钒对睾丸支持细胞／生精细胞的体外毒性研究

钒对睾丸支持细胞／生精细胞的体外毒性研究李宏霞，杨在昌，张天宝，曾祥贵（成都华西医科大学环境卫生学教研室６１００４１）已有研究表明，Ｖ２Ｏ５对雄性大鼠有明确的生殖毒性，但对其毒作用机制尚缺乏深入的研究。本实验在建立大鼠支持细胞／生精细胞（Ｓｅｒｔｏｌ...     

纳米氧化铝对大鼠肝组织细胞促凋亡作用研究

目的：纳米氧化铝（NAOs）是广泛应用的纳米材料,通过比较NAOs颗粒及非纳米氧化铝（nNAOs）颗粒对大鼠肝脏的影响研究其潜在的毒性作用。方法：将60只SD大鼠随机分为生理盐水对照组、50mg/kgNAOs组、50mg/kgnNAOs组,每组20只,隔日腹腔注射1次,共60d。采用原子吸收分光光度法测定铝元素在肝组织中含量的变化;免疫组织化学染色观察肝组织中枯否细胞（Kupffercells）的活化;RT-PCR检测凋亡相关基因Bax及Bcl-2mRNA表达的改变。结果：NAOs组大鼠肝脏中铝元素的浓度在染毒第4日达到峰值后逐渐降低,而nNAOs组大鼠肝脏中铝元素的浓度随染毒时间的延长而逐渐升高,两组大鼠均观察到枯否细胞的活化。nNAOs组Bax/Bcl-2比值为1.78,NAOs组为3.59,均显著高于对照组1.0（P均〈0.05）,且NAOs组与nNAOS组间的差异有统计学意义（P〈0.05）。结论：NAOs及nNAOs均能引起大鼠肝组织中枯否细胞活化,但NAOs引起肝组织细胞凋亡的程度高于nNAOs,可能与两种不同粒径的氧化铝在肝组织的代谢特征不同有关。     

长期摄入酒精对大鼠生精细胞增殖和凋亡的影响

目的：观察长期摄入酒精对大鼠生精细胞增殖和凋亡的影响,以探讨酒精致生精功能障碍的机制。方法：40只健康雄性成年SD大鼠随机分为3个不同酒精剂量的实验组（2.7、4.5、7.5g/kg）和1个对照组（蒸馏水）,共4组。各组每日分别灌胃给予受试物,连续13周,末次给予受试物24h后处死大鼠。在光镜下观察睾丸组织形态学,采用原位末端标记（TUNEL）法检测睾丸生精细胞凋亡,用流式细胞术（FCM）检测生精细胞凋亡率和计数各级生精细胞。用Western blot检测睾丸中Caspase-3以及核增殖抗原PCNA的表达。结果：光镜观察显示酒精组,尤其是7.5g/kg剂量组动物睾丸出现生精细胞核固缩、变性等细胞凋亡形态学改变,曲细精管腔中脱落细胞增多,且随酒精剂量的增加生精细胞的损伤加重。酒精4.5、7.5g/kg剂量组生精细胞凋亡率明显升高,FCM检测单倍体和四倍体细胞群计数下降（P〈0.05或P〈0.01）,PCNA表达降低（P〈0.05）,Caspase-3表达明显增强（P〈0.05或P〈0.01）。结论：长期摄入酒精可以诱导生精细胞凋亡增加和PCNA表达减弱,这可能是酒精致生精功能障碍的机制之一。     

缺血性急性肾损伤大鼠肾小管细胞凋亡及caspase-3表达

目的观察缺血性急性肾损伤(IAKI)大鼠肾小管细胞凋亡微细结构及caspase-3表达变化。方法应用光学和透射电镜技术、免疫组织化学和免疫印迹技术对缺血性急性肾损伤大鼠肾小管的细胞凋亡进行系统观察,并对caspase-3表达变化进行分析。结果肾缺血60 min再灌注24 h后,近髓质和髓质外带的近端小管出现了大量散在的凋亡细胞;凋亡细胞皱缩,核染色质固缩边聚,多数凋亡细胞脱落到小管腔内随尿液排除,小部分形成凋亡小体被邻近细胞所吞噬,在凋亡细胞内可见较多的自噬小体和自噬溶酶体。应用caspase-3免疫组化染色观察和免疫印迹分析结果显示,经caspase家族激活途径的细胞凋亡构成了IAKI诱导的近端小管细胞凋亡。结论大鼠肾缺血60 min再灌注24 h部分近端小管细胞发生了凋亡,推测这种细胞凋亡可能属于caspase依赖的细胞死亡;自噬作用参与了凋亡细胞处理细胞器的过程。     

磁性纳米四氧化三铁增强青蒿琥酯诱导的K562细胞凋亡及作用机制研究

本研究旨在观察青蒿琥酯共聚磁性纳米四氧化三铁（MNPs-Fe3O4）后,对K562细胞的细胞毒性效应以及是否增加K562细胞的凋亡,了解MNPs-Fe3O4是否可以增强青蒿琥酯的活性,并进一步探讨其可能的机制。方法:采用Western印迹检测K562细胞Bcl-2、Bax、Bcl-rambo,激活的Caspase-3和Survivin蛋白的表达,应用MTT法检测青蒿琥酯共聚MNPs-Fe3O4后对K562的细胞毒性,用流式细胞仪检测K562细胞的凋亡率。结果:青蒿琥酯可以抑制K562细胞的增殖,当青蒿琥酯共聚MNPs-Fe3O4后,对K562细胞的增殖抑制率显著高于单用青蒿琥酯组（P<0.05）,同时检测细胞凋亡率也发现,与单用青蒿琥酯组相比,青蒿琥酯共聚MNPs-Fe3O4组的细胞凋亡率显著增加,结果提示MNPs-Fe3O4可以增强青蒿琥酯的活性。而当加入泛Caspase抑制剂Z-VAD-FMK以后,MNPs-Fe3O4增强青蒿琥酯诱导细胞死亡的效应则被减弱了。Western印迹显示,青蒿琥酯共聚MNPs-Fe3O4组与单用青蒿琥酯组相比,Bcl-2,Bax,Bcl-rambo和Caspase-3蛋白的表达上调,而Survivin蛋白的表达则是下调的。结论:磁性纳米四氧化三铁可以增强青蒿琥酯诱导的K562细胞凋亡,其机制可能与上调Bcl-rambo和下调Survivin蛋白有关。      

X射线对血管平滑肌细胞作用机制的实验研究

目的：研究X射线外照射对体外原代培养的大鼠血管平滑肌细胞（VSMC）生长、增殖的影响及作用机制。方法：体外培养VSMC,给予单次8MVX射线照射,源皮距为100cm,剂量率400cGy/min。按照射剂量分为2、5、10、20Gy组,以0Gy为对照组,分别采用细胞计数法,克隆形成实验、四唑盐（MIT）比色实验、伊红排斥实验,流式细胞术及末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）技术,动态观察对VSMC生长、增殖、死亡率、凋亡的影响。结果：①照射后24hVSM数降低,72h后明显恢复（P＜0．05）。②照射后48h内VSMC吸光度（A570）值降低,72h2、5Gy组A570值升高,而10、15、20Gy组各高不明显（P＜0．05）。③72h内10、15、20Gy组VSMC死亡率较高,6d后,各剂量组死亡率下降至较低水平（P＜0．05）。④克隆形成实验提示X坶照射可直接导致NA链断裂,引起细胞死亡。⑤碘化丙啶（PI）染色流式细胞仪直方图上可见亚二倍体峰,TUNEL法阳性细胞核呈棕黄色,荧光镜下可见凋亡小体。结论：X射线外照射可抑制VSMC的生长和增殖,可能通过两种不同的机制即致死性和（或）亚致死性损伤及诱导凋亡导致SMC死亡。为应用放射治疗防治血管成形术后再狭窄提供了理论依据。     

PCB153对原代培养大鼠睾丸支持细胞SOD活性、DNA损伤及凋亡的影响

目的：探讨2,2′,4,4′,5-五氯联苯（2,2′,4,4′,5-hexachlorobiphenyl,PCB153）暴露对原代培养大鼠睾丸支持细胞（Sertoli cells,SC）超氧化物歧化酶（superoxide dismutase,SOD）活性、DNA损伤、细胞凋亡的影响以及抗氧化剂N-乙酰半胱氨酸（N-acetyl-L-cysteine,NAC）的干预作用。方法：原代培养出生18～20d雄性SD大鼠的睾丸支持细胞,设PCB153不同浓度的染毒组（加入10、20、30μmol/L PCB153）,NAC组（以300μmol/L NAC预处理1h后加入30μmol/L PCB153）,和对照组（加入与PCB153最大染毒量等体积的DMSO）,各组细胞经上述处理后继续培养24h,用SOD试剂盒测定各组细胞SOD活性,彗星实验测定DNA损伤程度,流式细胞术检测细胞凋亡,细胞荧光标记观察凋亡形态。结果：染毒24h后,大鼠睾丸支持细胞SOD活性随着PCB153染毒剂量的升高而降低,20、30μmol/L染毒组显著低于对照组（P〈0.05）,NAC预处理可提升SOD活性（P〈0.05）。各PCB153处理组及NAC预处理组与对照组相比,DNA损伤间的差异均无统计学意义（P〉0.05）,细胞凋亡率则均显著增加（P〈0.05）,NAC预处理可降低PCB153所致的凋亡率（P〈0.05）。结论：10～30μmol/L PCB153染毒24h可诱导的原代培养大鼠SCSOD活性降低,细胞凋亡增加,但并未引起DNA损伤,NAC预处理具有保护作用。     

碘对不同性别大鼠甲状腺细胞凋亡及相关蛋白表达的影响

目的观察短期碘摄入量异常对大鼠甲状腺滤泡上皮细胞凋亡及凋亡相关基因Bcl-2、Bax蛋白水平的表达及其在不同时间段不同性别中的表达差异。方法 90只Wistar大鼠随机分为低碘组、正常组和高碘组,雌雄各半,通过饮食饮水控制使各组碘摄入量分别为0.6μg/d、6.15μg/d和61.5μg/d。分别在饲养7、14和28 d后,处死动物并分离甲状腺。HE染色,光镜下进行形态学观察;免疫组化染色,MIAS-2000型图像分析系统观察分析甲状腺细胞凋亡相关基因Bcl-2、Bax蛋白水平的表达。结果各时间段各组大鼠甲状腺滤泡上皮细胞均未检出细胞凋亡。Bcl-2、Bax在低碘组和正常组均为阴性表达,在高碘组的表达高于正常组,且有随时间延长而有增强的趋势,其中,14 d时Bax表达出现阳性;28 d时Bcl-2、Bax表达均为阳性且高于正常组(P均<0.01)。7、14 d时,高碘组Bax在两性别中均有表达,表达水平在两性别中无统计学差别;28 d时,高碘组Bcl-2、Bax表达水平雄性均高于雌性,且差别均有统计学意义(P均<0.01)。结论短期碘缺乏和碘过量均不引起细胞凋亡,短期碘缺乏对凋亡相关基因无明显影响,短期碘过量既可促进促凋亡基因表达亦可促进抑凋亡基因表达。性别因素对甲状腺细胞凋亡相关基因的表达存在一定的影响。     

大鼠睾丸支持细胞的分离、鉴定与培养

背景与目的:分离培养高纯度的大鼠睾丸支持细胞.材料与方法:选用SD雄性大鼠(18～21 d),处死取出睾丸,采用0.25%胰蛋白酶、0.05%胶原酶二步酶消化法结合低速离心分离支持细胞,置于35℃,5%CO2的培养箱培养,48 h后用20 mmol/LTris-HC1低渗处理培养细胞.0.25%胰蛋白酶消化后二次贴壁培养,用油红0染色和透射电镜观察对所培养的支持细胞进行鉴定,并用MTT法绘制细胞生长曲线.结果:分离培养的支持细胞纯度达95%,体外培养的对数生长期为4～9 d. 结论:采用二步酶消化法与低速离心及低渗处理法分离培养的支持细胞纯度高,用油红0染色鉴定支持细胞是一种简便快速的方法.     

细胞凋亡机制研究的新进展

细胞凋亡 (Ａｐｏｐｔｏｓｉｓ)是由于细胞内外环境变化或死亡信号触发以及在基因调控下所引起细胞主动死亡的过程 ,这一过程对于消除机体内老化细胞或具有潜在性异常生长的细胞 ,以至于保持机体处于稳定状态 (Ｈｏｍｅｏｓｔａｓｉｓ)起着重要的作用。体内细胞凋亡调控机制发生紊乱将可引起人体发生多种疾患 ,其中肿瘤的形成及老年痴呆症均属这类典型的疾患[1] 。近年来 ,细胞凋亡的分子机制的研究取得了突破性进展 ,现已证明多种基因产物参与细胞凋亡过程 ,其中包括肿瘤坏死因子受体 (ＴＮＦＲ)基因超家族的产物即死亡受体 (Ｄｅａｔｈｒ…     

The effect of thermotherapy using magnetic nanoparticles on rat malignant glioma

Summary Thermotherapy using magnetic nanoparticles is a new technique for interstitial hyperthermia and thermoablation based on magnetic field-induced excitation of biocompatible superparamagnetic nanoparticles. To evaluate the potential of this technique for minimally invasive treatment, we carried out a systematic analysis of its effects on experimental glioblastoma multiforme in a rat tumor model. Tumors were induced by implantation of RG-2-cells into the brains of 120 male Fisher rats. Animals were randomly allocated to 10 groups of 12 rats each, including controls. Animals received two thermotherapy treatments following a single intratumoral injection of two different magnetic fluids (dextran- or aminosilane-coated iron-oxide nanoparticles). Treatment was carried out on days four and six after tumor induction using an alternating magnetic field applicator system operating at a frequency of 100 kHz and variable field strength of 0–18 kA/m. The effectiveness of treatment was determined by the survival time of the animals and histopathological examinations of the brain and the tumor. Thermotherapy with aminosilane-coated nanoparticles led up to 4.5-fold prolongation of survival over controls, while the dextran-coated particles did not indicate any advantage. Intratumoral deposition of the aminosilane-coated particles was found to be stable, allowing for serial thermotherapy treatments without repeated injection. Histological and immunohistochemical examinations after treatment revealed large necrotic areas close to particle deposits, a decreased proliferation rate and a reactive astrogliosis adjacent to the tumor. Thus, localized interstitial thermotherapy with magnetic nanoparticles has an antitumoral effect on malignant brain tumors. This method is suitable for clinical use and may be a novel strategy for treating malignant glioma, which cannot be treated successfully today. The optimal treatment schedules and potential combinations with other therapies need to be defined in further studies.     

单纯缺氧对大鼠心脏功能和结构影响的定量研究

目的定量研究在缺氧情况下,心脏结构和功能改变及其规律。方法W istar大鼠40只,雌雄各半,随机分为对照组和单纯缺氧组,置于本课题组设计并研制的常压低氧舱（氧浓度为10%）,采用生化、常规病理、超微病理、分子病理和定量病理等多种技术方法,对缺氧后心脏功能、结构和心肌细胞凋亡进行观察。结果缺氧后大鼠心肌酶谱（LDH、AST和CK）均明显高于正常值,且随实验时间延长而增加; PO2在缺氧1-7 d内呈持续性进行性下降,PCO2于缺氧1 d时显著升高,而于3-7 d内则呈持续性下降。pH值于缺氧1 d时显著低于正常对照组、而于3-7 d内则迅速恢复到对照组的水平。HCT（%）于缺氧1-7 d内呈持续性进行性升高; 缺氧后大鼠心肌细胞肿胀、变性、凋亡、坏死; 心肌纤维排列紊乱; 间质细胞肿胀、退变; 心肌细胞凋亡指数增加。结论缺氧引起大鼠心脏功能和结构明显损伤,且随缺氧时间延长呈进行性加重趋势; 缺氧后心肌细胞凋亡指数增加,可作为缺氧时心脏损伤的一个重要指标。     

长链非编码RNA CCAT2对结肠癌细胞增殖和凋亡的影响及机制探讨

目的:观察长链非编码RNA（lncRNA）结肠癌相关转录本2（CCAT2）在结肠癌细胞系中的表达及对细胞增殖和凋亡的影响,并探讨其机制。方法:采用荧光定量PCR技术（qRT-PCR）检测结肠癌细胞系HCT116、SW620、LOVO、HT29与正常结肠上皮细胞系NCM460中lncRNA CCAT2的表达。将结肠癌细胞系SW620分成CCAT2-siRNA组、Control-siRNA组及Mock组,CCAT2-siRNA组和Control-siRNA组经LipofectamineTM 2000分别转染CCAT2-siRNA及Control-siRNA,Mock组以PBST作对照。MTT实验和流式细胞术分别测定增殖和凋亡能力,Western blot测定p53、裂解型聚腺苷二磷酸-核糖聚合酶（PARP）及B细胞淋巴瘤/白血病-2（Bcl-2）蛋白的表达。结果:lncRNA CCAT2在结肠癌细胞系LOVO、HT29、HCT116、SW620中均比正常结肠上皮细胞系NCM460表达水平升高（P＜0.05)。MTT示:转染后0 h、24 h、48 h,CCAT2-siRNA组与Control-siRNA组OD490 nm值差异无统计学意义（P＞0.05)。转染后72 h、96 h,CCAT2-siRNA组OD490 nm值低于Control-siRNA组（P＜0.05)。CCAT2-siRNA组细胞凋亡率高于Control-siRNA组（P＜0.01）。与Control-siRNA组相比,CCAT2-siRNA组p53、裂解型PARP表达上调,Bcl-2蛋白表达下调。结论:lncRNA CCAT2在结肠癌细胞系中高表达,敲低lncRNA CCAT2表达可抑制结肠癌细胞增殖,并诱导凋亡,其机制可能与p53、裂解型PARP表达上调,Bcl-2蛋白表达下调有关。     

硒干预对DEHP暴露下SD大鼠血细胞参数的作用

目的：探讨不同剂量邻苯二甲酸二（2-乙基）己酯（DEHP）染毒后硒对大鼠外周血血细胞参数的影响。方法：将77只健康清洁级雄性SD大鼠,随机分为7组,即对照组、3个不同浓度（300、600、900 mg/kg）DEHP染毒组、1 mg/kg Se+不同剂量（300、600和900 mg/kg）DEHP染毒干预组,连续饲喂90 d,试验期间观察大鼠中毒状况（精神亢奋、被毛蓬松、局部脱毛现象）,试验期末称取大鼠体质量并取全血测定各类血细胞参数的变化。结果：与对照组比较,900 mg/kg DEHP染毒大鼠体质量明显下降（P < 0.05）,600和900 mg/kg DEHP染毒组大鼠出现中毒体征比例分别为63.63%（7/11）和100%（11/11）,均较对照组0（0/11）显著升高（P均 < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se干预后大鼠体质量均明显增加,差异均有统计学意义（P均 < 0.05）;300、600 mg/kg DEHP染毒组大鼠中毒体征明显降低（P均 < 0.05）。白细胞参数中,与对照组比较,600和900 mg/kg DEHP染毒组大鼠白细胞数（WBC）明显降低、单核细胞（MONO）显著升高,差异均有统计学意义（P均 < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se+600 mg/kg DEHP干预组白细胞数（WBC）明显升高、单核细胞（MONO）显著降低（P < 0.05）。红细胞参数中,与对照组比较,DEHP染毒后大鼠平均血红蛋白量（MCH）、血红蛋白含量分布宽度（HDW）均明显升高;600、900 mg/kg DEHP染毒组大鼠红细胞数（RBC）、红细胞压积（HCT）明显降低（P < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se干预后大鼠红细胞参数未见显著差异。血小板参数中,未发现DEHP染毒与Se干预对SD大鼠血小板各参数产生显著影响。结论：300~900 mg/kg DEHP染毒可对大鼠某些红细胞和白细胞参数产生影响,硒的干预在300~600 mg/kg DEHP染毒条件下可保护某些血细胞功能。     

Bioavailability and dose-dependent anti-tumour effects of 9-cis retinoic acid on human neuroblastoma xenografts in rat.

Neuroblastoma, the most common extracranial solid tumour in children, may undergo spontaneous differentiation or regression, but the majority of metastatic neuroblastomas have poor prognosis despite intensive treatment. Retinoic acid regulates growth and differentiation of neuroblastoma cells in vitro, and has shown activity against human neuroblastomas in vivo. The retinoid 9-cis RA has been reported to induce apoptosis in vitro, and to inhibit the growth of human neuroblastoma xenografts in vivo. However, at given dosage, the treatment with 9-cis RA caused significant toxic side effects. In the present study we investigated the bioavailability of 9-cis RA in rat. In addition, we compared two different dose schedules using 9-cis RA. We found that a lower dose of 9-cis RA (2 mg day(-1)) was non-toxic, but showed no significant effect on tumour growth. The bioavailability of 9-cis RA in rat was 11% and the elimination half-life (t1/2) was 35 min. Considering the short t1/2, we divided the toxic, but tumour growth effective dose 5 mg day(-1) into 2.5 mg p.o. twice daily. This treatment regimen showed no toxicity but only limited effect on tumour growth. Our results suggest that 9-cis RA may only have limited clinical significance for treatment of children with poor prognosis neuroblastoma.     

纳米羟基磷灰石对人骨肉瘤细胞U2OS增殖和凋亡的影响

目的:探索纳米羟基磷灰石（Nano-HAP）对人骨肉瘤细胞U2OS增殖和凋亡的影响。方法:不同浓度的Nano-HAP处理人骨肉瘤细胞U2OS后,通过FDA染色检测Nano-HAP对细胞黏附的影响;CCK8实验和克隆形成实验检测Nano-HAP对细胞生长增殖的影响;最后利用Annexinv-FITC凋亡检测试剂盒检测Nano-HAP对细胞凋亡的影响。结果:不同浓度的Nano-HAP对U2OS的黏附没有显著影响,但是对U2OS的克隆形成具有显著抑制作用,同时在50 μg/ml 和800 μg/ml时,可以显著抑制骨肉瘤细胞U2OS的增殖。结论:Nano-HAP对骨肉瘤细胞具有显著的抑制增殖促进凋亡作用,但效应与纳米粒子浓度并无直接的线性关系。     

Evaluation of the cytotoxic effects of hyperthermia and 5-fluorouracil-loaded magnetic nanoparticles on human colon cancer cell line HT-29

The purpose of this study was to evaluate the combined effects of heat and polylactic-co-glycolic acid (PLGA) nanoparticles, as 5-fluorouracil carriers with/without iron oxide core, on the viability and proliferation capacity of human colon cancer cell line HT-29 in the spheroid model. HT-29 spheroid cells were treated with different concentrations of 5-FU or 5-FU-loaded into both nanoparticles for 74?h. Hyperthermia was then performed at 43?°C for 60?min. Finally, the effects of the mentioned treatments on cell viability and proliferation capacity were evaluated using the trypan blue dye exclusion test and colony formation assay, respectively. Our results showed that hyperthermia, in combination with 5-FU or PLGA nanoparticles as 5-FU carriers, significantly enhanced the cytotoxic effects as compared to the control group. Considering that nanoparticles could increase the intracellular concentration of drugs in cancer cells, the extent of cytotoxic effects following treatment with 5-FU-loaded into both nanoparticles was significantly higher than that with free 5-FU. In addition, the presence of iron oxide cores in nanoparticles during hyperthermia enhanced the cytotoxic effects of hyperthermia compared with nanoparticles without iron oxide core. Based on this study, hyperthermia in combination with 5-FU-loaded PLGA nanoparticles with iron oxide core drastically reduced the proliferation capacity of HT-29 cells; therefore, it may be considered as a new direction in the treatment of colon cancer.     

Carboplatin toxic effects on the peripheral nervous system of the rat

Background: The most striking of carboplatin's advantages (CBDCA) over cisplatin (CDDP) is its markedly reduced rate of neurotoxic effects. However, the use of CBDCA higher-intensity schedules and the association with other neurotoxic drugs in polychemotherapy may cause some concern about its safety with respect to peripheral nervous system damage.Materials and methods: Two different schedules of CBDCA administration (10 mg/kg and 15 mg/kg i.p. twice a week for nine times) were evaluated in Wistar rats. Neurotoxicity was assessed for behavioral (tail-flick test), neurophysiological (nerve conduction velocity in the tail nerve), morphological, morphometrical and analytical effects.Results: CBDCA administration induced dose-dependent peripheral neurotoxicity. Pain perception and nerve conduction velocity in the tail were significantly impaired, particularly after the high-dose treatment. The dorsal root ganglia sensory neurons and, to a lesser extent, satellite cells showed the same changes as those induced by CDDP, mainly affecting the nucleus and nucleolus of ganglionic sensory neurons. Moreover, significant amounts of platinum were detected in the dorsal root ganglia and kidney after CBDCA treatment.Conclusions: CBDCA is neurotoxic in our model, and the type of pathological changes it induces are so closely similar to those caused by CDDP that it is probable that neurotoxicity is induced in the two drugs by the same mechanism. This model can be used alone or in combination with other drugs to explore the effect of CBDCA on the peripheral nervous system.     

长链非编码RNA H19对外阴鳞癌细胞A431增殖、迁移及凋亡的影响

目的:探讨长链非编码RNA H19在外阴鳞癌细胞系A431、人正常表皮细胞Hacat中的表达,及沉默H19表达后细胞增殖、迁移及凋亡的变化.方法:采用qRT-PCR方法检测A431细胞中H19的表达水平;用siRNA瞬时转染A431细胞,采用CCK8法、Transwell小室及Annexin V-FITC/PI双标记实验分别检测H19对A431细胞增殖、迁移及凋亡的影响.结果:H19在外阴鳞癌细胞系A431中的表达明显高于人正常表皮细胞Hacat,A431细胞中H19的表达下调能够抑制A431细胞的增殖及迁移能力,并且促进凋亡.结论:H19-siR-NA下调H19的表达,抑制A431细胞的增殖、迁移能力,促进凋亡,提示H19在外阴鳞癌中可能发挥促癌作用,其异常表达可能与外阴鳞癌的发生发展密切相关.