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胃型上皮Fas表达的调节:幽门螺杆菌致病的自身免疫机制之一 被引量:6
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作者 王继德 白杨 +3 位作者 林焕建 张亚历 黄文 周殿元 《第一军医大学学报》 CSCD 北大核心 2003年第11期1184-1187,共4页
目的探讨Fas介导的幽门螺杆菌(Hp)致胃上皮损伤机制。方法从Hp感染和非感染胃粘膜新鲜分离胃上皮细胞,流式细胞仪测定新分离及体外培养胃上皮细胞系中Fas的表达;调查Hp活菌及Hp感染时胃粘膜主要的Th1细胞因子干扰素-γ(IFN-γ)、肿瘤坏... 目的探讨Fas介导的幽门螺杆菌(Hp)致胃上皮损伤机制。方法从Hp感染和非感染胃粘膜新鲜分离胃上皮细胞,流式细胞仪测定新分离及体外培养胃上皮细胞系中Fas的表达;调查Hp活菌及Hp感染时胃粘膜主要的Th1细胞因子干扰素-γ(IFN-γ)、肿瘤坏死因子-α(TNF-α)对胃上皮Fas表达的调节作用,同时应用ELISA法探讨Fas介导的胃上皮细胞凋亡作用。结果Hp感染胃粘膜上皮Fas阳性数和表达量均高于非感染者(P<0.05),Hp、IFN-γ及TNF-α单独或合用均能提高胃上皮Fas的表达,而胃上皮表面的Fas分子能够介导其IgM单抗引起的致细胞凋亡作用,IFN-γ可增强这种作用。结论直接或间接通过Th1细胞因子增加Fas表达进而损伤胃上皮细胞,是Hp致胃上皮损伤的自身免疫机制之一。 展开更多
关键词 FAS 幽门螺杆菌 自身免疫机制 胃上皮损伤 感染
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幽门螺杆菌及其vacA基因亚型、cagA基因与胃上皮HLA—DR抗原表达的关系
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作者 何瑶 胡品津 《胃肠病学》 2001年第C00期51-51,共1页
关键词 幽门螺杆菌 vacA基因亚型 CAGA基因 胃上皮HLA-DR抗原 胃上皮损伤
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Effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in premalignant gastric lesions 被引量:10
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作者 Da-ZhongCao Wei-HaoSun +6 位作者 Xi-LongOu QianYu TingYu You-ZhenZhang Zi-YingWu Qi-PingXue Yun-LinCheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第11期1571-1576,共6页
AIM: To evaluate the effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in the tissues of premalignant gastric lesions. METHODS: Thirty-eight patients, with premalignant gastric lesions incl... AIM: To evaluate the effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in the tissues of premalignant gastric lesions. METHODS: Thirty-eight patients, with premalignant gastric lesions including 18 colonic-type intestinal metaplasia (IM) and 20 mild or moderate dysplasia, were randomly divided into a treatment group (n = 19) receiving folic acid 10 mg thrice daily and a control group (n = 19) receiving sucralfate 1 000 mg thrice daily for 3 mo. All patients underwent endoscopies and four biopsies were taken prior to treatment and repeated after concluding therapy. Folate concentrations in gastric mucosa were measured with chemiluminescent enzyme immunoassay. Epithelial apoptosis and the expression of Bcl-2 and p53 protein in gastric mucosa were detected with flow cytometric assay. RESULTS: The mean of folate concentration in gastric mucosa was 9.03±3.37 μg/g wet wt in the folic acid treatment group, which was significantly higher than 6.83±3.02 μg/g wet wt in the control group. Both the epithelial apoptosis rate and the tumor suppressor p53 expression in gastric mucosa significantly increased after folic acid treatment. In contrast, the expression of Bcl-2 oncogene protein decreased after folic acid therapy. CONCLUSION: These data indicate that folic acid may play an important role in the chemoprevention of gastric carcinogenesis by enhancing gastric epithelial apoptosis in the patients with premalignant lesions. 展开更多
关键词 Folic acid BCL-2 P53 Premalignant gastric lesions
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Ghrelin attenuates gastrointestinal epithelial damage induced by doxorubicin 被引量:3
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作者 Mohamed A Fahim Hazem Kataya +3 位作者 Rkia El-Kharrag Dena AM Amer Basel al-Ramadi Sherif M Karam 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第33期3836-3841,共6页
AIM:To examine the influence of ghrelin on the regenerative potential of gastrointestinal(GI)epithelium.METHODS:Damage to GI epithelium was induced in mice by two intravenous injections of doxorubicin(10 and 6 mg/kg).... AIM:To examine the influence of ghrelin on the regenerative potential of gastrointestinal(GI)epithelium.METHODS:Damage to GI epithelium was induced in mice by two intravenous injections of doxorubicin(10 and 6 mg/kg).Some of the doxorubicin-treated mice received a continuous subcutaneous infusion of ghrelin(1.25μg/h)for 10 d via implanted mini-osmotic pumps.To label dividing stem cells in the S-phase of the cell cycle,all mice received a single intraperitoneal injection of 5'-bromo-2'-deoxyuridine(BrdU)one hour before sacrifice.The stomach along with the duodenum were then removed and processed for histological examination and immunohistochemistry using anti-BrdU antibody.RESULTS:The results showed dramatic damage to the GI epithelium 3 d after administration of chemotherapy which began to recover by day 10.In ghrelintreated mice,attenuation of GI mucosal damage was evident in the tissues examined postchemotherapy.Immunohistochemical analysis showed an increase in the number of BrdUlabeled cells and an alteration in their distribution along the epithelial lining in response to damage by doxorubicin.In mice treated with both doxorubicin and ghrelin,the number of BrdUlabeled cells was reduced when compared with mice treated with doxorubicin alone.CONCLUSION:The present study suggests that ghrelin enhances the regenerative potential of the GI epithelium in doxorubicintreated mice,at least in part,by modulating cell proliferation. 展开更多
关键词 Gastrointestinal cell proliferation Gastrointestinal mucosal damage GHRELIN
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