半夏泻心汤及其拆方对幽门螺杆菌感染小鼠胃粘膜的形态学研究
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摘要
目的:探讨半夏泻心汤及其拆方对幽门螺杆菌感染小鼠胃粘膜形态学的影响及其作用机理,并比较半夏泻心汤全方及各拆方组对幽门螺杆菌感染小鼠胃组织的修复作用,为临床防治幽门螺杆菌感染性胃病提供实验依据。
方法:将120只C_(57)BL小鼠随机分为10组:Ⅰ半夏泻心汤全方组,Ⅱ半夏组,Ⅲ甘温组,Ⅳ苦寒组,Ⅴ半夏加苦寒组,Ⅵ半夏加甘温组,Ⅶ苦寒加甘温组,Ⅷ阳性药物对照组,Ⅸ模型纽,Ⅹ空白组。每组各12只小鼠,雌雄各半。先连续4天用氨苄西林给小鼠清肠消毒,第5天开始造模:第Ⅰ组至第Ⅸ组每只小鼠灌胃幽门螺杆菌菌液0.2ml,灌胃前禁食禁水,每隔一天灌胃一次,共8次。末次灌胃造模两天后,随机抽取四只小鼠进行胃粘膜细菌培养和尿素酶试验。结果:细菌培养,革兰氏染色镜检发现G~-弧形杆菌,菌尿素酶试验阳性,证实造模成功后开始药物灌胃。第Ⅰ组至第Ⅶ组按每只小鼠体重给予等效剂量的中药灌胃;第Ⅷ组灌胃等效剂量的氨苄青霉素,用蒸馏水稀释成所需浓度。模型组和空白组每只小鼠灌胃0.2ml的蒸馏水。连续灌胃8天,每天1次,灌药前禁水禁食6小时。灌胃结束后,动物禁食不禁水12小时,次日心脏采血处死动物,并完整取胃,观察胃组织的病理形态改变和检测胃细胞凋亡及T淋巴细胞亚群CD4~+和CD8~+的表达。
结果:1.半夏泻心汤全方组、阳性药物对照组大多数未见明显的炎细胞浸润,此两组与空白组相比无显著性差异(P＞0.05)。苦寒加甘温组、苦寒组和苦寒加半夏组可见少量炎细胞浸润,多累及胃粘膜的1/3。模型组可见大量炎细胞浸润,累及胃粘膜的2/3甚至全层。治疗组中全方组、阳性药物对照组、苦寒加甘温组与模型组对比均有显著性差异(P＜0.01)。2.模型组凋亡细胞增多,电镜下可观察到凋亡小体。药物治疗组中全方组、阳性药物对照组、苦寒加甘温组、苦寒组和苦寒加半夏组与模型组相比,均能有效减少胃粘膜细胞凋亡,比较有显著性差异(P＜0.01)。3.模型组CD4~+明显降低,CD8~+明显增多,CD4~+/CD8~+比例下降。各组CD4~+的表达依次为阳性药物对照组＞全方组＞苦寒加甘温组＞苦寒组＞半夏加苦寒组＞半夏加甘温组＞甘温组＞半夏组＞模型组。各组CD8~+表达水平由高至低依次为模型组＞半夏组＞半夏加甘温组＞甘温组＞苦寒组＞半夏加苦寒组＞苦寒加甘温组＞全方组＞阳性药对照组＞空白组药物治疗组。其中全方组、阳性药物对照组、苦寒加甘温组、苦寒组和苦寒加半夏组在胃粘膜细胞CD4~+和CD8~+的表达水平上以及CD4~+/CD8~+比例都与模型组有显著性差异(P＜0.01)。
结论:1.幽门螺杆菌感染可导致胃粘膜受损、细胞凋亡增多和T细胞亚群失调。抑制幽门螺杆菌活性,祛除邪气是治疗幽门螺杆菌感染胃粘膜相关疾病的重要环节。2.半夏泻心汤对于幽门螺杆菌感染小鼠胃粘膜有较好的修复作用。主要体现在半夏泻心汤保护胃粘膜,抑制细胞凋亡和调节CD4~+与CD8~+的表达。3.半夏泻心汤全方组与各拆方组比较,全方组对幽门螺杆菌感染的修复作用明显优于各拆方组,其原因与半夏泻心汤寒热并用、辛开苦降、扶正祛邪的精当配伍密切相关。各拆方组中以扶正祛邪兼施的苦寒加甘温组疗效最佳。综合各指标检测结果,各药物组对幽门螺杆菌感染胃粘膜的修复作用从大至小依次为阳性药物对照组＞半夏泻心汤全方组＞苦寒加甘温组＞苦寒组＞半夏加苦寒组＞甘温组＞半夏加甘温组＞半夏组。
AIM:Probe into tuber of Pinellia Heart-Purging Decoction and dismantle square to infect little mouse stomach influence and function mechanism,mucous membrane of morphology to pylorus spiral shell bacillus,and the whole side dismantle square group infect little mouse repair function that stomach organizes to pylorus spiral bacillus each, offer the experiment basis for the fact that prevent and cure the infectious stomach trouble of pylorus spiral bacillus clinically。
Method:Divide the little mouse of 120 C57BLs into 10 groups at random:ⅠPinellia Heart-Purging Decoction all square group,Ⅱtuber of pinellia group,Ⅲsweet warm group,Ⅳbitter cold group,Ⅴtuber of pinellia add bitter cold group,Ⅵtuber of pinellia add sweet warm group,Ⅶbitter cold add sweet warm group,Ⅷpositive medicine contrast group,Ⅸmodel group,Ⅹnormal group.12 little mice respectively of every group,the male and female are half and half.Give the little mouse clear intestines to disinfect with the ammonia and benzyl and west forest in 4 days in succession first,begin to make the mould on the 5th day:Ⅰgroup irritate stomach pylorus spiral shell bacillus fungus liquid 0.2ml toⅨgroup each little mouse,irritate stomach fasting prohibitted water, irritate the stomach once every other day,amounts to 8 times.The end time irritate stomach build one day such as mould,collect four little mouse carry on stomach mucous membrane bacterium train with the urea enzyme testing at random.Result:Bacterium train,leather blue one dye mirror is it find G-curved bacillus to examine,fungus urea enzyme tests the masculine gender,is it make mould begin medicine irritate the stomach after succeeding to verify.Ⅰgroup offer equivalent traditional Chinese medicine of dosage irritate the stomach toⅦgroup according to each little mouse weight;Ⅷgroup irritate stomach equivalent ammonia benzyl penicillin of dosage,dilute with the distilled water into the necessary density.Model group and normal group each little mouse irritate distilled water,stomach of 0.2ml.Irritate the stomach for 8 days in succession,1 times a day,prohibit water fasting for 6 hours before irritating medicines.Irritate after the stomach,animal fasting can't help 12 hours such as ink,the heart collects blood and puts animals to death next day,it is and the intact it fetch stomach,it observe pathology shape where stomach organize change and measure stomach the cells not to wither dying and T lymphocyte groups of CD4~+and CD8~+expression.
Result:1.Pinellia Heart-Purging Decoction square group,positive medicine contrast most of groups meet the obvious inflammation cell soak into all,compared with normal group this two groups do not have a significance difference(P＞0.05).Bitter cold add sweet warm group, bitter cold group and bitter cold add tuber of pinellia group can see a small amount of inflammation cell soak into,involve 1/3 of the stomach mucous membrane more.Model group can see a large number of inflammation cell soak into,involve 2/3,stomach of mucous membrane even the whole layer.Treat group square group,positive medicine contrast group,bitter cold add sweet warm group and model group is it have significance difference to compare with all(P＜0.01).2.Model group is it die cell increase,can is it is it lose the little body to wither to observe under the electric mirror to wither.Medication group square group,positive medicine contrast group,bitter cold add sweet warm group,bitter cold group and bitter cold add tuber of pinellia group compare with model group all,can reduce the stomach mucous membrane cell and wither and die,relatively has a significance difference(P＜0.01)effectively.3.The model group CD4~+is obviously reducing,CD8~+not obviously it increase,CD4~+/drop CD8~+ the proportion.Every group CD4 ~+expression to last group＞All square groups＞The bitter cold adds the sweet warm group＞Bitter cold group＞ The tuber of pinellia adds the bitter cold group＞The tuber of pinellia adds the sweet warm group＞Sweet warm group＞Tuber of pinellia group＞Model group.Every group CD8 express competence from high to successively a model group＞Tuber of pinellia group＞The tuber of pinellia adds the sweet warm group＞Sweet warm group＞Bitter cold group＞The tuber of pinellia adds the bitter cold group＞The bitter cold adds the sweet warm group＞All square groups＞The positive medicine contrasting and organizing＞The normal group medicine treats the group. All square groups among them,the positive medicine is contrasted and organized,the bitter cold adds the sweet warm group,last group at stomach mucous membrane cell CD4 ~+ the and CD8 ~+bitter cold group and bitter cold expression competence at and CD4 ~+/CD8~+ the proportion have significance difference as model group(P＜0.01).
Conclusion:1.Pylorus spiral shell bacillus is it can cause stomach to be mucous membrane damaged to infect,cell is it is it increase with T cell inferior group lacking proper care to die to wither.Suppressing the pylorus spiral shell's bacillus activation,it is to treat the important link of infecting the relevant diseases of mucous membrane of stomach of spiral shell's bacillus of pylorus to dispel perverse trend.2.Pinellia Heart-Purging Decoction infect to pylorus spiral shell bacillus little mouse stomach mucous membrane have better repair function.Mainly it embody in it rush down tuber of pinellia there aren't heart the soups,suppress cell not to wither not dying and not regulating it CD4 ~+and CD8 ~+ expression.3.Pinellia Heart-Purging Decoction all square group with dismantle square group compare,square group all obviously superior to each dismantling the square group to pylorus spiral shell repair function that bacillus is infect each,rush down heart soup fever and chills of reason of it and tuber of pinellia and with,the more hard to turn on more bitter to lower,compatibility not precise and appropriate not strengthen body resistance and eliminating evil closely related with. Dismantle square group in order to strengthen body resistance and eliminating evil each and concurrently bitter cold that construct add sweet warm curative effect best group.Synthesize every index measure result, every medicine group infect to pylorus spiral shell bacillus repair function,stomach of mucous membrane from heavy to light to contrast group＞Pinellia Heart-Purging Decoction in the all square groups of heart soup＞The bitter cold adds the sweet warm group＞Bitter cold group＞The tuber of pinellia adds the bitter cold group＞Sweet warm group＞The tuber of pinellia adds the sweet warm group＞Tuber of pinellia group.
方法:将120只C_(57)BL小鼠随机分为10组:Ⅰ半夏泻心汤全方组,Ⅱ半夏组,Ⅲ甘温组,Ⅳ苦寒组,Ⅴ半夏加苦寒组,Ⅵ半夏加甘温组,Ⅶ苦寒加甘温组,Ⅷ阳性药物对照组,Ⅸ模型纽,Ⅹ空白组。每组各12只小鼠,雌雄各半。先连续4天用氨苄西林给小鼠清肠消毒,第5天开始造模:第Ⅰ组至第Ⅸ组每只小鼠灌胃幽门螺杆菌菌液0.2ml,灌胃前禁食禁水,每隔一天灌胃一次,共8次。末次灌胃造模两天后,随机抽取四只小鼠进行胃粘膜细菌培养和尿素酶试验。结果:细菌培养,革兰氏染色镜检发现G~-弧形杆菌,菌尿素酶试验阳性,证实造模成功后开始药物灌胃。第Ⅰ组至第Ⅶ组按每只小鼠体重给予等效剂量的中药灌胃;第Ⅷ组灌胃等效剂量的氨苄青霉素,用蒸馏水稀释成所需浓度。模型组和空白组每只小鼠灌胃0.2ml的蒸馏水。连续灌胃8天,每天1次,灌药前禁水禁食6小时。灌胃结束后,动物禁食不禁水12小时,次日心脏采血处死动物,并完整取胃,观察胃组织的病理形态改变和检测胃细胞凋亡及T淋巴细胞亚群CD4~+和CD8~+的表达。
结果:1.半夏泻心汤全方组、阳性药物对照组大多数未见明显的炎细胞浸润,此两组与空白组相比无显著性差异(P＞0.05)。苦寒加甘温组、苦寒组和苦寒加半夏组可见少量炎细胞浸润,多累及胃粘膜的1/3。模型组可见大量炎细胞浸润,累及胃粘膜的2/3甚至全层。治疗组中全方组、阳性药物对照组、苦寒加甘温组与模型组对比均有显著性差异(P＜0.01)。2.模型组凋亡细胞增多,电镜下可观察到凋亡小体。药物治疗组中全方组、阳性药物对照组、苦寒加甘温组、苦寒组和苦寒加半夏组与模型组相比,均能有效减少胃粘膜细胞凋亡,比较有显著性差异(P＜0.01)。3.模型组CD4~+明显降低,CD8~+明显增多,CD4~+/CD8~+比例下降。各组CD4~+的表达依次为阳性药物对照组＞全方组＞苦寒加甘温组＞苦寒组＞半夏加苦寒组＞半夏加甘温组＞甘温组＞半夏组＞模型组。各组CD8~+表达水平由高至低依次为模型组＞半夏组＞半夏加甘温组＞甘温组＞苦寒组＞半夏加苦寒组＞苦寒加甘温组＞全方组＞阳性药对照组＞空白组药物治疗组。其中全方组、阳性药物对照组、苦寒加甘温组、苦寒组和苦寒加半夏组在胃粘膜细胞CD4~+和CD8~+的表达水平上以及CD4~+/CD8~+比例都与模型组有显著性差异(P＜0.01)。
结论:1.幽门螺杆菌感染可导致胃粘膜受损、细胞凋亡增多和T细胞亚群失调。抑制幽门螺杆菌活性,祛除邪气是治疗幽门螺杆菌感染胃粘膜相关疾病的重要环节。2.半夏泻心汤对于幽门螺杆菌感染小鼠胃粘膜有较好的修复作用。主要体现在半夏泻心汤保护胃粘膜,抑制细胞凋亡和调节CD4~+与CD8~+的表达。3.半夏泻心汤全方组与各拆方组比较,全方组对幽门螺杆菌感染的修复作用明显优于各拆方组,其原因与半夏泻心汤寒热并用、辛开苦降、扶正祛邪的精当配伍密切相关。各拆方组中以扶正祛邪兼施的苦寒加甘温组疗效最佳。综合各指标检测结果,各药物组对幽门螺杆菌感染胃粘膜的修复作用从大至小依次为阳性药物对照组＞半夏泻心汤全方组＞苦寒加甘温组＞苦寒组＞半夏加苦寒组＞甘温组＞半夏加甘温组＞半夏组。
AIM:Probe into tuber of Pinellia Heart-Purging Decoction and dismantle square to infect little mouse stomach influence and function mechanism,mucous membrane of morphology to pylorus spiral shell bacillus,and the whole side dismantle square group infect little mouse repair function that stomach organizes to pylorus spiral bacillus each, offer the experiment basis for the fact that prevent and cure the infectious stomach trouble of pylorus spiral bacillus clinically。
Method:Divide the little mouse of 120 C57BLs into 10 groups at random:ⅠPinellia Heart-Purging Decoction all square group,Ⅱtuber of pinellia group,Ⅲsweet warm group,Ⅳbitter cold group,Ⅴtuber of pinellia add bitter cold group,Ⅵtuber of pinellia add sweet warm group,Ⅶbitter cold add sweet warm group,Ⅷpositive medicine contrast group,Ⅸmodel group,Ⅹnormal group.12 little mice respectively of every group,the male and female are half and half.Give the little mouse clear intestines to disinfect with the ammonia and benzyl and west forest in 4 days in succession first,begin to make the mould on the 5th day:Ⅰgroup irritate stomach pylorus spiral shell bacillus fungus liquid 0.2ml toⅨgroup each little mouse,irritate stomach fasting prohibitted water, irritate the stomach once every other day,amounts to 8 times.The end time irritate stomach build one day such as mould,collect four little mouse carry on stomach mucous membrane bacterium train with the urea enzyme testing at random.Result:Bacterium train,leather blue one dye mirror is it find G-curved bacillus to examine,fungus urea enzyme tests the masculine gender,is it make mould begin medicine irritate the stomach after succeeding to verify.Ⅰgroup offer equivalent traditional Chinese medicine of dosage irritate the stomach toⅦgroup according to each little mouse weight;Ⅷgroup irritate stomach equivalent ammonia benzyl penicillin of dosage,dilute with the distilled water into the necessary density.Model group and normal group each little mouse irritate distilled water,stomach of 0.2ml.Irritate the stomach for 8 days in succession,1 times a day,prohibit water fasting for 6 hours before irritating medicines.Irritate after the stomach,animal fasting can't help 12 hours such as ink,the heart collects blood and puts animals to death next day,it is and the intact it fetch stomach,it observe pathology shape where stomach organize change and measure stomach the cells not to wither dying and T lymphocyte groups of CD4~+and CD8~+expression.
Result:1.Pinellia Heart-Purging Decoction square group,positive medicine contrast most of groups meet the obvious inflammation cell soak into all,compared with normal group this two groups do not have a significance difference(P＞0.05).Bitter cold add sweet warm group, bitter cold group and bitter cold add tuber of pinellia group can see a small amount of inflammation cell soak into,involve 1/3 of the stomach mucous membrane more.Model group can see a large number of inflammation cell soak into,involve 2/3,stomach of mucous membrane even the whole layer.Treat group square group,positive medicine contrast group,bitter cold add sweet warm group and model group is it have significance difference to compare with all(P＜0.01).2.Model group is it die cell increase,can is it is it lose the little body to wither to observe under the electric mirror to wither.Medication group square group,positive medicine contrast group,bitter cold add sweet warm group,bitter cold group and bitter cold add tuber of pinellia group compare with model group all,can reduce the stomach mucous membrane cell and wither and die,relatively has a significance difference(P＜0.01)effectively.3.The model group CD4~+is obviously reducing,CD8~+not obviously it increase,CD4~+/drop CD8~+ the proportion.Every group CD4 ~+expression to last group＞All square groups＞The bitter cold adds the sweet warm group＞Bitter cold group＞ The tuber of pinellia adds the bitter cold group＞The tuber of pinellia adds the sweet warm group＞Sweet warm group＞Tuber of pinellia group＞Model group.Every group CD8 express competence from high to successively a model group＞Tuber of pinellia group＞The tuber of pinellia adds the sweet warm group＞Sweet warm group＞Bitter cold group＞The tuber of pinellia adds the bitter cold group＞The bitter cold adds the sweet warm group＞All square groups＞The positive medicine contrasting and organizing＞The normal group medicine treats the group. All square groups among them,the positive medicine is contrasted and organized,the bitter cold adds the sweet warm group,last group at stomach mucous membrane cell CD4 ~+ the and CD8 ~+bitter cold group and bitter cold expression competence at and CD4 ~+/CD8~+ the proportion have significance difference as model group(P＜0.01).
Conclusion:1.Pylorus spiral shell bacillus is it can cause stomach to be mucous membrane damaged to infect,cell is it is it increase with T cell inferior group lacking proper care to die to wither.Suppressing the pylorus spiral shell's bacillus activation,it is to treat the important link of infecting the relevant diseases of mucous membrane of stomach of spiral shell's bacillus of pylorus to dispel perverse trend.2.Pinellia Heart-Purging Decoction infect to pylorus spiral shell bacillus little mouse stomach mucous membrane have better repair function.Mainly it embody in it rush down tuber of pinellia there aren't heart the soups,suppress cell not to wither not dying and not regulating it CD4 ~+and CD8 ~+ expression.3.Pinellia Heart-Purging Decoction all square group with dismantle square group compare,square group all obviously superior to each dismantling the square group to pylorus spiral shell repair function that bacillus is infect each,rush down heart soup fever and chills of reason of it and tuber of pinellia and with,the more hard to turn on more bitter to lower,compatibility not precise and appropriate not strengthen body resistance and eliminating evil closely related with. Dismantle square group in order to strengthen body resistance and eliminating evil each and concurrently bitter cold that construct add sweet warm curative effect best group.Synthesize every index measure result, every medicine group infect to pylorus spiral shell bacillus repair function,stomach of mucous membrane from heavy to light to contrast group＞Pinellia Heart-Purging Decoction in the all square groups of heart soup＞The bitter cold adds the sweet warm group＞Bitter cold group＞The tuber of pinellia adds the bitter cold group＞Sweet warm group＞The tuber of pinellia adds the sweet warm group＞Tuber of pinellia group.
引文
[1]Talley NJ.Chronic gastitis:athogenesis and manggement[J].DigDis.1989.7:61
[2]危北海.近年来消化系统疾病若干问题研究进展及对中医、中西医结合的挑战和启示[J].中华消化杂志,2000,20(4):221
[3]张万岱.幽门螺杆菌研究的现状与展望[J].中华消化杂志,1998,18(1):5
[4]周殿元,杨海涛,张万岱.幽门螺杆菌与胃十二指肠疾病.上海科学技术文献出版社,1992,4
[5]李宇航,李澎涛,王庆国,等.半夏泻心汤及其拆方对慢性胃溃疡大鼠溃疡灶形态变化的影响[J].中国中医基础医学杂志,2003,9(1):16-20
[6]柯雪帆.伤寒论选读。上海科学技术出版社,1996:92
[7]柯雪帆,赵章忠,张玉萍等.《伤寒论》和《金匮要略》中的药物剂量问题[J].上海中医药杂志,1983,(12):36
[8]柴可夫.慢性胃炎--疑难病中西医结合诊治从书.北京:科学技术文献出版社,1999.270
[9]中华医学会消化病学分会.全国慢性胃炎研讨会共识意见[J].中华消化杂志,2000,20:199-201
[10]邓铁涛.中医证候规范.广州:广东科学技术出版社,1990,303
[11]厉兰娜,孔繁智,沈金美,等.半夏泻心汤证与幽门螺杆菌感染关系的临床研究[J].中医杂志,1998,39(4):220
[12]张琳.半夏泻心汤治疗胃病的研究概况[J].上海中医药大学学报. 2002,16(3):62-65
[13]魏辉,司兆学,单罢安,等.加味半夏泻心汤对大鼠胃粘膜损伤的影响[J].中国中医药科技,1998,5(5):282
[14]吴丽芹,姜惟,姚欣.半夏泻心汤对幽门螺杆菌感染大鼠慢性胃炎模型胃粘液层磷脂、氨基己糖的影响[J].中国中医药信息杂志,2001,8(5):29-30
[15]孙艳.抗幽门螺杆菌的中药及临床运用[J].解放军药学报,2000,16(6):338-339
[16]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,2000,5(8):292-293.
[17]蔡仙德,谭剑萍,等.黄岑甙对小鼠细胞免疫功能的影响[J].南京铁道医学院学报,1994,13(2):65-68
[18]王本祥.现代中药药理与临床.天津科技翻译出版公司.2004;534-540
[19]Lee SK,Lee YC,Chung JB,Chon CY,Moon YM,Kang J-K,Park IS,Suh CO,Yang WI.Low grade gastric mucosa associated lymphoid tissue lymphoma:Treatment strategies based on 10 year follow -up.World J Gastroenterol 2004;10:223-226
[20]刘世增,袁吉云,赵群,等.Wistar大鼠Hp感染胃炎模型研究[J].苏州医学院学报,1997,17(6):1031-1032
[21]石碧坚,刘厚钰.幽门螺杆菌的致病机制.见胡伏莲/周殿元主编《幽门螺杆菌感染的基础与临床》修订版.北京,中国科学技术出版社.2002.1:54-71
[22]GrahemDYetal.Gastroenterology,1993,105;279-282
[23]Grahem D Yet al.Gastroenterology,1993,105;279-282
[24]Velle J et al.Disappearance of Gastritis after Eradication of Helicobacter Pylori.Scand J Gastro enterol.1991,26:0573
[25]吕宾.王慧萍.项柏康,等.幽门螺杆菌感染对胃上皮细胞凋亡及调节基因表达的影响[J].中华内科杂志.2000,39(4):255-258
[26]Shirim AH,Sordillo Em,Oh SH,et al.[J]Cancer Res,1999,59:2277-2281
[27]李志芳,林庚金,蔡定芳,等.幽门螺杆菌诱导胃上皮细胞凋亡的实验研究[J].上海医科大学学报.1999,5(26):31-33
[28]Moran AP,Wadstrom T.[J].Cur Opin Gastroenterol,1998,14(suppl 1):9-14
[29]Suzuki M,Miura S,Suematsu M,et al.[J].Am J physiol,1996,263:G719-705.
[30]孙燕.幽门螺杆菌致胃上皮细胞凋亡的机制及其在胃癌发生中的作用[J].国外医学内科学分册.2004,31(10):419-421
[31]Ernst P.Review article:the role of inflammation in the pathogenesis of gastric cancer.Aliment Pharmacol Ther 1999;13:13-18
[32]Houghton J-M,Macer-Bloch LS,Harrison L,Kim KH,Korah RM.Tumor necrosis facter alpha and interleukin 1 beta up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection.Infect Immun 2000,68:1189-1195
[33]Moran Ap,Wadstrom T.Pathogenesis of Helicobacter pylori.Cur Opin Gastroenterol,1998,14(Suppel):S9-14
[34]杨黎青.免疫学基础与病原微生物学.中国中医药出版社,2003: 71
[35]Engstrand L,et al.Infect Immun 1989,57:827-852
[36]门子荣,钱冬梅,刘复强,等.不同胃病患者外周血T淋巴细胞亚群的测定结果[J].基础医学与临床.1998,18(3):190-192
[37]Agnihotri N,Bhasin DK,Vohra H,Ray P,Singh K,Ganguly NK.Characterization of lymphocytic subsets and cytokine production in gastric biopsy samples from Helicobacter.pylori patients.Scand J Gastroenterol 1998,33:704-709
[38]纪开宇,胡伏莲.幽门螺杆菌与细胞因子研究进展[J].世界华人消化杂志.2002,10(5):503-508
[2]危北海.近年来消化系统疾病若干问题研究进展及对中医、中西医结合的挑战和启示[J].中华消化杂志,2000,20(4):221
[3]张万岱.幽门螺杆菌研究的现状与展望[J].中华消化杂志,1998,18(1):5
[4]周殿元,杨海涛,张万岱.幽门螺杆菌与胃十二指肠疾病.上海科学技术文献出版社,1992,4
[5]李宇航,李澎涛,王庆国,等.半夏泻心汤及其拆方对慢性胃溃疡大鼠溃疡灶形态变化的影响[J].中国中医基础医学杂志,2003,9(1):16-20
[6]柯雪帆.伤寒论选读。上海科学技术出版社,1996:92
[7]柯雪帆,赵章忠,张玉萍等.《伤寒论》和《金匮要略》中的药物剂量问题[J].上海中医药杂志,1983,(12):36
[8]柴可夫.慢性胃炎--疑难病中西医结合诊治从书.北京:科学技术文献出版社,1999.270
[9]中华医学会消化病学分会.全国慢性胃炎研讨会共识意见[J].中华消化杂志,2000,20:199-201
[10]邓铁涛.中医证候规范.广州:广东科学技术出版社,1990,303
[11]厉兰娜,孔繁智,沈金美,等.半夏泻心汤证与幽门螺杆菌感染关系的临床研究[J].中医杂志,1998,39(4):220
[12]张琳.半夏泻心汤治疗胃病的研究概况[J].上海中医药大学学报. 2002,16(3):62-65
[13]魏辉,司兆学,单罢安,等.加味半夏泻心汤对大鼠胃粘膜损伤的影响[J].中国中医药科技,1998,5(5):282
[14]吴丽芹,姜惟,姚欣.半夏泻心汤对幽门螺杆菌感染大鼠慢性胃炎模型胃粘液层磷脂、氨基己糖的影响[J].中国中医药信息杂志,2001,8(5):29-30
[15]孙艳.抗幽门螺杆菌的中药及临床运用[J].解放军药学报,2000,16(6):338-339
[16]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,2000,5(8):292-293.
[17]蔡仙德,谭剑萍,等.黄岑甙对小鼠细胞免疫功能的影响[J].南京铁道医学院学报,1994,13(2):65-68
[18]王本祥.现代中药药理与临床.天津科技翻译出版公司.2004;534-540
[19]Lee SK,Lee YC,Chung JB,Chon CY,Moon YM,Kang J-K,Park IS,Suh CO,Yang WI.Low grade gastric mucosa associated lymphoid tissue lymphoma:Treatment strategies based on 10 year follow -up.World J Gastroenterol 2004;10:223-226
[20]刘世增,袁吉云,赵群,等.Wistar大鼠Hp感染胃炎模型研究[J].苏州医学院学报,1997,17(6):1031-1032
[21]石碧坚,刘厚钰.幽门螺杆菌的致病机制.见胡伏莲/周殿元主编《幽门螺杆菌感染的基础与临床》修订版.北京,中国科学技术出版社.2002.1:54-71
[22]GrahemDYetal.Gastroenterology,1993,105;279-282
[23]Grahem D Yet al.Gastroenterology,1993,105;279-282
[24]Velle J et al.Disappearance of Gastritis after Eradication of Helicobacter Pylori.Scand J Gastro enterol.1991,26:0573
[25]吕宾.王慧萍.项柏康,等.幽门螺杆菌感染对胃上皮细胞凋亡及调节基因表达的影响[J].中华内科杂志.2000,39(4):255-258
[26]Shirim AH,Sordillo Em,Oh SH,et al.[J]Cancer Res,1999,59:2277-2281
[27]李志芳,林庚金,蔡定芳,等.幽门螺杆菌诱导胃上皮细胞凋亡的实验研究[J].上海医科大学学报.1999,5(26):31-33
[28]Moran AP,Wadstrom T.[J].Cur Opin Gastroenterol,1998,14(suppl 1):9-14
[29]Suzuki M,Miura S,Suematsu M,et al.[J].Am J physiol,1996,263:G719-705.
[30]孙燕.幽门螺杆菌致胃上皮细胞凋亡的机制及其在胃癌发生中的作用[J].国外医学内科学分册.2004,31(10):419-421
[31]Ernst P.Review article:the role of inflammation in the pathogenesis of gastric cancer.Aliment Pharmacol Ther 1999;13:13-18
[32]Houghton J-M,Macer-Bloch LS,Harrison L,Kim KH,Korah RM.Tumor necrosis facter alpha and interleukin 1 beta up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection.Infect Immun 2000,68:1189-1195
[33]Moran Ap,Wadstrom T.Pathogenesis of Helicobacter pylori.Cur Opin Gastroenterol,1998,14(Suppel):S9-14
[34]杨黎青.免疫学基础与病原微生物学.中国中医药出版社,2003: 71
[35]Engstrand L,et al.Infect Immun 1989,57:827-852
[36]门子荣,钱冬梅,刘复强,等.不同胃病患者外周血T淋巴细胞亚群的测定结果[J].基础医学与临床.1998,18(3):190-192
[37]Agnihotri N,Bhasin DK,Vohra H,Ray P,Singh K,Ganguly NK.Characterization of lymphocytic subsets and cytokine production in gastric biopsy samples from Helicobacter.pylori patients.Scand J Gastroenterol 1998,33:704-709
[38]纪开宇,胡伏莲.幽门螺杆菌与细胞因子研究进展[J].世界华人消化杂志.2002,10(5):503-508