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Inhibitory effect of octreotide on gastric cancer growth via MAPK pathway 被引量:33
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作者 chun-huiwang Cheng-WeiTang +1 位作者 Chun-LunLiu Li-PingTang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2003年第9期1904-1908,共5页
AIM: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreoti... AIM: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and its probable mechanisms.METHODS: Proliferation of gastric cancer cell line affected by octreotide was determined by 3H-thymidine incorporation.After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extracellular signalregulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and Western blot.Activator protein-1 binding activity was examined by electrophoretic mobility sift assay.RESULTS: 3H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a concentration dependent manner. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3% in octreotide group.The genes of somatostatin receptors 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially.CONCLUSION: Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms underlying the effect of octreotide on the growth of gastric adenocarcinoma. 展开更多
关键词 胃癌 肿瘤生长 MAPK途径 生长激素抑制剂 奥曲肽
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Probiotics inhibit TNF-α-induced interleukin-8 secretion of HT29 cells 被引量:12
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作者 Ai-PingBai QinOuyang +2 位作者 WenZhang chun-huiwang Sheng-FuLi 《World Journal of Gastroenterology》 SCIE CAS CSCD 2004年第3期455-457,共3页
AIM:To study the effect of probiotics on interleukin-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines.METHODS: Colonic adenocarcinoma HT29 cells were cultured and divided into four grou... AIM:To study the effect of probiotics on interleukin-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines.METHODS: Colonic adenocarcinoma HT29 cells were cultured and divided into four groups:control,TNF-α (group T in short),bifidobacterium (group B), lactobacillus (group L). B. Longum and L. bulgaricus were suspended in culture medium with a concentration of 1×10^8cfu/ml and added into 24 wells respectively. One hour later TNF-α (10ng/ml) was added into each well of groups T, B, L. The supernatants were collected and measured for IL-8 after 3 hours, nuclear factor-κB (NF-κB) p65 was also examined by Western blotting.RESULTS:There was less interleukin-8 secretion in HT29 cells when preincubated with B. Longum or L. bulgaricus compared with group T.Less p65 appeared in nuclei in groups B and L compared with group T,as detected by Westem blot.CONCLUSION:Probiotics can suppress interleukin-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines, which is most likely mediated by NF-κB. 展开更多
关键词 肿瘤坏死因子-α 白细胞介素-8 HT29细胞 细胞因子 细胞培养 炎症
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脂联素参与七氟醚预处理保护心肌缺血再灌注损伤后小鼠认知功能的机制研究
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作者 王春晖 岳毅 +3 位作者 刘少凯 刘小霞 柳元桢 张彦清 《中国现代医学杂志》 CAS 北大核心 2022年第17期33-37,共5页
目的探讨脂联素参与七氟醚预处理后心肌缺血再灌注(MIR)小鼠的认知功能保护作用的机制。方法将野生健康成年SPF级雄性C57BL/6小鼠随机分为sham组、MIR-Control组、MIR-SevoPre组,每组10只。将健康成年SPF级雄性脂联素基因敲除(APN KO)... 目的探讨脂联素参与七氟醚预处理后心肌缺血再灌注(MIR)小鼠的认知功能保护作用的机制。方法将野生健康成年SPF级雄性C57BL/6小鼠随机分为sham组、MIR-Control组、MIR-SevoPre组,每组10只。将健康成年SPF级雄性脂联素基因敲除(APN KO)小鼠随机分为KO-sham组、KO-MIR-Control组、KOMIR-Sevopre组、KO-MIR-Sevopre-AdipoRon组,每组10只。检测3组C57BL/6小鼠在模型复制或对照处理后12 h血浆的高、中和低分子量脂联素浓度;使用Morris水迷宫实验检测3组C57BL/6小鼠在模型复制或对照处理后24 h的游泳速率和潜伏期;检测4组APN KO小鼠在模型复制或对照处理后第1天、第2天、第4天的潜伏期。结果3组C57BL/6小鼠模型复制后第1天、第2天和第4天的游泳速率比较,采用重复测量设计的方差分析,结果:①不同时间点的小鼠游泳速率无差异(P>0.05);②3组小鼠游泳速率无差异(P>0.05);③3组小鼠游泳速率的变化趋势无差异(P>0.05)。3组C57BL/6小鼠模型复制后第1天、第2天和第4天的潜伏期比较,采用重复测量设计的方差分析,结果:①不同时间点的小鼠潜伏期有差异(P<0.05);②3组小鼠的潜伏期有差异(P<0.05),与sham组比较,MIR-Control组各时间点潜伏期延长(P<0.05),与MIR-Control组比较,MIR-Sevopre组小鼠各时间点潜伏期缩短(P<0.05);③3组小鼠的潜伏期变化趋势有差异(P<0.05)。3组C57BL/6小鼠血浆脂联素水平比较,总脂联素、高分子量脂联素、中分子量脂联素差异有统计学意义(P<0.05),低分子量脂联素差异无统计学意义(P>0.05)。Sham组小鼠的潜伏期与血浆脂联素水平呈负相关(r=-0.480,P=0.033),MIR-Control组小鼠的潜伏期与血浆脂联素水平呈负相关(r=-0.300,P=0.040),MIR-Sevopre组小鼠的潜伏期与血浆脂联素水平呈负相关(r=-0.730,P=0.019)。4组APN KO小鼠模型复制后第1天、第2天和第4天的潜伏期比较,采用重复测量设计的方差分析,结果:①不同时间点小鼠潜伏期有差异(P<0.05);②4组小鼠的潜伏期差异(P<0.05),与KO-sham组比较,KO-MIR-Control组潜伏期延长(P<0.05),与KO-MIR-Control组比较,KO-MIR-Sevopre组潜伏期无差异(P>0.05),与KO-MIR-Sevopre组比较,KO-MIR-Sevopre-AdipoRon组潜伏期缩短(P<0.05);③4组小鼠潜伏期的变化趋势无差异(P>0.05)。结论血浆脂联素参与七氟醚预处理对小鼠心肌MIR损伤后的认知保护作用,口服AdipoRon后可代替部分脂联素的保护作用。 展开更多
关键词 心肌缺血再灌注 小鼠 七氟醚 脂联素 认知功能
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