隆起糜烂性胃炎脾胃湿热证与IL-8、TNF-α、IL-10的相关性研究
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摘要
目的：
研究隆起糜烂性胃炎(Raised Erosive Gastritis,REG)脾胃湿热证与细胞因子(cytokine,CK)白介素8(Interleukin-8,IL-8)、白介素10(Interleukin-10,IL-10)、肿瘤坏死因子α(Tumor Necrosis Factor,TNF-α)表达之间的关系。
方法：
选择REG病例70例,按中医辨证标准分为脾胃湿热证、脾胃虚弱证两组,分别为34例、36例,同时设正常对照组13例。所有受试者均行胃镜检查,于胃镜下取胃窦部粘膜活检标本,用快速尿素酶试验及组织染色法检测幽门螺旋杆菌(Helicobacter Pylori,Hp),用免疫组织化学法检测IL-8、TNF-α、IL-10的表达量,活检标本同时行病理组织学诊断。
结果：
1.REG组IL-8的表达水平与正常组相比无明显差异(p>0.05)；REGHp(+)组、Hp(-)组、正常组三组间IL-8的表达水平无显著性差异(p>0.05)；REG脾胃湿热组、脾胃虚弱组IL-8的表达水平与正常组比较均有升高趋势,但其差异无统计学意义(p>0.05)；REG脾胃湿热组IL-8的表达水平与脾胃虚弱组相比无明显差异(p>0.05)；REG脾胃湿热组、脾胃虚弱组两组中Hp(+)组与Hp(-)组的IL-8表达水平无显著性差异(p>0.05)。
2.REG组TNF-α的表达水平高于正常组,有显著性差异(p<0.01)；REG Hp(+)组、Hp(-)组两组TNF-α的表达水平均高于正常组,有显著性差异(p<0.05)；REG Hp(-)组TNF-α的表达水平高于Hp(+)组,有显著性差异(p<0.05)；REG脾胃湿热组、脾胃虚弱组两组TNF-α的表达水平均高于正常组,有显著性差异(p<0.05)；脾胃湿热组TNF-α的表达水平与脾胃虚弱组相比,其差异无统计学意义(p>0.05)；REG脾胃湿热组中Hp(-)组TNF-α的表达水平高于Hp(+)组,有显著性差异(p<0.05)；脾胃虚弱组Hp(+)组TNF-α的表达水平与Hp(-)组相比,无显著性差异(p>0.05)。
3.REG组IL-10的表达水平高于正常组,有显著性差异(p<0.01);REG Hp(+)组、Hp(-)组两组IL-10的表达水平均高于正常组,有显著性差异(p<0.05);REG Hp(-)组IL-10的表达水平高于Hp(+)组,有显著性差异(p<0.01)；REG脾胃湿热组、脾胃虚弱组两组IL-10的表达水平均高于正常对照组,具有显著性差异(p<0.01)；脾胃湿热组、脾胃虚弱组IL-10的表达无显著性差异(p>0.05)；REG脾胃湿热组中Hp(+)组IL-10的表达水平与Hp(-)组相比,二者无显著性差异(p>0.05)；脾胃虚弱组中的Hp(-)组IL-10的表达水平高于Hp(+)组,差异有显著性意义(p<0.01)。
结论：
1.IL-8在REG的发生发展过程中可能不是主要的促炎因子。
2.TNF-α可能在促进REG的发生发展过程中起着重要作用。
3.IL-10可能在防止REG的组织损伤中起着重要作用。
4. IL-8、TNF-α、IL-10在REG脾胃湿热证与脾胃虚弱证之间表达无差异。
Objective:To study the relationship between the expression of IL-8,TNF-a, IL-10 and the Raised Erosive Gastritis (REG)with spleen-stomach dampness heat syndrome.
Method:70 Raised Erosive Gastritis patients whoses syndromes meet with spleen stomach-dampness-heat(SSDH) and spleen deficiency(SD) accroding to TCM dialectics were selected as research subjects.There were 34 patients in spleen-stomach dampness-heat(SSDH) group,36 patients in spleen deficiency(SD) group. And 13 healthy patients were considered as the control group. All subjects accepted gastroscopy examination.We got the samples from the gastric antrum,during the gastroscopy examination;and then the samples were used to do rapid urease test, detect the existence of Hp with histological stain method,do pathologic diagnosis and detect the expression of IL-8,TNF-a and IL-10 with immunohistochemistry.
Results:
1 There were no difference between the Raised Erosive Gastritis group and the control group about the expression of IL-8 (p>0.05). There were no significantly difference among the Hp positive group, the Hp negative group and the control group about the expression of IL-8(p>0.05). The expression of IL-8 in the SSDH group and the SD group were both higher than the control group, but the difference was not significant (p>0.05). The expression of IL-8 in the SSDH group and the SD group have no difference(p>0.05. In the SSDH, the expression of IL-8 between the Hp negative group and the control group was not different(p>0.05),and the result was the same in the SD group.
2 The expression level of TNF-a in the Raised Erosive Gastritis group was obviously higher than the control group(p<0.01),the expression level of TNF-a in the Hp positive group and the Hp negative group were both higher compared with the control group,while the Hp negative group is higher than the Hp positive group (p<0.05). Both the SSDH group and the SD group were obviously different from the control group about the expression of TNF-a (p<0.01).Though the SSDH group expressed more TNF-a than the SD group, the different was not significan(p>0.05). In the SSDH group, the expression of TNF-a in the Hp negative group was enhanced and obviously different from the Hp positive group (p<0.01).In the SD group, the expression of TNF-a between the Hp negative group and the Hp positive group was not different (p<0.01).
3 The expression of IL-10 in the Raised Erosive Gastritis group was obviously higher than the control group(p<0.01).The expression of IL-10 in the Hp positive group and the Hp negative group were both higher compared with the control group,and the Hp negative group is higher than the Hp positive group (p<0.05).The expression of IL-10 in the SSDH group and the SD group was both enhanced and obviously different from the control group(p<0.01).The SSDH group expressed more IL-10 than the SD group, but the different was not significant(p>0.05). There were no difference between the SSDH group and the SD group about the expression of IL-10 (p>0.05).In the SSDH group, The expression of IL-10 was not different between the Hp positive group and the Hp negative group (p>0.05).In the SD group, the expression of IL-10 in the Hp negative group was enhanced and obviously different fome the Hp positive group(p<0.05).
Conclusion:
1 IL-8 may not be a major proinflammatory cytokine in the the occurrence and development of REG
2 TNF-αmay play an important role in promoting the occurrence and development of REG
3 IL-10 may an important role in preventing tissue from damage in the REG
4 It was not different between the REG SSDH group and the REG SD group about the expression of IL-8、TNF-a and IL-10.
研究隆起糜烂性胃炎(Raised Erosive Gastritis,REG)脾胃湿热证与细胞因子(cytokine,CK)白介素8(Interleukin-8,IL-8)、白介素10(Interleukin-10,IL-10)、肿瘤坏死因子α(Tumor Necrosis Factor,TNF-α)表达之间的关系。
方法：
选择REG病例70例,按中医辨证标准分为脾胃湿热证、脾胃虚弱证两组,分别为34例、36例,同时设正常对照组13例。所有受试者均行胃镜检查,于胃镜下取胃窦部粘膜活检标本,用快速尿素酶试验及组织染色法检测幽门螺旋杆菌(Helicobacter Pylori,Hp),用免疫组织化学法检测IL-8、TNF-α、IL-10的表达量,活检标本同时行病理组织学诊断。
结果：
1.REG组IL-8的表达水平与正常组相比无明显差异(p>0.05)；REGHp(+)组、Hp(-)组、正常组三组间IL-8的表达水平无显著性差异(p>0.05)；REG脾胃湿热组、脾胃虚弱组IL-8的表达水平与正常组比较均有升高趋势,但其差异无统计学意义(p>0.05)；REG脾胃湿热组IL-8的表达水平与脾胃虚弱组相比无明显差异(p>0.05)；REG脾胃湿热组、脾胃虚弱组两组中Hp(+)组与Hp(-)组的IL-8表达水平无显著性差异(p>0.05)。
2.REG组TNF-α的表达水平高于正常组,有显著性差异(p<0.01)；REG Hp(+)组、Hp(-)组两组TNF-α的表达水平均高于正常组,有显著性差异(p<0.05)；REG Hp(-)组TNF-α的表达水平高于Hp(+)组,有显著性差异(p<0.05)；REG脾胃湿热组、脾胃虚弱组两组TNF-α的表达水平均高于正常组,有显著性差异(p<0.05)；脾胃湿热组TNF-α的表达水平与脾胃虚弱组相比,其差异无统计学意义(p>0.05)；REG脾胃湿热组中Hp(-)组TNF-α的表达水平高于Hp(+)组,有显著性差异(p<0.05)；脾胃虚弱组Hp(+)组TNF-α的表达水平与Hp(-)组相比,无显著性差异(p>0.05)。
3.REG组IL-10的表达水平高于正常组,有显著性差异(p<0.01);REG Hp(+)组、Hp(-)组两组IL-10的表达水平均高于正常组,有显著性差异(p<0.05);REG Hp(-)组IL-10的表达水平高于Hp(+)组,有显著性差异(p<0.01)；REG脾胃湿热组、脾胃虚弱组两组IL-10的表达水平均高于正常对照组,具有显著性差异(p<0.01)；脾胃湿热组、脾胃虚弱组IL-10的表达无显著性差异(p>0.05)；REG脾胃湿热组中Hp(+)组IL-10的表达水平与Hp(-)组相比,二者无显著性差异(p>0.05)；脾胃虚弱组中的Hp(-)组IL-10的表达水平高于Hp(+)组,差异有显著性意义(p<0.01)。
结论：
1.IL-8在REG的发生发展过程中可能不是主要的促炎因子。
2.TNF-α可能在促进REG的发生发展过程中起着重要作用。
3.IL-10可能在防止REG的组织损伤中起着重要作用。
4. IL-8、TNF-α、IL-10在REG脾胃湿热证与脾胃虚弱证之间表达无差异。
Objective:To study the relationship between the expression of IL-8,TNF-a, IL-10 and the Raised Erosive Gastritis (REG)with spleen-stomach dampness heat syndrome.
Method:70 Raised Erosive Gastritis patients whoses syndromes meet with spleen stomach-dampness-heat(SSDH) and spleen deficiency(SD) accroding to TCM dialectics were selected as research subjects.There were 34 patients in spleen-stomach dampness-heat(SSDH) group,36 patients in spleen deficiency(SD) group. And 13 healthy patients were considered as the control group. All subjects accepted gastroscopy examination.We got the samples from the gastric antrum,during the gastroscopy examination;and then the samples were used to do rapid urease test, detect the existence of Hp with histological stain method,do pathologic diagnosis and detect the expression of IL-8,TNF-a and IL-10 with immunohistochemistry.
Results:
1 There were no difference between the Raised Erosive Gastritis group and the control group about the expression of IL-8 (p>0.05). There were no significantly difference among the Hp positive group, the Hp negative group and the control group about the expression of IL-8(p>0.05). The expression of IL-8 in the SSDH group and the SD group were both higher than the control group, but the difference was not significant (p>0.05). The expression of IL-8 in the SSDH group and the SD group have no difference(p>0.05. In the SSDH, the expression of IL-8 between the Hp negative group and the control group was not different(p>0.05),and the result was the same in the SD group.
2 The expression level of TNF-a in the Raised Erosive Gastritis group was obviously higher than the control group(p<0.01),the expression level of TNF-a in the Hp positive group and the Hp negative group were both higher compared with the control group,while the Hp negative group is higher than the Hp positive group (p<0.05). Both the SSDH group and the SD group were obviously different from the control group about the expression of TNF-a (p<0.01).Though the SSDH group expressed more TNF-a than the SD group, the different was not significan(p>0.05). In the SSDH group, the expression of TNF-a in the Hp negative group was enhanced and obviously different from the Hp positive group (p<0.01).In the SD group, the expression of TNF-a between the Hp negative group and the Hp positive group was not different (p<0.01).
3 The expression of IL-10 in the Raised Erosive Gastritis group was obviously higher than the control group(p<0.01).The expression of IL-10 in the Hp positive group and the Hp negative group were both higher compared with the control group,and the Hp negative group is higher than the Hp positive group (p<0.05).The expression of IL-10 in the SSDH group and the SD group was both enhanced and obviously different from the control group(p<0.01).The SSDH group expressed more IL-10 than the SD group, but the different was not significant(p>0.05). There were no difference between the SSDH group and the SD group about the expression of IL-10 (p>0.05).In the SSDH group, The expression of IL-10 was not different between the Hp positive group and the Hp negative group (p>0.05).In the SD group, the expression of IL-10 in the Hp negative group was enhanced and obviously different fome the Hp positive group(p<0.05).
Conclusion:
1 IL-8 may not be a major proinflammatory cytokine in the the occurrence and development of REG
2 TNF-αmay play an important role in promoting the occurrence and development of REG
3 IL-10 may an important role in preventing tissue from damage in the REG
4 It was not different between the REG SSDH group and the REG SD group about the expression of IL-8、TNF-a and IL-10.
引文
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[1]窦肇华,张远强,郭顺根.免疫细胞学与疾病[M].北京：中国医药科技出版社,2004：25,860-901.
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[3]王孟春,李岩,古田隆久.幽门螺杆菌感染者胃粘膜中IL-1βmRNA的竞争RT-PCR检测[J].中华微生物学和免疫学杂志,1998,18(2)：159-161.
[4]徐克强,张万岱,王继德,等.幽门螺杆菌细胞毒素促进胃粘膜分泌白介素8作用[J].世界华人消化杂志,2002,10(8)：907-911.
[5]余柏林,刘重贞,余开森,等.消化性溃疡患者Hp感染与IL-6、IL-8活性的关系[J].中国内镜杂志,1997,3(6)：3-11.
[6]凌贤龙,房殿春,周晓东,等.幽门螺杆菌感染与胃粘膜炎症反应和IL-8活性的关系[J].第三军医大学学报,2001,23(9)：1046-1047.
[7]SEGAL E D, LANGE C, COVACCI A, et al.Induction of host signal transduction pathways by Hel-icobaeter pylori[J].Proc Natl Acad Sci USA,1997,94(14):7595-7599.
[8]KASSAI K.YOSHIKAWA T.YOSHIDA N, et al.Helicobacter pylori water extract induces interleukin-8 production by gastric epitheial cells.[J].Dig Dis Sci,1999,44(2):237-2 42.
[9]ZHANG Q B, DAWODU J B.HUSAIN A. et al.Association of antral mucosal levels of interleukin 8 and reactive oxygen radicals in patients infected with Helicobacter pylori [J].clin Sci(Lond),1997,92(1):69-73.
[10]PEEK P M.MOSS S F.THAM K T, et al.Helicobacter pylori CaPA+ strains and dissociation of gastric epithelial cell proliferation from apoptosis[J].Natl Cancer Inst,1997,89 (2):863-868.
[11]林焕建,王继德,张亚历,等.TH1细胞因子(IFN-γ)在幽门螺杆菌致病中的作用[J].中国微生态学杂志,2003,15(3)：126-127.
[12]高玮,黄仕和,余跃,等.儿童幽门螺杆菌感染根除前后IL-18,IFN-γ水平变化[J].中华微生物学和免疫学杂志,2005,25(7)：543.
[13]KARTTUNEN R A, KARTTUNEN T J, YOUSFI M M, et al.Expression of mRNA for IFN-γ,IL-10, and IL-12(p42)in normal gastric mucosa and in mucosa infected with H. pylori.Scand[J].Gas-troenterol,1997,32(1):22-27.
[14]林谦,王大为,唐英姿,等.IL-12和IL-10在儿童幽门螺旋杆菌相关性胃炎中的表达研究[J].南京医科大学学报·自然科学版2005,25(9)：647-650.
[15]温忠慧,欧阳钦.IL-18在肠道疾病中的致病作用机制[J].国外医学·消化系疾病分册2003,23(4)：237-239
[16]FIORUCCI S,SANTUCCI L,MIGLIORATI G, et al.Isolated guinea pig gastric chief cells expr-ess tumor necrosis factor receptors coupled with the sphingomyelin pathway[J].Gut,1996 ,3(8):182-189.
[17]NEU B, PUSCHMANN A J, MAYERHOFER A, et al.TNF-α induces apoptosis of parietal cells[J]. Biochem Pharmacol,2003,65(10):1755-1760.
[18]KOYAMA S.Flow cytometric measurement of tumor necrosis factor-related apoptosis-indu-cing ligand and its receptors in gastric epithelium and infiltrating mucosal lymphocyt-es in Helicobacter pylori-associated gastritis[J].Gastroenterology and Hepatology, 2003,18:(7)763-770.
[19]胡伏莲,周殿元,贾博琦,等.幽门螺杆菌感染的基础与临床[M].北京：中国科学技术出版社,1997：150-159.
[20]朱慧芳.幽门螺旋杆菌感染者的Th1/Th2及Treg细胞免疫应答及其相关性分析[D].南京：南京师范大学,2006.
[21]孟凡科,林志恒,王福德,等.十二指肠球部溃疡处粘膜白细胞介素-10、白细胞介素-12和干扰素-γ的水平及其临床意义[J].潍坊医学院学报,2003,25(3)：181-183.
[22]刘伟.EGF与胃肠关系的研究新进展[J].国外医学·消化系疾病分册,2002,22(4)：207.
[23]马强,张方信,张振书.幽门螺杆菌相关性胃炎活动性与TNF-α,EGF的相关性[J].世界华人消化杂志,4,12(9)：2190-2192.
[24]刘利民,张万岱,宋余刚,等.慢性胃病不同中医证型Hp感染的比较研究[J].现代消化及介入诊疗,2003,8(4)：212-214.
[25]徐艺,叶柏,单兆伟,等.中草药单味与复方对幽门螺杆菌抑菌作用研究[J].中国中西医结合脾胃杂志,2000,8(5)：292-293.
[26]魏辉,余志坚.中医药诊治幽门螺杆菌感染的研究近况[J].解放军广州医高专学报,1996,19(2)：159-160.
[27]罗云坚,黄穗平,陈慧,等.慢性胃炎中医证候与胃窦十二指肠运动及胃炎程度的相关性[J].广州中医药大学学报,2000,17(3)241-244.
[28]杨春波,黄可成,肖丽春,等.脾胃湿热证的临床研究-附400例资料分析[J].中医杂志,1994,35(7)：425-427.
[29]危北海.宏观辩证和微观辩证的结合的研究[J].北京中医杂志,1992,11(1)：19-21.
[30]翟兴红,赵荣莱,赵子厚,等.慢性胃病与胃粘膜细胞保护因子的相关性研究[J].中国中西医结合脾胃杂志,1998,6(1)：9-11.
[31]冯春霞,劳绍贤,黄志新,等.慢性浅表性胃炎脾胃湿热证胃粘膜病理、幽门螺杆菌感染及胃粘膜分泌特点[J].广州中医药大学学报,2003,20(3)：187-190.
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