L)组S期细胞比例明显下降(P<0.01);G2/M期细胞比例整体呈下降趋势。NaAsO2单独作用于HaCaT细胞,细胞周期相关蛋白Cyclin D1和CDK4的蛋白表达随NaAsO2染毒浓度的增加而明显下降(P<0.01);tBHQ预处理后,Cyclin D1和CDK4蛋白表达均明显高于相同浓度NaAsO2单独作用组(P<0.01)。结论 tBHQ对无机砷致人皮肤角质细胞细胞周期异常变化具有一定的拮抗作用。     

亚砷酸钠对黑色素瘤细胞A375和G361色素代谢的影响

目的 探讨亚砷酸钠(NaAsO2)暴露对黑色素瘤细胞A375(以下简称A375)和G361(以下简称G361)的色素水平及酪氨酸酶(TYR)活力的影响,以及两种细胞色素代谢能力的差异.方法 以0.0(对照)、0.1、1.0 μmol/L NaAsO2作用于A375和G361细胞,72 h后,以阿尔玛蓝还原法检测细胞活力水平,同时测定细胞中黑色素水平及TYR的活力水平.结果 NaAsO2作用72h后,0.1 μmol/L剂量组的A375和G361细胞均呈轻度增殖表现,细胞活力[A375:(103.32±1.26)％;G361:(104.10±1.76)％]与对照组[A375:(100.00±1.08)％;G361:(100.00±1.79)％]比较,差异无统计学意义(P均＞0.05);1.0μmol/L剂量组细胞活力[A375:(75.32±1.59)％;G361:(78.26±2.10)％]与对照组相比均显著下降(P均＜0.05).对照、0.1、1.0μmol/L剂量组的G361细胞的黑色素水平[(7.19±0.35)、(7.34±0.83)、(8.19±0.86) pg/细胞]均高于A375细胞[(4.35±0.72)、(4.54±0.01)、(4.60±0.59)pg/细胞,P均＜0.05],G361细胞的TYR活力水平[(54.13±1.21)、(54.56±0.21)、(56.25±0.85)贝克勒尔(Bq)]均高于A375细胞[(42.00±0.21)、(42.90±0.54)、(42.91±0.01)Bq,P均＜0.05].2种细胞的黑色素生成水平及TYR活力水平均随NaAsO2剂量增高而呈增高趋势,但组间比较,差异均无统计学意义(P均＞ 0.05).结论 砷致色素代谢异常可能与砷暴露致黑色素水平及TYR活力增高有关;不同个体间色素代谢差异,可能与个体的黑色素代谢本底水平及TYR本底活力差异有关.     

亚砷酸钠诱导人膀胱上皮永生化细胞氧化损伤作用观察

目的 观察亚砷酸钠(NaAsO2)诱导人膀胱上皮永生化细胞(SV-HUC-1)氧化损伤作用.方法 以不同浓度NaAsO2[0(对照)、1、2、4、8、10μmol/L]对SV-HUC-1细胞染砷24 h,利用流式细胞仪检测细胞内活性氧(ROS)水平,采用酶联免疫吸附实验(EHSA法)检测细胞内硝基酪氨酸(NT)含量和细胞培养液中8-羟基脱氧鸟嘌呤核苷(8-OHdG)水平.结果 1、2、4、8、10 μmol/L染砷组SV-HUC-1细胞ROS水平(81.76±4.91、95.23±2.17、126.61±17.95、126.74±27.77、114.18±9.65)明显高于对照组(69.84±1.28,P＜ 0.05或＜ 0.01),ROS水平与染砷剂量呈显著正相关(r=0.818,P＜ 0.01).10 μmol/L染砷组SV-HUC-1细胞内NT含量[ (919.66±206.33)μg/L]显著高于对照组[(238.19±38.28) μg/L,P＜ 0.01],NT含量与染砷剂量呈显著正相关(r=0.617,P＜0.01).各组细胞培养液中8-OHdG含量比较,差异无统计学意义(F=2.127,P＞0.05).结论 NaAsO2能够引起SV-HUC-1细胞氧化损伤.     

tBHQ对NaAsO2诱导HaCaT细胞凋亡的拮抗作用

目的探讨叔丁基对苯二酚(tertiary butylhydroquinone,tBHQ)对亚砷酸钠(NaAsO2,sodium arsenite)诱导人角质上皮HaCaT细胞凋亡的拮抗作用。方法 tBHQ(10、25、50μmol/L)预处理12 h,再与NaAsO2(5、10、30μmol/L)共同处理HaCaT细胞24 h。用Annxin V/PI染色流式细胞术法检测细胞凋亡率;DAPI染色观察细胞形态学改变;JC-1法测定线粒体膜电位。结果将实验数据进行ANOVA分析处理后表明,5,10、30μmol/L NaAsO2单独作用时,细胞凋亡率与对照组相比显著升高,而线粒体膜电位则显著下降(P<0.05或P<0.01),形态学观察可见高强度DAPI染色细胞数目增加和凋亡小体出现;当给予tBHQ(10、25、50μmol/L)预处理后,NaAsO2致HaCaT细胞凋亡率升高和线粒体膜电位下降均明显受到抑制(P<0.05),形态学观察可见高强度DAPI染色细胞数目和细胞核碎片明显减少。结论实验结果表明tBHQ可能通过线粒体凋亡途径抑制NaAsO2引起的HaCaT细胞凋亡。     

卵磷脂对砷染毒非洲绿猴肾细胞细胞膜损伤的作用

目的 观察卵磷脂对亚砷酸钠(NaAsO2)染毒非洲绿猴肾细胞(Vero)细胞膜损伤的作用.方法 将体外培养Vero细胞分为4组:对照组(生理盐水)、砷模型组(2.20 mg/L NaAsO2)、卵磷脂高剂量+砷干预组(53.33 mg/L卵磷脂+2.20 mg/L NaAsO2)、卵磷脂低剂量+砷干预组(13.32 mg/L卵磷脂+2.20 mg/L NaAsO2),每组6瓶细胞,每2天换液1次,培养120 h.采用分光光度法测定细胞膜Na+,K+-ATP酶活性,高效液相法测定细胞膜磷脂组分磷脂酰丝氨酸(PS)、磷脂酰乙醇胺(PE)、磷脂酰胆碱(PC)和神经鞘磷脂(SM).结果 对照组、砷模型组、卵磷脂高剂量+砷干预组、卵磷脂低剂量+砷干预组细胞膜Na+,K+-ATP酶活性分别为(O.962 ±0.081)×106、(0.544±0.037)×106、(0.647±0.043)×106、(0.550±0.020)× 106 U·kg-1·h-1,各组间比较,差异有统计学意义(F=43.58,P<0.01).与对照组比较,其他3组细胞膜Na+,K+-ATP酶活性明显降低(P均<0.05);与砷模型组比较,卵磷脂高剂量+砷干预组明显增高(P<0.05),而卵磷脂低剂量+砷十预组未见明显改变(P>0.05).与对照组[(0.087±0.003)、(0.127±0.053)、(0.588±0.105)、(0.07l±0.029)g/L]比较,砷模型组PS、PE、PC、SM水平[(0.051±0.018)、(0.073±0.030)、(0.240 4-0.038)、(0.047±0.121)g/L]均明显降低(P均<0.05);卵磷脂高剂量+砷干预组PS、PE、PCI(0.084±0.011)、(0.109±0.363)、(0.591±0.476)g/L]未见明显改变(P均>0.05),而SM[(0.057±0.004)g/L]明显降低(P<0.05);卵磷脂低剂量+砷干预组PS、PE、SM[(0.058±0.020)、(0.086±0.177)、(0.048±0.103)g/L]明显降低(P均<0.05),而PCI(0.521±0.098)g/L]未见明显改变(P>0.05).与砷模型组比较,卵磷脂高剂量+砷干预组PS、PE、PC、SM明显增高(P均<0.05);卵磷脂低剂量+砷干预组PS、PE、SM未见明显改变(P均>0.05),PC明显增高(P<0.05).结论 高剂量卵磷脂对砷染毒Vero细胞膜损伤具有一定的保护作用.

Abstract：

Objective To observe the lecithin's effect on membrane of African green monkey kidney cells (Vero) exposed to sodium arsenite(NaAsO2). Methods Vero cells cultured in vitro were divided into 4 groups:control group (saline), model group (2.20 mg/L NaAsO2), high eoncentration of lecithin and arsenic group (53.33mg/L lecithin + 2.20 mg/L NaAsO2), low eoncentration of lecithin and arsenic group( 13.32 mg/L lecithin + 2.20 mg/L NaAsO2), 6 bottles of cells in each group, medium was changed every 2 days, cultured for 120 h. Na+ ,K+-ATPase activities of membrane were measured by spectrophotometry, and membrane phospholipids composition including phosphatidylserine (PS), phosphatidylethano-lamine (PE), phosphatidylcholine (PC) and sphingmyelin (SM) were measured by high performance liquid chromatography (HPLC). Results The Na~, K+-ATPase activities of membrane of control group, model group, high concentration of lecithin and arsenic group, low concentration of lecithin and arsenic group were (0.962 ± 0.081) × 106, (0.544 ± 0.037) × 106, (0.647 ± 0.043) x 106, (0.550±Compared with control group, the Na+ ,K+-ATPase activities of other 3 groups were significantly reduced (all P < 0.05). Compared with model group, the Na+ ,K+-ATPase activity in high concentration of lecithin and arsenic group was significantly higher (P < 0.05),but in low concentration of lecithin and arsenic group did not change significantly (P > 0.05). Compared with control group[(0.087 ± 0.003), (0.127 ± 0.053), (0.588 ± 0.105),(0.071 ± 0.029)g/L], PS, PE, PC, SM levels in model group[(0.051 ± 0.018), (0.073 + 0.030), (0.240 ±0.038), (0.047 ± 0.121 )g/L] were significantly lower(all P < 0.05) ;PS, PE, PC in high concentration of lecithin and arsenic group[(0.084 ± 0.011), (0.109 ± 0.363), (0.591 ± 0.476)g/L] did not change significantly(all P > 0.05), but SM[(0.057 ± 0.004)g/L] significantly decreased(P < 0.05) ;PS, PE, SM levels of low concentration of lecithin and arsenic group[(0.058 ± 0.020), (0.086 ± 0.177), (0.048 ± 0.103)g/L] significantly reduced (all P < 0.05), the PC did not change significantly [(0.521±0.098 )g/L, P > 0.05]. Compared with model group,the levels of PS, PE, PC, SM in high concentration of lecithin and arsenic group were significantly higher(all P <0.05);PS, PE, SM levels in low concentration of lecithin and arsenic group did not change significantly(all P > 0.05), and PC was significantly higher(P < 0.05). Conclusions High concentration lecithin has certain protective effect on Vero cell membrane exposured to sodium arsenite.     

亚砷酸钠诱导人膀胱上皮细胞环氧化酶2和前列腺素E2表达的实验观察

目的 观察不同浓度亚砷酸钠(NaAsO2)对人膀胱上皮细胞(SV-HUC-1)环氧化酶2(COX-2)和前列腺素E2(PGE2)表达的诱导作用.方法 不同浓度NaAsO2[0(对照)、1、2、4、8、10 μmol/L]作用于SV-HUC-1细胞24h后,应用实时定量(RT)-PCR法检测SV-HUC-1细胞内COX-2 mRNA表达水平,酶联免疫吸附试验(ELISA)测定细胞培养液中PGE2含量.结果 与对照组(1.00±0.00)比较,2、4、8、10μmol/L NaAsO2 组SV-HUC-1细胞内COX-2 mRNA表达(1.73±0.25、245±0.23、1.94±0.71、1.75±0.43)明显升高(P均＜0.05),并且4μmol/L NaAsO2组SV-HUC-1细胞内COX-2 mRNA表达达到最高;随NaAsO2浓度的增高,细胞培养液中PGE2含量呈升高趋势,表现为剂量反应关系,其中4、8、10 μmol/L NaAsO2组细胞培养液中PGE2含量[(9.59±1.27)、(10.40±2.19)、(12.93±1.33)ng/g]明显高于对照组[(6.64±1.46)ng/g,P均＜0.05].结论 NaAsO2能够诱导SV-HUC-1细胞COX-2 mRNA表达和PGE2分泌.     

tBHQ对无机砷诱导HaCaT细胞凋亡中的保护作用

目的观察tBHQ对内源性线粒体凋亡通路和凋亡相关蛋白Bel-2等蛋白表达的影响,探讨tBHQ在无机砷诱导HaCaT细胞凋亡过程中的作用。方法采用分光光度法检测Caspase-3蛋白活力;Westernblot法分析细胞内Caspase-3、CytC、Bcl-2和Bax蛋白表达水平。结果NaAsO2单独作用于HaCaT细胞24h,线粒体中CytC蛋白表达降低,而胞浆中CytC蛋白表达则随染砷剂量的增加而明显升高。tBHQ预处理12h后再分别暴露于NaAsO2,线粒体中CytC蛋白表达明显恢复,胞浆中CytC蛋白表达则随tBHQ剂量的增加而明显回落。此外,NaAsO。单独作用于HaCaT细胞24h,Procaspase-3蛋白表达降低,而Caspase-3活化程度均显著高于对照组（P〈0．01）,tBHQ预处理12h后再暴露于NaAsO2,Procaspase-3蛋白表达均明显高于相同浓度砷单独作用组,而且Caspase-3酶活力得到明显抑制,差异均具有统计学意义（P〈0．05）。NaAsO：单独作用于HaCaT细胞24h,与对照组相比Bcl-2蛋白表达降低,而Bax蛋白表达明显升高。tBHQ预处理12h后再分别暴露于NaAsO2,Bcl-2蛋白表达明显恢复,而Bax蛋白表达则随tBHQ剂量的增加而减少。结论tBHQ能够影响线粒体凋亡途径拮抗NaAsO2诱导的人皮肤角质细胞凋亡;tBHQ能够诱导调控凋亡相关蛋白Bcl-2／Bax从而发挥抗凋亡作用。     

不同剂量亚砷酸钠染毒大鼠多药耐药相关蛋白2表达水平的变化

目的观察不同剂量亚砷酸钠染毒大鼠肝细胞膜转运蛋白——多药耐药相关蛋白2(multidrugresistance-associatedprotein2,MRP2)表达水平的变化及与砷代谢的关系。方法24只健康雄性Wistar大鼠随机分为4组:第1组为对照组,给予生理盐水;第2～4组为染砷组,分别给予4、10和20mg/kg体质量的亚砷酸钠溶液,隔天灌胃染毒1次,2周后将大鼠处死。原子吸收分光光度法测定胆汁、全血和肝组织中的总砷含量。蛋白印记法测定肝细胞膜上MRP2的改变。结果经方差分析检验,胆汁和肝脏中含砷量随着染砷剂量的增加而逐渐增加(P<0.05)。两两比较发现,3个染毒组的血砷与对照组之间差异有统计学意义,而3个染毒组间差异无统计学意义。随着染砷剂量增加,MRP2表达有增加的趋势,且MRP2表达量与胆汁含砷量呈正相关(r=0.986,P<0.05)。结论亚砷酸钠可以诱导MRP2的表达,随染砷剂量增加,MRP2表达量增加。MRP2在砷及其代谢产物的胆汁排泄过程中发挥了重要作用。     

姜黄素对砷中毒小鼠急性肝脏毒性与氧化损伤的拮抗作用观察

目的探讨姜黄素对砷中毒小鼠急性肝脏毒性与氧化损伤的拮抗作用。方法选取60只健康的昆明种雌性小鼠,将60只小鼠分为对照组、单纯染毒组、干预组1和干预组2。对照组6只,单纯染毒组、干预组1和干预组2各18只。各实验组小鼠以自由饮水方式饮用浓度为10mg/L、50mg/L、100mg/L的含砷水,时间6周。干预组1、2分别给予姜黄素以200mg/kg、600mg/kg剂量进行灌胃干预,每周2次。对各实验组小鼠肝脏丙二醛含量、血清谷草转氨酶及谷丙转氨酶水平、肝脏和全血谷胱甘肽含量进行测定。结果单纯染毒组血清谷草转氨酶和谷丙转氨酶水平高于对照组,差异具有统计学意义(P0.05)。单纯染毒组各水砷浓度条件下肝脏丙二醛含量均高于对照组,差异具有统计学意义(P0.05)。水砷浓度相同的条件下,与单纯染毒组比较,干预组1及干预组2谷丙转氨酶和谷草转氨酶水明显降低,肝脏丙二醛含量下降,全血和肝脏谷胱甘肽含量上升,差异均具有统计学意义(P0.05)。结论姜黄素对砷中毒小鼠急性肝脏毒性与氧化损伤具有一定的拮抗作用。     

Protective effects of apocynin and allopurinol on ischemia/reperfusion-induced liver injury in mice

AIM： To determine the effects of allopurinol, an inhibitor of xanthine oxidase, and apocynin, an inhibitor of NADPH oxidase, on oxidant stress and liver injury caused by hepatic ischemia/reperfusion （I/R） procedure in mice.
METHODS： Mice were pretreated with a xanthine oxidase inhibitor, allopurinol, or NADPH oxidase （NOX） inhibitor, apocynin before the hepatic I/R procedure. Then treated or untreated mice underwent the hepatic I/R procedure. The effects on hepatic injury and superoxide anions were determined after starting reperfusion.
RESULTS： A standard warm hepatic I/R procedure led to a marked increase in superoxide anion production as indicated by a superoxide anion tracer, MCLA. At the same time, the procedure caused profound acute liver injury, as indicated by elevated serum alanine aminotransferase and tumor necrosis factor-α levels, reduced liver glutathione levels and elevated malondialdehyde contents, as well as a high apoptotic cell count. All these changes were reversed by the use of apocynin or allopurinol prior to the hepatic I/R procedure.
CONCLUSION： Allopurinol and apocynin exerted protective effects on hepatic ischemia/reperfusion injury. The protection is associated with blocking the generationof superoxide anions during the hepatic I/R procedure by inhibiting xanthine oxidase and NADPH oxidase activity.     

氧自由基清除剂对砷所致细胞DNA损伤的保护作用

目的：探讨砷引起细胞DNA损伤和细胞毒性的机理。方法：用羟基自由基（．OH／OH－）清除剂DMSO和过氧化氢（H2O2）清除剂过氧化氢酶（catalase,CAT)与不同浓度的砷共同处理人类早幼粒细胞系HL60细胞和人淋巴细胞,用单细胞凝胶电泳（SCGE）检测细胞DNA损伤,结果：2．4和4．8umol的砷分别引起了HL60的人淋巴细胞显著的DNA损伤,DMSO和CAT完全消除了低剂量砷引起的DNA损伤,减少了70％以上的高剂量砷引起的DNA损伤。结论：微量砷可引起人类细胞不同程度的DNA损伤,DMSO和CAT可保护或减轻细胞的这些损伤,表明砷通过活性氧自由基,主要是H2O2和O2－,引起人类细胞DNA损伤。     

NADPH氧化酶在氧化应激中的作用

NADPH氧化酶（Nox）是血管内生成活性氧簇（ROS）的主要酶体，在外来信号刺激下激活或失活，从而迅速升高或降低细胞内的ROS水平。ROS过多与炎性反应、甲状腺功能减退、糖尿病和心血管疾病的发生密切相关。Nox亚单位的表达与氧化应激、动脉硬化的发生相关；Nox在有丝分裂活跃的细胞和组织如肿瘤细胞中过度表达，使ROS水平升高。糖尿病患者细胞Nox的活性、p22^phox亚单位mRNA和蛋白质的表达均明显升高，p22^phoxmRNA的升高与糖化血红蛋白（Hb）A1C水平和糖尿病病程呈正相关。通过抑制Nox减少ROS的产生，为有效防治ROS相关的临床疾病提供新思路和新的药物靶点。     

脂联素与氧化应激关系的研究进展

脂联素是具有抗炎、抗动脉粥样硬化作用的脂肪细胞因子，在肥胖、糖尿病、冠心病等患者中血浆脂联素均降低，其机制尚未明确。体外培养及动物实验显示，氧化应激抑制脂联素mRNA表达和脂联素分泌，而脂联素又可调节氧化应激。临床研究显示，肥胖患者血浆脂联素与氧化应激指标呈负相关，在健康人两者无明显相关。脂联素可能抑制核因子-κB等途径，抑制氧化应激，具有抗氧化性。脂联素可能为治疗肥胖及肥胖相关性疾病提供新的药理靶点。     

Cd Se/Zn S quantum dots induce photodynamic effects and cytotoxicity in pancreatic cancer cells

AIM: To investigate the photodynamic effect of Cd Se/Zn S quantum dots(QDs) on pancreatic cancer cells and elucidate the probable mechanisms.METHODS: The pancreatic cancer cell line SW1990 was treated with different concentrations of Cd Se/Zn S QDs(0, 0.5, 1.0, 1.5, 2.0, 2.5 μmol/L), with or without illumination. The viability of SW1990 cells was tested using the Cell Counting Kit-8(CCK-8) assay. The ultrastructural changes of SW1990 cells were observed by transmission electron microscopy. Apoptosis was detected by nuclear staining and flow cytometry(FCM). Reactive oxygen species(ROS) were measured by dichlorofluorescein diacetate via fluorescence microscopy. Expression of Bax, Bcl-2 and caspase-3 was measured by real-time polymerase chain reaction(PCR) and protein immunoblotting 24 h after SW1990 cells were treated with Cd Se/Zn S QDs and illuminated.RESULTS: The CCK-8 assay results showed that both Cd Se/Zn S QDs with and without illumination suppressed SW1990 cell proliferation. Cell viability was significantly lower when illuminated or with a longer incubation time and a higher light dose. Cd Se/Zn S QDs with illumination caused ultrastructural changes in SW1990 cells, such as organelle degeneration and chromatin condensation and aggregation at the periphery of the nucleus. Fluorescence microscopy and FCM showed that Cd Se/Zn S QDs(1.5 μmol/L) with illumination increased SW1990 cell apoptosis(53.2%) and ROS generation compared with no illumination. Real-time PCR showed that expression of Bax and caspase-3 was upregulated and Bcl-2 was downregulated. Immunoblotting results were consistent with real-time PCR results. Inhibition of ROS and apoptosis both attenuated QD-photodynamictherapy-induced cell death.CONCLUSION: Cd Se/Zn S QDs can be used as a photosensitizer to inhibit SW1990 cell proliferation through ROS generation and apoptotic protein expression regulation.     

氧化应激与阻塞性睡眠呼吸暂停低通气综合征的研究进展

阻塞性睡眠呼吸暂停低通气综合征(OSHAS)是多种全身疾病的独立危险因素.OSHAS可导致慢性间歇性低氧、睡眠片段、睡眠结构紊乱和神经调节功能失衡.上述病理生理改变可引起体内活性氧增多,从而导致氧化应激,也有很多证据证明OSHAS患者体内存在氧化应激.氧化应激与各系统疾病密切相关.故氧化应激有可能在OSAHS各种并发症的发生发展中起着重要的作用.     

Total oxidative/anti-oxidative status and relation to bone mineral density in osteoporosis

The aim of this study was to evaluate the total antioxidant status (TAS), total oxidative status (TOS) and oxidative stress index (OSI) in patients with postmenopausal osteoporosis. We also investigate the relation between bone mineral density and oxidative/antioxidative parameters. Thirty-nine patients with osteoporosis and 26 healthy controls were included in the study. Plasma TAS, TOS levels were determined by using a novel automated methods. Plasma TOS and OSI value were significantly higher, and plasma TAS level was lower in patients than in healthy controls (P < 0.001 for all). There was a significant negative correlation between OSI and BMD in lumbar and femoral neck region (r = −0.63, P < 0.001; r = 0.40, P = 0.018). The results of this study indicated that increased osteoclastic activity and decreased osteoblastic activity may be associated with an imbalance between oxidant and antioxidant status in postmenopausal osteoporosis. Therefore, supplementation of antioxidant-enriched diet to the therapy might shed light on the development of novel therapeutic strategies for osteoporosis.     

关于氧化应激致动脉粥样硬化的研究进展

许多疾病状态如高血压、糖尿病、高胆固醇血症可产生过量的活性氧(ROS),引起氧化应激。近年研究显示,ROS在血管病变,尤其是在动脉粥样硬化中扮演重要角色。大量研究揭示,血管壁可产生多种ROS,它们独自或联合参与了动脉粥样硬化的形成过程。