CAJ | 학술논문

目的：通过检测幽门螺杆菌（Hp）相关胃病脾胃湿热证患者白细胞介素－8（IL －8）及热休克蛋白70（HSP70）的表达，探讨 Hp 相关胃病脾胃湿热证发生的病理机制。方法选择脾胃湿热证和脾气虚证的慢性胃炎、消化性溃疡患者75例，招募健康志愿者10例作为正常对照。采用免疫组织化学标记法、荧光定量 PCR 法检测各组胃黏膜 HSP70、IL －8蛋白及 mRNA 的表达。结果HSP70、IL －8蛋白和 mRNA 表达水平呈现脾胃湿热证患者＞脾气虚证患者＞正常对照者的趋势。 Hp 感染者 HSP70、IL －8蛋白和 mRNA 表达水平较非感染者有偏高趋势。结论HSP70、IL －8的表达与证型及 Hp 感染可能存在一定的相关性，HSP70表达水平与 Hp 感染的关系可能部分体现脾胃湿热证的“正邪交争”状态，IL －8的高表达可能为脾胃湿热证 Hp 作用于胃黏膜的机制之一。
목적：통과검측유문라간균（Hp）상관위병비위습열증환자백세포개소－8（IL －8）급열휴극단백70（HSP70）적표체，탐토 Hp 상관위병비위습열증발생적병리궤제。방법선택비위습열증화비기허증적만성위염、소화성궤양환자75례，초모건강지원자10례작위정상대조。채용면역조직화학표기법、형광정량 PCR 법검측각조위점막 HSP70、IL －8단백급 mRNA 적표체。결과HSP70、IL －8단백화 mRNA 표체수평정현비위습열증환자＞비기허증환자＞정상대조자적추세。 Hp 감염자 HSP70、IL －8단백화 mRNA 표체수평교비감염자유편고추세。결론HSP70、IL －8적표체여증형급 Hp 감염가능존재일정적상관성，HSP70표체수평여 Hp 감염적관계가능부분체현비위습열증적“정사교쟁”상태，IL －8적고표체가능위비위습열증 Hp 작용우위점막적궤제지일。
Objective To explore the pathogenesis of the Helicobacter pylori (Hp) -related gastropathy with splenogastric hygropyrexia syndrome by detecting heat shock protein 70 (HSP70) and interleukin -8 (IL -8) expres-sions.Methods Seventy -five patients with chronic gastritis and peptic ulcer , complicated with splenogastric hygropy -rexia syndrome or deficiency of spleen -QI syndrome were collected; with 10 healthy volunteers as normal controls .The protein and mRNA expression of HSP70 and IL -8 were detected by immunohistochemistry and fluorescence quantitative polymerase chain reaction.Results The protein and mRNA expression of HSP70 and IL -8 were highest in patients with splenogastric hygropyrexia syndrome , and followed by deficiency of spleen -QI syndrome patients and normal controls . Protein and mRNA expressions of HSP70 and IL -8 in Hp infection patients were higher than those in non -infected pa-tients.Conclusion HSP70 and IL -8 expression may be prompted with the certificate type of syndrome , and correlated with Hp infection.The correlation between HSP70 expression and Hp infection may partly reflect the "antipathogenic qi fighting with pathogenic factors "state of the plenogastric hygropyrexia syndrome .IL -8 high expression is possibly one of the mechanisms that Hp attack on gastric mucosa in splenogastric hygropyrexia syndrome .