共查询到19条相似文献,搜索用时 250 毫秒
1.
目的观察1,25-二羟维生素D,[1,25-(OH)2D3]对高糖状态下人近端肾小管上皮细胞(HK-2)维生素D受体(VDR)以及血管紧张素Ⅱ(AngⅡ)表达的影响。方法体外培养HK-2细胞,实验分为对照组(糖浓度5.5mmol/L)、甘露醇组(19.5mmol/L)、高糖组(糖浓度25.0mmoL/L)、高糖+1,25-(OH),D,组(浓度1.0×10^-6、1.0×10^-7、1.0×10^-8mol/L)和高糖+1,25-(OH)2D3+siRNAVDR干扰组,实时荧光定量聚合酶链反应(PCR)法检测VDRmRNA表达,Westernblotting检测VDR蛋白表达,双荧光素酶报告基因系统检测VDR基因转录活性,放射免疫法检测AngⅡ含量。多个样本间比较采用单因素方差分析,两组间比较采用g检验。结果与对照组相比,高糖组HK-2细胞中VDRmRNA、蛋白的表达及基因转录活性均明显降低(分别为1.34±0.22比2.47±0.31、0.51±0.06比1.14±0.13、0.51±0.21比1.42±0.28,均P〈0.05)。1,25-(OH)2D3上调高糖条件下HK-2细胞中VDRmRNA、蛋白的表达及基因转录活性,且呈浓度依赖性(分别为1.964-0.31比1.34±0.22、0.934-0.08比0.51±0.06、1.12±0.23比0.51±0.21,均P〈0.05)。与对照组相比,高糖使HK-2细胞分泌AngⅡ增加[(88±10)比(17±2)ng/L,P〈0.05]。1,25-(OH)2D3浓度依赖性下调高糖诱导的AngII高表达[(44±5)比(884-10)ng/L,P〈0.05]。利用RNA干扰诱导VDR基因沉默后,1,25-(OH)2D3不能下调高糖诱导的AngⅡ高表达[(87±12)比(88±10)ng/L,P〉0.05]。结论1,25-(OH)2D,可能通过VDR介导的方式负性调节高糖环境下人肾小管上皮细胞AnglI表达,从而对糖尿病肾脏疾病的进展起到延缓作用。 相似文献
2.
人端粒保护蛋白1(hPOT1)的主要作用为保护端粒和调节端粒长度。目的:探讨hPOT1在人胃癌细胞中对端粒长度的调节作用及其可能机制。方法:以RNA干扰(RNAi)技术抑制人胃癌细胞株BGC-823中hPOT1的表达.以实时荧光定量聚合酶链反应(PCR)检测细胞端粒长度,以半定量逆转录聚合酶链反应(RT—PCR)检测人端粒酶逆转录酶(hTERT)mRNA表达。结果:以RNAi技术抑制hPOT1表达后,BGC-823细胞端粒长度明显缩短,反映端粒相对长度的T/S值显著小于亲本BGC-823细胞组和阴性对照组(1.383±0.091对2.758±0.647和3.043±0.548,P〈0.05),亲本细胞组与阴性对照组之间则无明显差异。hPOT1RNAi组细胞hTERTmRNA表达亦明显下调。结论:在人胃癌细胞中,hPOT1能正性调节端粒长度;在hPOT1下调引起端粒缩短的环节中,hTERT表达下降可能起一定作用。 相似文献
3.
端粒酶逆转录酶基因反义寡核苷酸抑制肺癌细胞端粒酶活性和诱导细胞凋亡 总被引:11,自引:0,他引:11
目的 研究端粒酶逆转录酶(hTERT)基因反义寡核苷酸(ASODN)对肺癌细胞端粒酶活性和细胞凋亡的影响。方法 实验分为ASODN组、正义寡核苷酸(SODN)组和空白对照组,所用ASODN和SODN的浓度分别为10μmol/L,脂质体为16mg/L,采用端粒重复扩增法、逆转录-聚合酶链反应、Western Blot及流式细胞术分别观察各组端粒酶活性、hTERP mRNA和蛋白质表达以及细胞凋亡。结果 ASODN组显著下调或抑制肺癌细胞端粒酶活性和hTERT表达,但直到第21天才出现细胞凋亡增多。结论 端粒酶活性与hTERT表达密切相关。 相似文献
4.
采用MTT试验比较了不同浓度的丁酸钠干预后,结肠癌HT-29细胞和结肠癌Lovo细胞的生长曲线变化,并采用流式细胞术研究了丁酸钠对结肠癌细胞周期的影响。结果与对照组相比,1.25mmol/L浓度组在各观察时间点均未显示出对Lovo细胞的抑制;2.5mmol/L以上浓度(2.5、5、10mmol/L)在各观察点显示出明显的生长抑制作用,各组之间差异有显著性(P〈0.01);随着丁酸钠浓度的升高,越来越多的HT-29细胞被阻滞在G0/G1期,越来越多的Lovo细胞处于G2/M期。证实丁酸钠对肿瘤细胞增殖的抑制作用具有浓度、时间依赖性,这种作用是通过G2/M期或G0/G1期阻滞实现的。 相似文献
5.
6.
目的:观察1,25二羟基维生素D3[1,25(OH)2D3]对成骨细胞增殖及其与乳腺癌细胞黏附的影响。方法取对数生长期人成骨细胞hFOB1.19,随机分为三组,正常对照组用DMEM/F12培养基培养;溶剂对照组用含0.1 mL/L乙醇的DMEM/F12培养基培养;1,25(OH)2D3组分别用含1×10-7、1×10-8、1×10-9、1×10-10mol/L 1,25(OH)2D3的DMEM/F12培养基培养。1~3 d后于酶标仪上450 nm处测定吸光度值,计算细胞增殖抑制率;采用微量酶标仪法检测hFOB1.19细胞培养上清中碱性磷酸酶( ALP)活力。取对数生长期人乳腺癌细胞MDA-MB-231、T47D,分组及处理同上,各组培养24 h后加入对数生长期hFOB1.19细胞,采用细胞黏附法计算MDA-MB-231或T47D与hFOB1.19细胞黏附率。结果正常对照组、溶剂对照组及1×10-7、1×10-8、1×10-9、1×10-10 mol/L 1,25(OH)2D3组细胞增殖抑制率第3天分别为0、-1.63%±2.04%、16.02%±1.13%、10.78%±0.98%、8.82%±2.59%、5.55%±0.57%,各组间比较,P均<0.05;ALP活力分别为(1.77±0.03)、(1.76±0.01)、(2.11±0.02)、(1.96±0.01)、(1.84±0.04)、(1.81±0.03)金氏单位/100 mL,1×10-7、1×10-8moL/L 1,25(OH)2D3组与其他四组比较,P 均<0.05;MDA-MB-231与 hFOB1.19细胞黏附率分别为58.80%±3.11%、59.80%±3.96%、42.00%±1.87%、46.40%±2.30%、53.80%±0.84%、57.00%±3.24%,T47D与hFOB1.19细胞黏附率分别为55.75%±2.22%、56.25%±1.71%、47.80%±3.11%、50.60%±2.07%、54.40%±2.70%、57.20%±1.48%,1×10-7、1×10-8moL/L 1,25(OH)2D3组与其他四组比较,P均<0.05。结论1,25(OH)2D3能抑制成骨细胞增殖,促进成骨细胞分化,降低乳腺癌细胞与成骨细胞的黏附。 相似文献
7.
目的研究酰基化ghrelin在高糖诱导的血管内皮细胞凋亡中的作用。方法通过Western-Blot、分光光度比色法分别检测Akt(Ser473)磷酸化水平及caspase-3活性。结果(1)不同浓度ghrelin(10^-6mol/L、10^-7mol/L)作用内皮细胞30min对Akt磷酸化作用的差异有统计学意义(P〈0.05),而ghrelin(10^-7mol/L、10^-8mol/L、10^-9mol/L)浓度之间没有统计学差异(P〉0.05),暴露于酰基化ghrelin(10^-7mol/L)中细胞内Akt迅速磷酸化,在30min达高峰。(2)P13K抑制剂LY294002可以减弱ghrelin对高糖(33.3mmol/L)环境下caspase-3活化的抑制作用。结论酰基化ghrelin通过P13K/Akt通路抑制高糖诱导的内皮细胞凋亡,在糖尿病血管并发症的防治中可能有一定的意义。 相似文献
8.
目的:研究端粒酶在肺良、恶性病变和正常肺组织中表达的定位,以阐明端粒酶在上述疾病发病机制中的作用,以及在正常肺组织中的生物学意义。方法:对38例肺癌、7例良性实质性病变及35例病灶旁正常肺组织标本用核酸原位杂交和免疫组织化学技术对端粒酶逆转录酶(hTERT)mRNA和蛋白质的定位表达进行了研究,同时与端粒酶活性进行了对比。结果:肺癌、良性实质性病变和病灶旁正常肺组织端粒酶活性阳性分别31/38、3/7、7/35(P<0.001);肺癌组织癌细胞、肺良性实质性病变中的淋巴细胞、纤维母细胞、巨噬细胞等以及病灶旁正常 肺组织小气道、细支气管上皮的部分细胞和少部分肺泡上皮细胞hTERT蛋白有阳性表达,在有淋巴小结的肺组织其生发中心可见hTERT表达,多数巨噬细胞也有hTERT阳性表达。hTERTmRNA所表达的细胞与免疫组织化学结果类似。肺癌hTERT免疫染色平均吸光度比较:鳞癌A值比腺癌略高,Ⅲ期比I期、Ⅱ期稍高,分化程度越低A值也越高,但P>0.05。结论:(1)端粒酶除了参与肺癌的发病机制外,也参与肺良性实质性病变发生发展。(2)端粒酶对于维持正常肺组织支气管上歧细胞、肺泡巨噬细胞和淋巴细胞的功能可能有重要的生物学意义。(3)端粒酶是一种增殖指标,而非肺癌的恶性特异性标志,端粒酶作为肺癌诊断标记物时可能有一定的假阳性。 相似文献
9.
目的探讨1,25(OH)_2D_3对脂多糖诱导下人肾小管上皮细胞(HK-2细胞)增殖与凋亡的影响。方法体外培养HK-2细胞,随机分为正常对照组、脂多糖(1μg/ml)组、1,25(OH)_2D_3(10~(-8)mol/L)组、脂多糖联合1,25(OH)_2D_3组,干预培养48 h,采用细胞计数试剂盒(CCK)-8法检测各组HK-2细胞的增殖,流式细胞术分别检测各组HK-2细胞的细胞周期与细胞凋亡。结果与正常对照组比较,脂多糖组HK-2细胞增殖明显被促进,G0/G1期细胞明显减少,S期及G2/M期细胞明显增加,且细胞凋亡率明显下降;1,25(OH)_2D_3组HK-2细胞增殖明显被抑制,G0/G1期细胞明显增加,S期及G2/M期细胞明显减少,且细胞凋亡率明显增加。与脂多糖组比较,脂多糖联合1,25(OH)_2D_3组HK-2细胞增殖明显被抑制,G0/G1期细胞明显增加,S期及G2/M期细胞明显减少,且细胞凋亡率明显增加。结论 1,25(OH)_2D_3可抑制HK-2细胞的增殖,诱导其凋亡,且1,25(OH)2D3可逆转脂多糖对HK-2细胞的促增殖、抑制凋亡的作用。 相似文献
10.
碘对人甲状腺细胞凋亡的影响 总被引:18,自引:1,他引:18
目的:研究碘对人甲状腺细胞亡的影响,探讨其在甲状腺疾病发病机制中的作用和意义。方法:分别以不同浓度Nal刺激单层培养的人正常甲状腺上皮细胞,采用流式细胞术,Western印迹和半定量RT-PCR等方法分别检测刺激前后细胞凋亡率,凋亡相关蛋白Fas,Bcl-2和Bak以及Fas,可溶性Fas(sFas)mRNA表达的变化。并以ELISA法检测细胞培养液中sFas的含量。结果:(1)低浓度NaI(10^-8mol/L)明显抑制细胞凋亡(P<0.05),中,高浓度(10^-6-10^-4mol/L)时显著增加细胞凋亡(P<0.05);(2)低浓度NaI显著促进sFas蛋白及mRNA的表达(P<.05),不影响Fas蛋白及mRNA的表达;(3)中、高浓度NaI则明显增加Fas蛋白及mRNA表达,但抑制sFas蛋白及mRNA表达(P<0.05);(4)在10^-8-10^-4mol/L浓度范围内,NaI剂量依赖性地抑制甲状腺上皮细胞表达Bcl-2蛋白,但显著增加Bak蛋白的表达(P<0.05),结论:碘可通过调节Fas,sFas,Bcl-2及Bak的表达,影响甲状腺细胞凋亡的发生,其中低浓度碘可抑制凋亡,而中,高浓度碘则促进细胞凋亡。 相似文献
11.
目的 研究1.25二羟基维生素D3[1,25(OH)2D3]抑制辅助性T细胞17(Th17)的分化与STAT5调控的关系。方法 通过分选出的CD4+T细胞,在1,25(OH)2D3和/或STAT5抑制剂的作用下,采用ELISA法检测抑制剂处理后细胞培养上清液Th17细胞因子(IL-17A、IL-22)水平的变化;采用细胞免疫荧光技术检测STAT5的磷酸化水平,采用Western blot技术检测STAT5蛋白表达水平。结果 1,25(OH)2D3组细胞培养上清IL-17A和IL-22水平(12.5±0.5 ng/ml,48.5±0.9 pg/ml)明显低于对照组(22.7±0.5 ng/ml,73.8±1.9 pg/ml),而STAT5抑制剂组IL-17A和IL-22水平明显升高(33.5±0.7 ng/ml,89.1±1.4 pg/ml),1,25(OH)2D3与STAT5抑制剂联合作用细胞IL-17A和IL-22水平(18.5±0.7 ng/ml,54.1±1.6 pg/ml)显著高于1,25(OH)2D3组,但低于STAT5抑制剂组,差异有统计学意义(P<0.01);1,25(OH)2D3组细胞p-STAT5表达显著强于对照组,1,25(OH)2D3联合STAT5抑制剂组p-STAT5表达量低于对照组,而STAT5抑制剂组细胞p-STAT5表达量最低;1,25(OH)2D3组STAT5蛋白表达明显升高,而1,25(OH)2D3联合STAT5抑制剂组或STAT5抑制剂组STAT5蛋白表达明显降低,以STAT5抑制剂组细胞表达最弱,差异均具有统计学意义(P<0.01)。结论 1,25(OH)2D3通过STAT5信号通路能抑制Th17细胞分化。 相似文献
12.
Oliver Schrder Sinan Turak Carolin Daniel Tanja Gaschott Jürgen Stein 《World journal of gastroenterology : WJG》2005,11(45)
AIM: To investigate the possible involvement of 25-hydroxyvitamin D3-1α-hydroxylase [1α-25(OH)2D3] in butyrate-induced differentiation in human intestinal cell line Caco-2 cells.METHODS: Caco-2 cells were incubated either with 3 mmol/L butyrate and 1 μmol/L 25(OH)2D3 or with 1μmol/L 1α-25(OH)2D3 for various time intervals ranging from 0 to 72 h. Additionally, cells were co-incubated with butyrate and either 25(OH)2D3 or 1α-25(OH)2D3.1α-25(OH)2D3 mRNA was determined semi-quantitatively using the fluorescent dye PicoGreen. Immunoblotting was used for the detection of 1α-25(OH)2D3 protein.Finally, enzymatic activity was measured by ELISA.RESULTS: Both butyrate and 1α-25(OH)2D3 stimulated differentiation of Caco-2 cells after a 48 h incubation period, while 25(OH)2D3 had no impact on cell differentiation. Synergistic effects on differentiation were observed when cells were co-incubated with butyrate and vitamin D metabolite. Butyrate transiently upregulated 1α-25(OH)2D3 mRNA followed by a timely delayed protein upregulation. Coincidently, enzymatic activity was enhanced significantly. The induction of the enzyme allowed for comparable differentiating effects of both vitamin D metabolites.CONCLUSION: Our experimental data pr ovide a further mechanism for the involvement of the vitamin D signaling pathway in colonic epithelial cell differentiation by butyrate. The enhancement of 1α-25(OH)2D3 followed by antiproliferative effects of the vitamin D prohormone in the Caco-2 cell line suggest that 25(OH)2D3 in combination with butyrate may offer a new therapeutic approach for the treatment of colon cancer. 相似文献
13.
目的 体内体外观察1,25(OH)2D3通过调节miR-146a水平抑制大鼠肝纤维化的作用机制。方法 建立CCl4诱导的大鼠肝纤维化模型,体外转染肝星状细胞(HSCs)miR-146a 模拟剂/抑制剂,观察1,25(OH)2D3处理对动物肝组织变化和HSC增殖和凋亡的影响。采用qPCR法检测肝组织miR-146a水平,采用CCK8法检测细胞增殖,使用流式细胞术检测HSC凋亡。结果 在干预8 w末,1,25(OH)2D3干预组大鼠肝纤维化程度明显减轻; 1,25(OH)2D3干预组大鼠肝组织miR-146a水平为(0.70± 0.03),显著高于橄榄油组【(0.33±0.17,P<0.05)】; 1,25(OH)2D3组细胞增殖率为58.8%,较DMSO组下降了15.9%,转染miR-146a 模拟剂组大鼠HSC增殖率为46.5%,较对照组下降了53.3%,转染miR-146a 抑制剂组HSC增殖率为132.8%,较对照物组升高了32.8%(P<0.05),1,25(OH)2D3干预组细胞凋亡率为12.6%,较DMSO组增加了5.2%,转染miR-146a 模拟剂组细胞凋亡率为16.8%,较对照组细胞凋亡率增加了8.2%,转染miR-146a 抑制剂组细胞凋亡率为6.3%,较对照组细胞凋亡率减少了2.2%(P<0.05),提示1,25(OH)2D3具有抑制HSC增殖、促进凋亡作用。结论 1,25(OH)2D3可能通过调节miR-146a水平抑制HSC活化和抑制大鼠肝纤维化。 相似文献
14.
Schröder O Turak S Daniel C Gaschott T Stein J 《World journal of gastroenterology : WJG》2005,11(45):7136-7141
AIM: To investigate the possible involvement of 25-hydroxyvitamin D(3)-1(alpha)-hydroxylase [1alpha-25(OH) (2) D(3)] in butyrate-induced differentiation in human intestinal cell line Caco-2 cells. METHODS: Caco-2 cells were incubated either with 3 mmol/L butyrate and 1 micromol/L 25(OH) (2) D(3) or with 1 micromol/L 1alpha-25(OH) (2) D(3) for various time intervals ranging from 0 to 72 h. Additionally, cells were co-incubated with butyrate and either 25(OH) (2) D(3) or 1alpha-25(OH) (2) D(3). 1alpha-25(OH) (2) D(3) mRNA was determined semi-quantitatively using the fluorescent dye PicoGreen. Immunoblotting was used for the detection of 1alpha-25(OH) (2) D(3) protein. Finally, enzymatic activity was measured by ELISA. RESULTS: Both butyrate and 1alpha-25(OH) (2) D(3) stimulated differentiation of Caco-2 cells after a 48 h incubation period, while 25(OH) (2) D(3) had no impact on cell differentiation. Synergistic effects on differentiation were observed when cells were co-incubated with butyrate and vitamin D metabolite. Butyrate transiently upregulated 1alpha-25(OH) (2) D(3) mRNA followed by a timely delayed protein upregulation. Coincidently, enzymatic activity was enhanced significantly. The induction of the enzyme allowed for comparable differentiating effects of both vitamin D metabolites. CONCLUSION: Our experimental data provide a further mechanism for the involvement of the vitamin D signaling pathway in colonic epithelial cell differentiation by butyrate. The enhancement of 1alpha-25(OH) (2) D(3) followed by antiproliferative effects of the vitamin D prohormone in the Caco-2 cell line suggest that 25(OH) (2) D(3) in combination with butyrate may offer a new therapeutic approach for the treatment of colon cancer. 相似文献
15.
结肠癌的发生与肠腔内脱氧胆酸引起的DNA损伤有关,聚腺苷二磷酸核糖聚合酶-1(PARP-1)对DNA损伤具有修复作用.目的:探讨PARP-1在脱氧胆酸钠促结肠癌细胞增殖中的作用及其可能机制.方法:选用不同浓度的脱氧胆酸钠、PARP-1抑制剂5-氨基异喹啉酮(5-AIQ)或两者联合分别作用于人结肠腺癌细胞株HT-29.MTT实验检测细胞增殖情况,流式细胞仪检测细胞周期和细胞凋亡,免疫细胞化学染色检测环氧合酶-2(COX-2)、caspase-3、PARP-1蛋白表达.结果:10~50 μmol/L脱氧胆酸钠能促进HT-29细胞增殖,增加COX-2、PARP-1蛋白表达,减低caspaae-3蛋自表达.100μmol/L 5-AIQ单独作用对HT-29细胞增殖无明显影响,但能减低COX-2、PARP-1蛋白表达.与单独作用相比,10μmol/L脱氧胆酸钠与100 μmol/L 5-AIQ联合能显著抑制HT-29细胞生长,阻滞细胞周期,诱导细胞凋亡,COX-2、PARP-1蛋白表达减低,caspase-3蛋白表达无明显变化.结论:COX-2与PARP-1在脱氧胆酸钠促结肠癌细胞增殖的过程中可能存在相互作用,PARP-1抑制剂5-AIQ可能用于预防脱氧胆酸诱发的结肠癌. 相似文献
16.
M. R. HAUSSLER D. J. BAYKLINK M. R. HUGHES P. F. BRUMBAUGH J. E. WERGEDAL F. H. SHEN R. L. NIELSEN S. J. COUNTS K. M. BURSAC T. A. McCAIN 《Clinical endocrinology》1976,5(S1):s151-s165
A sensitive radioreceptor assay for 1α,25-dihydroxyvitamin D3 (1α,25-(OH)2 D3 ) is utilized to quantitate the circulating concentration of this sterol in experimental animals and humans. When weanling rats are grown for 2 weeks on low calcium or low phosphate diets, limited availability of either ion elicits a five-fold increase in the plasma level of 1α,25-(OH)2 D3 . The enhancement of 1α,25-(OH)2 D3 in calcium deficiency is dependent upon the presence of the parathyroid and/or thyroid glands, which is consistent with parathyroid hormone (PTH) mediation of this effect. In contrast, the response to phosphate deficiency is independent of these glands and may result from a direct action of low phosphate on the renal synthesis of 1α,25-(OH)2 D3 . Studies in humans indicate that the normal level of 1α,25-(OH)2 D is 2.1-4.5 ng/100 ml plasma. Patients with chronic renal failure have markedly lower circulating 1α,25-(OH)2 D and this kidney hormone is undectectable in anephirc subjects, but returns to normal within 1 day after successful renal transplantation. Hypoparathyroidism and pseudohypoparatghyroidism are associated with reduced plasma 1α,25-(OH)2 D while patients with primary hyperparathyroidism have significantly elevated sterol hormone levels. Thus, from measurements in rats and humans, it appears that circulating 1α,25-(OH)2 D3 is regulated by PTH and/or phosphate and that abnormal plasma 1α,25-(OH)2 D3 is a part of the pathophysiology of renal osteodystrophy and parathyroid disorders. 相似文献
17.
Retinoic acid has previously been shown to alter 1-25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptors in tumorigenic (ROS 17/2A, UMR 106M) and nontumorigenic (RCJ 1.20) bone-derived cells. The mechanism of this regulation is unclear. In the present series of experiments, we have investigated the mechanism of the retinoic acid-induced increase in 1,25-(OH)2D3 receptors by studying the effects of sodium butyrate on this process. In ROS 17/2A rat osteosarcoma cells, retinoic acid induced a 2-4-fold increase in 1,25-(OH)2D3 receptors in proliferating cells but only a 1.5- to 2-fold increase in nonproliferating cells. The retinoic acid-induced increase in 1,25-(OH)2D3 receptors in proliferating ROS 17/2A cells was inhibited by sodium butyrate, but sodium butyrate had no effect on the retinoic acid-induced increase in 1,25-(OH)2D3 receptors in nonproliferating cells. Pretreatment with hydroxyurea of low density cells decreased the effect of retinoic acid, and abolished the sodium butyrate inhibition, indicating that the differing effects of retinoic acid in high and low density cells are related to cell proliferation and not to cell density or time of exposure to retinoic acid. In low density UMR 106M cells, the effects of retinoic acid and sodium butyrate on the number of 1,25-(OH)2D3 receptors were similar to those in ROS 17/2A cells. However, in RCJ 1.20 cells, a nontumorigenic cell line with some of the characteristics normally attributed to osteoblasts, the effects of retinoic acid and sodium butyrate were opposite: retinoic acid caused a decrease in the number of 1,25-(OH)2D3 receptors, which was inhibited by sodium butyrate. The possibility that the different responses observed between the two osteosarcoma cell lines and the RCJ 1.20 cells constitute differences in response pattern between tumorigenic and nontumorigenic cell lines is of interest, but requires further experimentation to verify. 相似文献
18.
对于肠易激综合征(IBS)内脏感觉功能异常的研究,需建立合适的动物模型。目的:以丁酸钠溶液灌肠建立大鼠结肠感觉过敏模型,观察其内脏感觉功能和结肠黏膜改变。方法:16只大鼠随机分为实验组和对照组。实验组予1 ml 200mmol/L丁酸钠溶液灌肠,对照组予1 ml 0.9%NaCl溶液灌肠,每天2次,连续3d。分别于灌肠前和实验开始后第3、6、9、12、15、18d行结直肠扩张(CRD),观察腹壁回撤反射(AWR)评分和内脏感觉压力闽值,以反映内脏感觉功能。实验结束后处死大鼠,行结肠黏膜大体形态观察和组织学检查。结果:实验第3-12d.实验组不同CRD压力下AWR评分均显著高于对照组(P〈0.05),疼痛感觉压力阈值显著低于对照组(P〈0.05);第15-18d,上述指标恢复至初始状态。实验结束后,实验组与对照组结肠黏膜大体形态和组织学改变均无明显差异。结论:丁酸钠溶液反复灌肠可诱导大鼠结肠感觉过敏,内脏感觉功能恢复后,结肠黏膜改变同步恢复。该模型可用于IBS病理生理机制的研究。 相似文献
19.
背景:塞来昔布为环氧合酶.2(COX-2)选择性抑制剂,近年研究发现其具有抗肿瘤作用。目的:观察塞来昔布对人结肠癌细胞株HT-29巨噬细胞游走抑制因子(MIF)、抑癌基因蛋白PFEN和凋亡相关蛋白Caspase-3表达的影响,探讨其防治结肠癌可能的分子机制。方法:25、50、100μmol/L塞来昔布分别作用于HT-29细胞24h后,以逆转录聚合酶链反应(RT-PCR)检测HT-29细胞MIFmRNA表达,蛋白质印迹法检测MIF、PTEN、Caspase-3蛋白表达。结果:经25~100μmol/L塞来昔布处理后,HT-29细胞MIFmRNA和蛋白表达随塞来昔布浓度的增加而减低,PTEN和Caspase-3蛋白表达随塞来昔布浓度的增加而增加,与正常对照组相比差异均有统计学意义(P〈0.05)。结论:塞来昔布的抗结肠癌作用可能与下凋MIF表达和上调PTEN、Caspase-3表达有关。 相似文献