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1.
目的探讨雌二醇对去卵巢后EAE大鼠的免疫抑制作用及其机制.方法制备去卵巢后10 d的EAE大鼠模型,随机分为EAE组、E2治疗组和佐剂组.E2治疗组在免疫后（post-inoculation,p.i.）0～5 d每日肌注E2（250μg/kg）一次.在p.i.6,8,10,12,14,16 d处死动物,用免疫组化技术检测脑和脊髓不同部位ICAM-1,IFN-γ的表达,并对EAE组ICAM-1和IFN-γ进行相关分析.结果与EAE组相比较,在p.i.6～12 d,E2治疗组血清E2浓度升高,临床症状评分降低,体重减轻减少,发病率较低,上述差异均有统计学意义;在p.i.10～16 d,E2治疗组ICAM-1与IFN-γ的表达降低,且具有统计学意义.EAE组ICAM-1与IFN-γ表达呈显著正相关性.结论E2能够有效抑制EAE,其抑制机制与E2下调ICAM-1,IFN-γ的表达进而促使Th细胞发生转分化有关。 相似文献
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《赤峰学院学报(自然科学版)》2017,(5)
目的:通过建立体外大鼠终板软骨细胞自然退变模型,探讨miR-125a-5p在自然传代诱导大鼠终板软骨细胞退变中的表达,通过生物信息学软件预测相关靶基因.方法:取大鼠原代终板软骨细胞,应用胰酶消化法和自然传代法培养终板软骨细胞,分别选取P2、P5、P8代细胞进行甲苯胺蓝及阿辛蓝染色观察细胞形态改变.qRT-PCR检测终板软骨细胞中miR-125a-5p表达情况,通过生物信息学软件预测相关靶基因.结果:细胞传到P5代时细胞由多角形变成长梭形,外基质分泌减少,细胞形态发生退变改变,qRT-PCR检测结果显示mi R-125a-5p表达含量随细胞代数增加逐渐减少.结论:大鼠终板软骨细胞自然传代至P5代出现退变改变,miR-125a-5p与终板软骨退变有密切联系. 相似文献
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目的 :探讨 p2 7Kip1、VEGF在胆管癌中的表达及相互关系。 方法 :采用免疫组化技术检测 32例胆管癌标本中p2 7Kip1及VEGF的表达。结果 :p2 7Kip1、VEGF在胆管癌和正常胆管组织中的阳性表达率分别为 5 6 .2 5 %和 11.1% (P <0 .0 1) ;81.2 5 %和 33.3% (P <0 .0 1)。p2 7Kip1、VEGF在胆管癌中的表达具有相关性 (P <0 .0 5 ) ,与分化程度、转移水平有关 ,与大小、生存期无关。结论 :p2 7Kip1、VEGF在胆管癌中高表达 ,p2 7Kip1、VEGF与胆管癌的发生、发展有关。 相似文献
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目的：探讨益肾活血平喘合剂对哮喘大鼠气道TGFβ1表达的影响。方法：健康雌性SD大鼠60只。随机分为4组,即正常组、模型组、地塞米松阳性对照组、益肾活血平喘合剂组,每组15只大鼠。除正常组外,其余3组均利用哮喘模型。各组于造模后14d开始每天给药及雾化吸入。造模后28d处死动物,取同一部位肺叶,包埋,切片,HE染色及免疫组化检测气道TGFβ1的表达。结果：益肾活血平喘合剂组气道TGFβ1的表达明显少于模型组（P〈0．01）及阳性对照组（P〈0．05）。结论：益肾活血平喘合剂通过抑制气道TGFβ1的表达,减轻哮喘气道炎症及重塑的发生。 相似文献
5.
目的:研究缺血对左室心肌细胞凋亡和凋亡相关基因表达的影响,探讨心肌细胞凋亡的分子机制。方法:采用结扎冠脉左前降支(LAD)法制作大鼠心肌缺血模型;运用DNA琼脂糖凝胶电泳技术鉴定基因组DNA的断裂情况;使用Northern Blot检测缺血心肌细胞p53、c-myc及bcl-2的表达活性。结果;a.缺血能够诱导左室心肌细胞凋亡;b.缺血明显上调p53基因的转录;c.缺血的左室心肌细胞c-myc mRNA含量显著增加;d.缺血减弱了bcl-2基因的转录。结论:内源性促凋亡基因p53、c-myc及抗凋亡基因bcl-2表达活性的改变介导了缺血诱导的心肌细胞凋亡,凋亡是心肌缺血时心肌细胞缺失的一个重要原因。 相似文献
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《莆田学院学报》2020,(2):57-61
观察p62/SQSTM1 (简称p62)在胃癌组织中的表达水平,探讨p62与自噬的关系及临床意义。采用免疫组织化学检测胃癌石蜡标本中p62的表达情况,并分析p62与临床病理资料及预后的关系,同时检测胃癌和癌旁新鲜组织中p62 mRNA及蛋白的表达水平。结果,190例胃癌石蜡标本中p62阳性率高于癌旁正常组织(P <0. 05); p62的表达与浸润深度、淋巴结转移、临床分期有关(P <0. 05); p62阳性患者5年生存率为33. 2%,低于p62阴性患者的55. 3%(P <0. 05);在新鲜胃癌组织中,p62 mRNA和蛋白的表达水平显著高于相应癌旁正常组织。结果表明:p62促进胃癌的发生发展及转移,是评估胃癌术后患者预后的一个重要标志。 相似文献
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慕博华 《泰州职业技术学院学报》2002,2(3):46-49
目的 探讨c erbB 2、p53和nm2 3蛋白在乳腺癌组织中的表达与乳腺癌临床病理参数、雌激素受体 (ER)、孕激素受体 (PR)的关系。方法 应用免疫组化ABC法对 5 5例乳腺癌组织中的c erbB 2、p53和nm2 3蛋白表达进行检测。结果 5 5例乳腺癌中c erbB 2、p53及nm2 3的阳性率分别为 49 1 % (2 7/5 5 )、47 3 % (2 6 /5 5 )和 49 1 % (2 7/5 5 ) ,c erbB 2和p53蛋白在乳腺癌中的阳性率与肿瘤病理分级及淋巴结转移有显著意义 (P <0 0 5 ) ,与雌孕激素受体状况呈负相关 (P <0 0 1 )。nm2 3蛋白在乳腺癌中的阳性率与肿瘤病理分级、淋巴结转移有密切的关系 (p <0 0 5 ) ,与雌孕激素受体状呈正相关 (p <0 0 1 )。 70 9% (3 9/5 5 )肿瘤有上述蛋白的异常表达 ,其中 49 1 % (2 7/5 5 )的肿瘤同时有多个蛋白异常表达。结论 肿瘤的多因素分析比单因素分析更有价值 ,癌基因c erbB 2、nm2 3和抑癌基因p53蛋白的表达异常及协同作用在乳腺癌的发生发展中起重要使用 相似文献
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探讨空间学习记忆训练后大鼠海马Caveolin-1（Cav-1）蛋白表达的变化。采用Morris水迷宫实验检测大鼠的空间学习记忆能力,WesternBlot方法检测大鼠海马Cav-1蛋白表达的变化。结果显示：水迷宫实验中,与青年训练组比,老年训练组大鼠的逃避潜伏期明显延长（P〈0．05,P〈0．01）,穿台次数明显减少（P〈0．05）,在原平台象限的停留时间明显缩短沪〈0．05）。WesternBlot检测表明,与青年和老年对照组比,青年和老年水迷宫训练组大鼠海马Cav-1蛋白表达显著增加（P〈0．05）;与青年对照组比,老年对照组大鼠海马Cav-1蛋白表达显著升高（P〈0．01）;与青年训练组比,老年训练组大鼠海马Cav-1蛋白表达显著升高（P〈0．01）。结果提示Cav-1蛋白可能参与了空间学习记忆过程。 相似文献
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目的:探讨影响大鼠胚胎成纤维细胞(REF)分离和培养的一些因素,以建立稳定的REF培养体系.方法:取SD大鼠胚胎分离成纤维细胞,利用体外培养体系,对REF的生长形态、生长曲线进行观察,以探讨不同胚胎日龄以及不同胰酶作用时间对REF分离及培养的影响,并对其进行免疫细胞化学鉴定.结果:13.5d 胎龄鼠胚的REF分离效果优于10.5d、18.5d 胎龄鼠胚;REF在体外为贴壁生长型细胞,第三代细胞增殖旺盛;并表达波形蛋白(vimentin)、层黏连蛋白(laminin,LN)和纤维连接蛋白(fibronectin,FN)蛋白.结论:13.5d 胎龄SD大鼠REF以H-DMEM做培养基,在第3代增殖旺盛,合成多种细胞外基质,最适宜作胚胎干细胞或其它悬浮培养细胞的饲养层. 相似文献
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目的:探讨意向性运动疗法干预后与神经可塑性相关的信号通路。创新点:首次发现意向性运动疗法干预后信号传导与转录激活因子3(STAT3)表达增高,以及STAT3直接调控神经可塑性相关基因。方法:将大脑中动脉梗死(MCAO)模型大鼠随机分为MCAO组、环境改变组和意向性运动疗法组。18天后测量三组大鼠的脑梗死面积。应用逆转录聚合酶链反应(RT-PCR)和荧光免疫染色法分别检测STAT3的基因和蛋白的表达;应用染色质免疫共沉淀检测STAT3是否绑定脑源性神经营养因子(BDNF)、突触素以及蛋白激酶Cα相互作用蛋白1(PICK1)。结论:研究结果显示:意向性运动疗法干预15天后,STAT3的基因与蛋白均增高;STAT3绑定皮层神经元BDNF、PICK1和突触素的启动子区;意向性运动干预后STAT3的升高可能与神经可塑性相关。 相似文献
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采用免疫组化技术和PCR-SSCP技术对高、中、低分化大肠腺癌、癌旁粘膜、正常粘膜及大肠腺瘤型息肉的P21、P53蛋白表达和K-ras基因、p53基因突变进行了检测,检测结果高、中、低分化大肠腺癌、癌旁粘膜、正常粘膜和大肠腺瘤型息肉六组P21蛋白表达阳性率分别为57.5％、62.5％、75％、13.3％、6.7％、50％,p53蛋白表达阳性率分别为30％、37.5％、50％、4.4％、22％、33.3％,K-ras基因突变率分别为32.5％、37.5％、62.5％、2.2％、0％、16.7％,p53基因突变率分别为22.5％、25％、37.5％、0％、0％、0％.结果表明大肠腺癌P21、P53蛋白表达比大肠腺瘤增多,但增加不显著(P>0.05), 二组均比癌旁粘膜和正常粘膜P21、P53蛋白表达阳性率高(P<0.01);大肠腺癌K-ras基因和p53基因突变率比大肠腺瘤、癌旁粘膜和正常粘膜组显著增加(P<0.01);高、中、低分化大肠癌各组中,随恶性程度增加,P21、P53蛋白表达增加,K-ras基因和p53基因突变率增加,但均不显著(P>0.05).说明K-ras基因、p53基因突变及其蛋白表达产物P21、P53在细胞癌变、癌细胞恶性表型维持中起重要作用。 相似文献
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INTRODUCTION Bronchioloalveolar carcinoma (BAC) is a par-ticular subtype of pulmonary adenocarcinoma de-rived from clara cell and type II pneumocyte. BAC cells grow along and within alveolar spaces while the alveolar framework of the lung is preserved. The incidence of BAC appears to be rising recently. The etiology and pathogenesis of this unique neoplastic disease are still unclear; many studies of oncogene and tumor suppressor gene expression include BAC with all adenocarcinoma o… 相似文献
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目的：探讨Skp2蛋白表达与上皮性卵巢癌发生、发展及预后评价的意义。方法：采用免疫组化法检测15例卵巢上皮性良性肿瘤、10例卵巢上皮性交界性肿瘤及58例上皮性卵巢癌中Skp2蛋白的表达情况。结果：Skp2在卵巢上皮性良性及交界性肿瘤中的表达均为阴性，而在上皮性卵巢癌中高表达，阳性率为48．28％（28／58），Skp2在中低分化组、Ⅲ／Ⅳ期组及有淋巴结转移组分别高于高分化组（P〈0．01）、Ⅰ／Ⅱ期组（P〈0．01）及无淋巴结转移组（P〈0．01）。在不同年龄及组织类型的卵巢癌中表达无显著性差异。结论：Skp2在上皮性卵巢癌中表达，表达水平越高提示预后越差。 相似文献
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INTRODUCTION Diabetes is the largest morbidity of patients with heart failure and adversely affects outcomes of car- diovascular diseases (Beller, 2001). Oxidative stress has been associated with the pathogenesis of chronic diabetic complications including cardiomyopathy (Cai and Kang, 2003). The ability of antioxidants to inhibit these injuries has raised the possibility of newer therapeutic treatment for diabetic heart dis- eases. Recently, Bcl-2 gene has been focused because it was in… 相似文献
15.
Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats 总被引：9，自引：0，他引：9
To investigate the inhibiting effect of β-Aescin on nuclear factor-κB(NF-κB)activation and the expression of tumornecrosis factor-α(TNF-α)protein after traumatic brain injury(TBI)in the rat brain,62 SD rats were subjected to lateral corticalimpact injury caused by a free-falling object and divided randomly into four groups:(1)sham operated(Group A);(2) injured(Group B);(3)β-Aescin treatment(Group C);(4) pyrrolidine dithocarbamate(PDTC) treatment(Group D).β-Aescin was ad-ministered in Group C and PDTC treated in Group D immediately after injury.A series of brain samples were obtained directly 6h,24 h and 3 d respectively after trauma in four groups.NF-κB activation was examined by Electrophoretic Mobility Shift Assay(EMSA);the levels of TNF-α protein were measured by radio-immunoassay(RIA);the water content of rat brain was measuredand pathomorphological observation was carried out.NF-κB activation,the levels of TNF-α protein and the water content of ratbrain were significantly increased(P＜0.0 相似文献
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17.
Zhao LL Chen HJ Chen JZ Yu M Ni YL Zhang WF 《Journal of Zhejiang University. Science. B》2008,9(6):448-454
Objective: To assess the effect of angiotensin Ⅱ type 1 (AT1) receptor antagonist losartan on myocardium connexin43 (Cx43) gap junction (GJ) expression in spontaneously hypertensive rats (SHRs) and investigate possible mechanisms. Methods: Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto (WKY) rats were included in this study. SHRs were randomly divided into two groups to receive losartan at 30mg/(kg·d) by oral gavage once daily for 8 weeks (SHR-L) or vehicle (0.9% saline) to act as controls (SHR-V); WKY rats receiving vehicle for 8 weeks served as normotensive controls. At the end of the experiment, rats were sacrificed and the hearts were removed. Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65) proteins in all three groups were observed and further investigations on the effect of angiotensin Ⅱ type 1 receptor antagonist losartan (30mg/(kg·d), 8 weeks) on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot. Results: Left ventricular (LV) hypertrophy was prominent in SHRs, Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface. Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium. The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment. Conclusion: Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy. Angiotensin Ⅱ type l receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles, possibly through the NF-κB pathway. 相似文献
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Purpose: To investigate the relationship between expression of cell cycle-related protein cyclin D1, p27kipl and the pathogenesis of bronchioloalveolar carcinoma (BAC) and the value of prediction of prognosis. Methods: Cyclin D 1 and p27kip 1 protein were detected by immunohistochemical En Vision method in 43 BACs. Results: The positivity of cyclin D 1 in BAC was 65.1% (28/43), which was significantly higher than that in normal pulmonary tissue (0/13), P＜0.01. No statistically significant association was found between cyclin D1 expression data and sex, age, tobacco-use history, histologic subtype (mucinous vs nonmucinous), stromal fibrosis, lymph node metastasis, clinical stage or postoperative survival period (P＞0.05), while cyclin D1 expression was found to be negatively correlated with tumor size (P＜0.05). The positivity of p27kipl in BACs was 51.2% (22/43), significantly lower than that in normal pulmonary tissue (12/13), P＜0.01. p27kipl expression level was not associated with sex, age, tobacco-use history, tumor size or histologic subtype (P＞0.05), but was negatively correlated with stromal fibrosis, lymph node metastasis and clinical stage (P＜0.05); and positively associated with postoperative survival period (P＜0.01). The survival rate of p27kipl positive group was significantly higher than that of p27kipl negative group (P＜0.01). No statistically significant correlation was found between cyclin D 1 and p27kipl expression. Conclusions: Increased cyclin D1 expression and decreased p27kip 1 expression are related to the pathogenesis of BAC;decreased p27kipl expression is associated with metastasis progression; immunodetection ofp27kip 1 is useful for assessment of prognosis. 相似文献
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Study on the neurotoxic effects of low-level lead exposure in rats 总被引：10，自引：0，他引：10
Objective: To investigate effects of developmental lead exposure on nitric oxide synthase (NOS) activity in different brain regions and on N-methyl-D-aspartate (NMDA) receptor mRNA expression in the hippocampus of rats. On the basis of these observations, we explored possible mechanisms by which lead exposure leads to impaired learning and memorizing abilities in children. Methods: A series of rat animal models exposed to low levels of lead during the developing period was established (drinking water containing 0.025%, 0.05% and 0.075% lead acetate). NOS activities in the hippocampus, the cerebral cortex, the cerebellum and the brain stem were determined with fluorescence measurement and levels of mRNA expression of the NMDA receptor 2A (NR2A) subunit and NMDA receptor 2B (NR2B) subunit in the rat hippocampus were measured with Retro-translation (RT-PCR). Results: There were no differences in the body weight of rat pups between any of the groups at any given time (P>0.05). The blood lead level of Pb-exposed rat pups showed a systematic pattern of change: at 14 d of age, it was lower than that at 7 d of age, then rising to the peak level at 21 d and finally falling to lower levels at 28 d. The hippocampal NOS activities of lead-exposed groups were all lower than that of the control group on the 21st and 28th day (P<0.01). NOS activities in the cerebellum of lead-exposed groups were all lower than that of the control group on the 21st and 28th day (P<0.001) and the NOS activity of the 0.025% group was significantly lower than that of the 0.05% and 0.075% groups on the 28th day (P<0.05). NOS activity in the cerebral cortex of the 0.075% group was significantly lower than that of the control, 0.025% and 0.05% groups on the four day spans (P<0.001). There was no significant difference of NOS activity in the brain stem between any lead-exposed group and the control group on the four day spans. In the 0.05% and the 0.075% groups, the level of NR2A mRNA expression was higher than that in the control group at 7 d and 14 d of age (P<0.05). In the 0.025% group, the level of NR2A was found to be higher than that in the control group at 7 d of age only (P<0.05). No significant differences were found for the levels of NR2B mRNA expression between any of the groups at any given time. Conclusions: NOS activity in the hippocampus, the cerebral cortex and the cerebellum are inhibited by lead exposure. The degree of the inhibitory effect depends on the time span of exposure and the lead concentration. Developmental low-level lead exposure was found to raise the level of NR2A mRNA expression in the hippocampus of rats. Developmental low-level lead exposure does not affect the level of NR2B mRNA expression in the hippocampus. 相似文献
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目的：探讨转化生长因子β1（TGF-β1）、半胱氨酸天冬氨酸蛋白酶3（Caspase-3）及肾母细胞瘤抑癌基因蛋白（WT1）在肾活检肾小球肾炎组织中的表达及其意义。方法：采用Envision法对40例肾小球肾炎组织及7例对照组肾组织进行TGF-β1、Caspase-3和WT1免疫组织化学染色标记、分析。结果：TGF-β1、Caspase-3、WT1在各种肾炎组织中均有表达,各实验组与对照组差异有统计学意义（P〈0.05）。TGF-β1在系膜增生性肾小球肾炎组的表达明显低于膜性肾病组（t=-4.131,P=0.002）;Caspase-3在各组别中其表达差异无统计学意义;WT1在大量高蛋白尿组表达低于非大量蛋白尿组（t=-2.130,P=0.046）;其余组别差异无统计学意义。WT1的低表达与TGF-β1、Caspase-3的高表达相关。结论：TGF-β1、Caspase-3表达的上调及WT1表达的下调与肾病理改变密切相关,蛋白尿和足细胞减少可能是肾脏病进展的预测因子及肾小球硬化的原因。 相似文献