目的阐明幽门螺杆菌(Helicobacter pylori,Hp)感染对胃粘膜上皮细胞凋亡的作用及其与 p53和 bc(?)-2表达的关系。方法本研究观察了28例幽门螺杆菌 Hp 阳性和17例 Hp 阴性慢性浅表性胃炎患者和20例 Hp 阴性正常胃粘膜对照者胃粘膜上皮细...目的阐明幽门螺杆菌(Helicobacter pylori,Hp)感染对胃粘膜上皮细胞凋亡的作用及其与 p53和 bc(?)-2表达的关系。方法本研究观察了28例幽门螺杆菌 Hp 阳性和17例 Hp 阴性慢性浅表性胃炎患者和20例 Hp 阴性正常胃粘膜对照者胃粘膜上皮细胞凋亡百分率及其 p53和bc(?)-2表达水平。结果:正常胃粘膜和 Hp 阴性慢性浅表性胃炎患者胃粘膜上皮细胞凋亡百分率低,p53蛋白低表达和 bc(?)-2蛋白高表达。而 Hp阳性慢性浅表性胃炎患者胃粘膜上皮细胞凋亡百分率高,p53蛋白高表达而 bc(?)-2蛋白低表达。结论 Hp 可诱导胃粘膜上皮细胞凋亡,其作用途径与上调 p53蛋白表达水平及下调 bc(?)-2蛋白表达水平有关。展开更多
In this study,we examined the expression of inducible nitric oxide synthase(iNOS) and vascular endothelial growth factor(VEGF) by immunohistochemical staining in 76 tissue sections collected from bepa-tocellular carci...In this study,we examined the expression of inducible nitric oxide synthase(iNOS) and vascular endothelial growth factor(VEGF) by immunohistochemical staining in 76 tissue sections collected from bepa-tocellular carcinoma(HCC) patients undergoing hepatectomy.Microvascular density (MVD) was determined by counting endothelial cells immunostained using anti-CD34 antibody.We performed DNA-flow cytometric analyses to elucidate the impact of iNOS and VEGF expression on the cell cycle of HCC.Most of the HCC cells that invaded stroma were markedly immunostained by iNOS antibody.The iNOS stain intensity of the liv-er tissue close to the tumor edge was stronger than that of HCC tissue,and the strongest was the hepatocytes colser to the tumor tissue.However,iNOS expression in 10 normal hepatic samples was undetectable.VEGF positive expression ratio was 84.8% in iNOS positive expression cases,and the ratio was 35.3% in negative cases.There was significant correlation(P=0.000) between iNOS and VEGF expression.Moreover,iNOS expression was significantly associated with bcl-2 and MVD,but without p53 expression.DNA-flow cytometric analyses showed that combined expression of iNOS and VEGF had significant impact on the cell cycle in HCC.PI(Proliferating Index) and SPF(S-phase fraction)in the combined positive expression of iNOS and VEGF group was significantly higher than that in the combined negative group.The present findings suggested that iNOS expression was significantly associated with angiogenesis,bcl-2 and cell proliferation of HCC.展开更多
文摘目的阐明幽门螺杆菌(Helicobacter pylori,Hp)感染对胃粘膜上皮细胞凋亡的作用及其与 p53和 bc(?)-2表达的关系。方法本研究观察了28例幽门螺杆菌 Hp 阳性和17例 Hp 阴性慢性浅表性胃炎患者和20例 Hp 阴性正常胃粘膜对照者胃粘膜上皮细胞凋亡百分率及其 p53和bc(?)-2表达水平。结果:正常胃粘膜和 Hp 阴性慢性浅表性胃炎患者胃粘膜上皮细胞凋亡百分率低,p53蛋白低表达和 bc(?)-2蛋白高表达。而 Hp阳性慢性浅表性胃炎患者胃粘膜上皮细胞凋亡百分率高,p53蛋白高表达而 bc(?)-2蛋白低表达。结论 Hp 可诱导胃粘膜上皮细胞凋亡,其作用途径与上调 p53蛋白表达水平及下调 bc(?)-2蛋白表达水平有关。
文摘In this study,we examined the expression of inducible nitric oxide synthase(iNOS) and vascular endothelial growth factor(VEGF) by immunohistochemical staining in 76 tissue sections collected from bepa-tocellular carcinoma(HCC) patients undergoing hepatectomy.Microvascular density (MVD) was determined by counting endothelial cells immunostained using anti-CD34 antibody.We performed DNA-flow cytometric analyses to elucidate the impact of iNOS and VEGF expression on the cell cycle of HCC.Most of the HCC cells that invaded stroma were markedly immunostained by iNOS antibody.The iNOS stain intensity of the liv-er tissue close to the tumor edge was stronger than that of HCC tissue,and the strongest was the hepatocytes colser to the tumor tissue.However,iNOS expression in 10 normal hepatic samples was undetectable.VEGF positive expression ratio was 84.8% in iNOS positive expression cases,and the ratio was 35.3% in negative cases.There was significant correlation(P=0.000) between iNOS and VEGF expression.Moreover,iNOS expression was significantly associated with bcl-2 and MVD,but without p53 expression.DNA-flow cytometric analyses showed that combined expression of iNOS and VEGF had significant impact on the cell cycle in HCC.PI(Proliferating Index) and SPF(S-phase fraction)in the combined positive expression of iNOS and VEGF group was significantly higher than that in the combined negative group.The present findings suggested that iNOS expression was significantly associated with angiogenesis,bcl-2 and cell proliferation of HCC.
