胃炎Ⅰ号对慢性萎缩性胃炎大鼠血清胃泌素和血浆胃动素的调控作用
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摘要
背景：慢性萎缩性胃炎(Chronic atrophic gastritis, CAG)是以胃粘膜局部性或广泛性的固有腺体萎缩,数量减少,粘膜层变薄,粘膜肌层变厚为主要病理改变的一种慢性胃炎。由于腺体萎缩或消失,胃粘膜有不同程度的变薄,并常伴有肠上皮化生、炎性反应及不典型增生。临床上可有胃内游离盐酸减少或缺乏、消化不良、上腹不适或钝痛、贫血等症状。
CAG是消化系统常见病、多发病,且反复发作,缠绵难愈,发病率随年龄增长而增高,故中老年人多发此病。本病可由慢性浅表性胃炎发展而来,也可两者并存。有的呈隐袭性,发现时即为本病。本病可能与遗传有关,呈现出家族中发病集中的趋势。因其与胃癌的发生有一定关系,1978年WHO将其列为胃癌的癌前疾病或癌前状态,而在CAG伴发的肠上皮化生和异型增生,则是胃癌的癌前病变,癌变的可能性大,成为目前研究的重点。一般认为,胃粘膜发生癌肿并非由正常细胞一跃而变成癌细胞,而是一个由量变到质变的多步骤癌变过程。目前,慢性胃炎->胃粘膜萎缩->肠化->异型增生->胃癌的发展模式已为国内外多数学者所赞同。CAG在中国的发病率很高,临床随诊10—20年后约8%病例有胃癌发生。因此,及早识别、防治癌前疾病和癌前病变,成为降低胃癌发生率和死亡率较为行之有效的方法。
胃泌素(Gastrin, Gas)是一种重要的胃肠激素,它主要由G细胞分泌。G细胞是典型的开放型细胞,以胃窦部最多,其次是胃底、十二指肠和空肠等处。人胰岛的D细胞亦能分泌胃泌素。近年发现,颊粘膜、舌、食道、中枢神经系统也含有胃泌素,1978年Rehfeld证明人的脑脊液和某些脑组织中存在胃泌素,胃泌素几乎对整个胃肠道均有作用,它可促进胃肠道的分泌功能；增加胃肠道的运动；松弛幽门括约肌；胆道口括约肌和回盲部括约肌；促进胃及上部肠道粘膜细胞的分裂增殖；促进胰岛素和降钙素的释放。
胃动素(Motilin, MOT)是由22个氨基酸残基组成的直链多肽类胃肠激素,由Brown等于1972年自动物十二指肠液中分离纯化。主要由十二指肠和近端空肠粘膜隐窝中Mo细胞释放,此外在胃底、胃窦及下部小肠粘膜也有少量Mo细胞.胃动素直接作用于消化道平滑肌细胞的受体,导致平滑肌收缩。胃动素在消化间期呈周期性释放,故称为消化间期激素。消化道肿瘤患者胃动素的水平较正常人显著增高,其机制尚不明确,胃动素水平增高的原因可能为：①除胃肠道粘膜外,胃动素也存在于神经组织中。含有胃动素的神经细胞存在于食道、胃、小肠、大肠的粘膜下层和肌层,当这些部位有肿瘤生长时,可能使含有胃动素的神经细胞刺激增强而促使胃动素的水平增高。②胃癌和结肠癌细胞中有促胃液素受体,早期胃癌和结肠癌的癌细胞可产生一种促胃液素样物,它可刺激胃动素的释放。患胃肠道肿瘤时,胃肠道的运动功能发生紊乱,可能反馈地引起血浆胃动素水平的升高。
导师刘友章教授根据中医脾胃为后天之本,气血生化之源的理论,结合临床,运用健脾益气,养血和胃生肌的方法治疗慢性萎缩性胃炎,创制了纯中药方剂胃炎1号。胃炎1号选用党参、白芍健脾养胃,柔肝生肌为君；珍珠层粉、蒲公英、白花蛇舌草、七叶一枝花、莪术、当归清热化瘀,行气活血为臣；鸡骨草、砂仁理气和胃止痛为佐；甘草调和诸药为使,共凑健脾益气,和胃生肌之功效。早在20世纪90年代初,刘友章教授与日本京都大学合作研究的“胃炎1号对萎缩性胃炎病人胃粘膜修复作用的研究”已初步证实了胃炎1号对脾胃虚弱型慢性萎缩性胃炎病人胃粘膜修复有一定的疗效,并有一定的抗上皮化生的作用。刘友章教授主持的广东省中医药管理局科研课题——胃炎1号治疗萎缩性胃炎作用机理的临床与实验研究,运用了随机对照的方法从血清胃肠激素的变化、胃粘膜组织的病理变化等方面发现胃炎Ⅰ号对大鼠CAG模型以及慢性萎缩性胃炎患者的胃粘膜改变具有明显的防治作用。
目的：本实验研究以血清胃泌素和血浆胃动素为切入点,对胃炎Ⅰ号治疗大鼠慢性萎缩性胃炎的作用机制进行更深入探讨,为胃炎Ⅰ号的临床疗效提供科学的实验依据,可以为开发临床治疗慢性萎缩性胃炎有效中成药胃炎Ⅰ号提供理论实验依据。
方法：本研究包括文献研究和实验研究两部分。本论文对古代历代医家及现代历代中医家对本病病因病机、辩证分型以及治疗原则进行了系统论述。随着科学技术发展,现代医学对本病的病因、发病机制及诊疗技术等方面研究不断深入,本文对其进展也进行了综述。
实验研究部分,选用健康SD大鼠84只,雌雄各半。共分六个组：模型组24只,空白组12只,高剂量组12只,中剂量组12只,低剂量组12只,西药对照组12只。采用50μg/ml甲基-硝基-亚硝基胍(MNNG)避光自由饮用、3mg/ml雷尼替丁灌胃每天一次2ml、加上2天给食1天停食的饥饱失常综合造模法构建大鼠慢性萎缩性胃炎模型,造模20周。经病理检查模型构建成功后,高剂量治疗组给予5g/(kg·d)胃炎Ⅰ号,中剂量治疗组给予2.5g/(kg·d)胃炎Ⅰ号,低剂量组给予1.25g/(kg·d)胃炎Ⅰ号,西药对照组给予0.86 g/(kg·d)维酶素,空白组正常饮食。
采用放射免疫法检测慢性萎缩性胃炎大鼠血清胃泌素和血浆胃动素的浓度。全部实验数据均采用SPSS13统计软件处理,各组数据以均数±标准差(X±S)形式表示。
结果：
1、本实验研究表明,本实验采用的造模方法能够成功复制大鼠慢性萎缩性胃炎动物模型。但本实验所用的方法也存在所构建模型病变不够典型,造模时间长死亡率较高,采用的造模试剂MNNG为致癌物质,对实验人员及环境均存在危害,实验试剂价格较贵等缺点。因此,本实验造模方案可成功构建大鼠慢性萎缩性胃炎模型,但并非一个良好的方案。
2、各组大鼠血清胃泌素含量变化,经一维方差分析及LSD两两比较,各组与模型组比较P<0.05,均具有统计学意义,说明本实验慢性萎缩性胃炎大鼠模型构建成功,且各组胃炎Ⅰ号及维酶素干预对提高血清胃泌素水平均有疗效。胃炎Ⅰ号高、中剂量与空白组比较P>0.05,无统计学意义,组间没有明显差别,低剂量组与空白组比较P<0.05,差别有统计学意义,胃炎Ⅰ号高剂量与中剂量比较P>0.05,故胃炎Ⅰ号对慢性萎缩性胃炎大鼠血清胃泌素的以高、中剂量疗效均为最佳。西药维酶素疗效优于胃炎Ⅰ号低剂量组疗效(P<0.05)。
3、各组大鼠血浆胃动素含量变化,经一维方差分析及LSD两两比较,各组与模型组比较P<0.01,均具有统计学意义,说明本实验慢性萎缩性胃炎大鼠模型构建成功,且各组胃炎Ⅰ号及维酶素干预对降低血浆胃动素水平均有疗效。高剂量、低剂量胃炎Ⅰ号及酶素组与空白组比较P<0.05,差别有统计学意义,中剂量组与空白组比较P>0.05,差别无统计学意义,故在各治疗组中以胃炎Ⅰ号中剂量疗效最佳。维酶素组与低剂量组比较P<0.05,差别具有统计学意义。
结论：本论文通过实验研究探讨了胃炎Ⅰ号对慢性萎缩性胃炎大鼠血清胃泌素和血浆胃动素的调控作用。研究结果表明：
1、本实验采用的综合造模法可以成功构建慢性萎缩性胃炎大鼠模型。
2、胃炎Ⅰ号可以改善慢性萎缩性胃炎大鼠胃黏膜病理改变。
3、本实验研究发现,慢性萎缩性胃炎模型大鼠血清胃泌素水平低于正常大鼠血清胃泌素水平。胃炎Ⅰ号治疗后,慢性萎缩性胃炎模型大鼠血清胃泌素水平上升。
4、本实验研究发现,慢性萎缩性胃炎模型大鼠血浆胃动素水平高于正常大鼠血浆胃动素水平。胃炎Ⅰ号治疗后,慢性萎缩性胃炎模型大鼠血浆胃动素水平降低。
综合以上研究结果,胃炎Ⅰ号可能通过提高CAG大鼠血清胃泌素和降低血浆胃动素的水平,起到改善CAG大鼠胃黏膜损伤,促进病变胃黏膜修复的治疗效果。
Objective:Chronic atrophic gastritis (CAG) is a refractory disease of digestive system diseases, which's main pathological changes including gastric mucosa and gastric glands thinning, lamina muscularis mucosae thickening, intestinal metaplasia, etc. Due to the atrophy of the gastric glandular organ, the gastric mucosa is thinner, together with intestinal metaplasia, inflammatory reaction and atypical hyperplasia. The clinical symptoms are including dyspepsia, epigastric discomfort or dull pain and anemia.
CAG is a commonly encountered disease and frequently encountered disease of digestive system, characteristic with recurrent attacks. The disease rate rise with the age increase, soit is higher in the aged. Chronic superficial gastritis could develop to CAG. Because of relating to the gastric cance, CAG was classified as precancerous disease or precancerous disease by the WHO in 1978. According to the linkage theory of gastric cancer carcinogenesis, the pathological changes of gastric cancer carcinogenesis follow the step from chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia, atypical hyperplasia and the end to gastric cancer. CAG as a kind of lesion precancerous has been generally accepted. The incidence of CAG is very high in China, and about 8% will develop to gastric cancer after 10 to 20 years. So discerning and preventing the precancerous disease and lesion precancerous of s digestive system as early as possible, are effective methods to decrease the incidence rate and death rate of gastric cancer.
Gastrin is a kind of important gastrointestinal hormone, secreted by G cells. Gastrin affects the most functions of the gastrointestinal tract, promoting gastrointestinal secretion, promoting gastrointestinal movement, loosening pyloric sphincter and sphincter of Oddi and ileocecal junction, promoting gastrointestinal mucous cell division growth, promoting releasing trypsin and calcitonin.
Motilin is a kind of straight chain polypeptides gastrointestinal hormone, constitute by 22 amino-acid residue. Motilin is secreted by Mo cells in the duodenum and proximate jejunal mucous membrane cryptae. Motilin directly affect to the acceptor of enteron smooth muscle cell, inducing smooth muscle contraction. Motilin secretes periodicity in interdigestive phase. The level of motilin in the digestive tract cancer patients is higher than health persons, and the mechanisms are indefinite.
Gastritis I is an effective prescription which was found by Professor Liu Youzhang in his several decade clinical practices It has the effectiveness of strengthening spleen, benefiting vital energy, nourishing blood, regulating stomach and promoting granulation, and has been confirmed it's effectiveness in reconditioning gastric mucosa and resisting epithelial metaplasia of CAG. The purpose of our empirical study is to lucubrate the mechanism of gastritis I curing the CAG rats by lucubrating the mechanism of gastritis I regulating to serum gastrin and blood plasma motilin in stomach of the CAG rats, and to provide scientific experimental evidence of the clinical therapeutic effect of gastritis I.
Methods:Our research was divided into overview and empirical study. We expounded the etiological factor, pathogenesis and therapeutic principle of ancient and contemporary doctor of TCM. We also expounded the advancement of modern medicine. In the empirical study,84 healthy SD rats were divided into 6 groups, including model group (24), normal group (12), western medicine control group (12), and 3 Gastritis I treatment group including high dose group (12), medium dose group (12), low-dose group (12). the CAG model rats was constructed by freely drinking the MNNG solution (50μg/ml), being intragastric administration and irregular diet. After the CAG model was constructed successfully, giving 5g/(kg·d) Gastritis I to high dose treatment group, giving 2.5g/(kg·d) Gastritis I to medium dose group, giving 1.25g/(kg·d) Gastritis I to low-dose group, giving 0.86 g/(kg·d) Wei Mei Su Pian to western medicine control group, the normal group was feed normally. We adopted radio-immunity echnology to detect the level of serum gastrin and blood plasma motilin.
Result:①Our empirical study indicated that the method adopted to copy the CAG rats animal models was success. But the pathological changes were not typical enough, and persistence time was too long, the death rate was high, and the reductant MNNG is a kind of carcinogen, harm to the experimenter and the environment. Accordingly, our experiment program had successful, but not excellent enough.②The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group (P<0.05). After treated by gastritis I, the curative effect of high and medium dose were better than low dose and Wei Mei Su Pian (P<0.05).③The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group (P<0.01). After treated by gastritis I, the curative effect of medium dose was better than other groups (P<0.05).
Conclusion:Our experiment had study the mechanism of gastritis I regulating to the serum gastrin and blood plasma motilin of the CAG rats by empirical study. The experimental results indicated:①Our study adopted synthetic methods to construct the CAG model rats. Those methods were able to build the CAG model rats successfully;②Gastritis I could improve the gastric mucosal lesion of the CAG rats;③The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group. After treated by Gastritis I, the serum gastrin level of the CAG model group rats was rising.④The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group. After treated by Gastritis I, the blood plasma motilin level of the CAG model group rats was decreasing.
Gastritis I could improve the gastric mucosa damage of the CAG rats, and promote gastric mucosa plerosis, by raising the serum gastrin level and decreasing the blood plasma motilin level.
CAG是消化系统常见病、多发病,且反复发作,缠绵难愈,发病率随年龄增长而增高,故中老年人多发此病。本病可由慢性浅表性胃炎发展而来,也可两者并存。有的呈隐袭性,发现时即为本病。本病可能与遗传有关,呈现出家族中发病集中的趋势。因其与胃癌的发生有一定关系,1978年WHO将其列为胃癌的癌前疾病或癌前状态,而在CAG伴发的肠上皮化生和异型增生,则是胃癌的癌前病变,癌变的可能性大,成为目前研究的重点。一般认为,胃粘膜发生癌肿并非由正常细胞一跃而变成癌细胞,而是一个由量变到质变的多步骤癌变过程。目前,慢性胃炎->胃粘膜萎缩->肠化->异型增生->胃癌的发展模式已为国内外多数学者所赞同。CAG在中国的发病率很高,临床随诊10—20年后约8%病例有胃癌发生。因此,及早识别、防治癌前疾病和癌前病变,成为降低胃癌发生率和死亡率较为行之有效的方法。
胃泌素(Gastrin, Gas)是一种重要的胃肠激素,它主要由G细胞分泌。G细胞是典型的开放型细胞,以胃窦部最多,其次是胃底、十二指肠和空肠等处。人胰岛的D细胞亦能分泌胃泌素。近年发现,颊粘膜、舌、食道、中枢神经系统也含有胃泌素,1978年Rehfeld证明人的脑脊液和某些脑组织中存在胃泌素,胃泌素几乎对整个胃肠道均有作用,它可促进胃肠道的分泌功能；增加胃肠道的运动；松弛幽门括约肌；胆道口括约肌和回盲部括约肌；促进胃及上部肠道粘膜细胞的分裂增殖；促进胰岛素和降钙素的释放。
胃动素(Motilin, MOT)是由22个氨基酸残基组成的直链多肽类胃肠激素,由Brown等于1972年自动物十二指肠液中分离纯化。主要由十二指肠和近端空肠粘膜隐窝中Mo细胞释放,此外在胃底、胃窦及下部小肠粘膜也有少量Mo细胞.胃动素直接作用于消化道平滑肌细胞的受体,导致平滑肌收缩。胃动素在消化间期呈周期性释放,故称为消化间期激素。消化道肿瘤患者胃动素的水平较正常人显著增高,其机制尚不明确,胃动素水平增高的原因可能为：①除胃肠道粘膜外,胃动素也存在于神经组织中。含有胃动素的神经细胞存在于食道、胃、小肠、大肠的粘膜下层和肌层,当这些部位有肿瘤生长时,可能使含有胃动素的神经细胞刺激增强而促使胃动素的水平增高。②胃癌和结肠癌细胞中有促胃液素受体,早期胃癌和结肠癌的癌细胞可产生一种促胃液素样物,它可刺激胃动素的释放。患胃肠道肿瘤时,胃肠道的运动功能发生紊乱,可能反馈地引起血浆胃动素水平的升高。
导师刘友章教授根据中医脾胃为后天之本,气血生化之源的理论,结合临床,运用健脾益气,养血和胃生肌的方法治疗慢性萎缩性胃炎,创制了纯中药方剂胃炎1号。胃炎1号选用党参、白芍健脾养胃,柔肝生肌为君；珍珠层粉、蒲公英、白花蛇舌草、七叶一枝花、莪术、当归清热化瘀,行气活血为臣；鸡骨草、砂仁理气和胃止痛为佐；甘草调和诸药为使,共凑健脾益气,和胃生肌之功效。早在20世纪90年代初,刘友章教授与日本京都大学合作研究的“胃炎1号对萎缩性胃炎病人胃粘膜修复作用的研究”已初步证实了胃炎1号对脾胃虚弱型慢性萎缩性胃炎病人胃粘膜修复有一定的疗效,并有一定的抗上皮化生的作用。刘友章教授主持的广东省中医药管理局科研课题——胃炎1号治疗萎缩性胃炎作用机理的临床与实验研究,运用了随机对照的方法从血清胃肠激素的变化、胃粘膜组织的病理变化等方面发现胃炎Ⅰ号对大鼠CAG模型以及慢性萎缩性胃炎患者的胃粘膜改变具有明显的防治作用。
目的：本实验研究以血清胃泌素和血浆胃动素为切入点,对胃炎Ⅰ号治疗大鼠慢性萎缩性胃炎的作用机制进行更深入探讨,为胃炎Ⅰ号的临床疗效提供科学的实验依据,可以为开发临床治疗慢性萎缩性胃炎有效中成药胃炎Ⅰ号提供理论实验依据。
方法：本研究包括文献研究和实验研究两部分。本论文对古代历代医家及现代历代中医家对本病病因病机、辩证分型以及治疗原则进行了系统论述。随着科学技术发展,现代医学对本病的病因、发病机制及诊疗技术等方面研究不断深入,本文对其进展也进行了综述。
实验研究部分,选用健康SD大鼠84只,雌雄各半。共分六个组：模型组24只,空白组12只,高剂量组12只,中剂量组12只,低剂量组12只,西药对照组12只。采用50μg/ml甲基-硝基-亚硝基胍(MNNG)避光自由饮用、3mg/ml雷尼替丁灌胃每天一次2ml、加上2天给食1天停食的饥饱失常综合造模法构建大鼠慢性萎缩性胃炎模型,造模20周。经病理检查模型构建成功后,高剂量治疗组给予5g/(kg·d)胃炎Ⅰ号,中剂量治疗组给予2.5g/(kg·d)胃炎Ⅰ号,低剂量组给予1.25g/(kg·d)胃炎Ⅰ号,西药对照组给予0.86 g/(kg·d)维酶素,空白组正常饮食。
采用放射免疫法检测慢性萎缩性胃炎大鼠血清胃泌素和血浆胃动素的浓度。全部实验数据均采用SPSS13统计软件处理,各组数据以均数±标准差(X±S)形式表示。
结果：
1、本实验研究表明,本实验采用的造模方法能够成功复制大鼠慢性萎缩性胃炎动物模型。但本实验所用的方法也存在所构建模型病变不够典型,造模时间长死亡率较高,采用的造模试剂MNNG为致癌物质,对实验人员及环境均存在危害,实验试剂价格较贵等缺点。因此,本实验造模方案可成功构建大鼠慢性萎缩性胃炎模型,但并非一个良好的方案。
2、各组大鼠血清胃泌素含量变化,经一维方差分析及LSD两两比较,各组与模型组比较P<0.05,均具有统计学意义,说明本实验慢性萎缩性胃炎大鼠模型构建成功,且各组胃炎Ⅰ号及维酶素干预对提高血清胃泌素水平均有疗效。胃炎Ⅰ号高、中剂量与空白组比较P>0.05,无统计学意义,组间没有明显差别,低剂量组与空白组比较P<0.05,差别有统计学意义,胃炎Ⅰ号高剂量与中剂量比较P>0.05,故胃炎Ⅰ号对慢性萎缩性胃炎大鼠血清胃泌素的以高、中剂量疗效均为最佳。西药维酶素疗效优于胃炎Ⅰ号低剂量组疗效(P<0.05)。
3、各组大鼠血浆胃动素含量变化,经一维方差分析及LSD两两比较,各组与模型组比较P<0.01,均具有统计学意义,说明本实验慢性萎缩性胃炎大鼠模型构建成功,且各组胃炎Ⅰ号及维酶素干预对降低血浆胃动素水平均有疗效。高剂量、低剂量胃炎Ⅰ号及酶素组与空白组比较P<0.05,差别有统计学意义,中剂量组与空白组比较P>0.05,差别无统计学意义,故在各治疗组中以胃炎Ⅰ号中剂量疗效最佳。维酶素组与低剂量组比较P<0.05,差别具有统计学意义。
结论：本论文通过实验研究探讨了胃炎Ⅰ号对慢性萎缩性胃炎大鼠血清胃泌素和血浆胃动素的调控作用。研究结果表明：
1、本实验采用的综合造模法可以成功构建慢性萎缩性胃炎大鼠模型。
2、胃炎Ⅰ号可以改善慢性萎缩性胃炎大鼠胃黏膜病理改变。
3、本实验研究发现,慢性萎缩性胃炎模型大鼠血清胃泌素水平低于正常大鼠血清胃泌素水平。胃炎Ⅰ号治疗后,慢性萎缩性胃炎模型大鼠血清胃泌素水平上升。
4、本实验研究发现,慢性萎缩性胃炎模型大鼠血浆胃动素水平高于正常大鼠血浆胃动素水平。胃炎Ⅰ号治疗后,慢性萎缩性胃炎模型大鼠血浆胃动素水平降低。
综合以上研究结果,胃炎Ⅰ号可能通过提高CAG大鼠血清胃泌素和降低血浆胃动素的水平,起到改善CAG大鼠胃黏膜损伤,促进病变胃黏膜修复的治疗效果。
Objective:Chronic atrophic gastritis (CAG) is a refractory disease of digestive system diseases, which's main pathological changes including gastric mucosa and gastric glands thinning, lamina muscularis mucosae thickening, intestinal metaplasia, etc. Due to the atrophy of the gastric glandular organ, the gastric mucosa is thinner, together with intestinal metaplasia, inflammatory reaction and atypical hyperplasia. The clinical symptoms are including dyspepsia, epigastric discomfort or dull pain and anemia.
CAG is a commonly encountered disease and frequently encountered disease of digestive system, characteristic with recurrent attacks. The disease rate rise with the age increase, soit is higher in the aged. Chronic superficial gastritis could develop to CAG. Because of relating to the gastric cance, CAG was classified as precancerous disease or precancerous disease by the WHO in 1978. According to the linkage theory of gastric cancer carcinogenesis, the pathological changes of gastric cancer carcinogenesis follow the step from chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia, atypical hyperplasia and the end to gastric cancer. CAG as a kind of lesion precancerous has been generally accepted. The incidence of CAG is very high in China, and about 8% will develop to gastric cancer after 10 to 20 years. So discerning and preventing the precancerous disease and lesion precancerous of s digestive system as early as possible, are effective methods to decrease the incidence rate and death rate of gastric cancer.
Gastrin is a kind of important gastrointestinal hormone, secreted by G cells. Gastrin affects the most functions of the gastrointestinal tract, promoting gastrointestinal secretion, promoting gastrointestinal movement, loosening pyloric sphincter and sphincter of Oddi and ileocecal junction, promoting gastrointestinal mucous cell division growth, promoting releasing trypsin and calcitonin.
Motilin is a kind of straight chain polypeptides gastrointestinal hormone, constitute by 22 amino-acid residue. Motilin is secreted by Mo cells in the duodenum and proximate jejunal mucous membrane cryptae. Motilin directly affect to the acceptor of enteron smooth muscle cell, inducing smooth muscle contraction. Motilin secretes periodicity in interdigestive phase. The level of motilin in the digestive tract cancer patients is higher than health persons, and the mechanisms are indefinite.
Gastritis I is an effective prescription which was found by Professor Liu Youzhang in his several decade clinical practices It has the effectiveness of strengthening spleen, benefiting vital energy, nourishing blood, regulating stomach and promoting granulation, and has been confirmed it's effectiveness in reconditioning gastric mucosa and resisting epithelial metaplasia of CAG. The purpose of our empirical study is to lucubrate the mechanism of gastritis I curing the CAG rats by lucubrating the mechanism of gastritis I regulating to serum gastrin and blood plasma motilin in stomach of the CAG rats, and to provide scientific experimental evidence of the clinical therapeutic effect of gastritis I.
Methods:Our research was divided into overview and empirical study. We expounded the etiological factor, pathogenesis and therapeutic principle of ancient and contemporary doctor of TCM. We also expounded the advancement of modern medicine. In the empirical study,84 healthy SD rats were divided into 6 groups, including model group (24), normal group (12), western medicine control group (12), and 3 Gastritis I treatment group including high dose group (12), medium dose group (12), low-dose group (12). the CAG model rats was constructed by freely drinking the MNNG solution (50μg/ml), being intragastric administration and irregular diet. After the CAG model was constructed successfully, giving 5g/(kg·d) Gastritis I to high dose treatment group, giving 2.5g/(kg·d) Gastritis I to medium dose group, giving 1.25g/(kg·d) Gastritis I to low-dose group, giving 0.86 g/(kg·d) Wei Mei Su Pian to western medicine control group, the normal group was feed normally. We adopted radio-immunity echnology to detect the level of serum gastrin and blood plasma motilin.
Result:①Our empirical study indicated that the method adopted to copy the CAG rats animal models was success. But the pathological changes were not typical enough, and persistence time was too long, the death rate was high, and the reductant MNNG is a kind of carcinogen, harm to the experimenter and the environment. Accordingly, our experiment program had successful, but not excellent enough.②The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group (P<0.05). After treated by gastritis I, the curative effect of high and medium dose were better than low dose and Wei Mei Su Pian (P<0.05).③The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group (P<0.01). After treated by gastritis I, the curative effect of medium dose was better than other groups (P<0.05).
Conclusion:Our experiment had study the mechanism of gastritis I regulating to the serum gastrin and blood plasma motilin of the CAG rats by empirical study. The experimental results indicated:①Our study adopted synthetic methods to construct the CAG model rats. Those methods were able to build the CAG model rats successfully;②Gastritis I could improve the gastric mucosal lesion of the CAG rats;③The results of the serum gastrin level analysised by analysis of variance found that the serum gastrin level of the CAG model group rats was lower than normal control group. After treated by Gastritis I, the serum gastrin level of the CAG model group rats was rising.④The results of the blood plasma motilin level analysised by analysis of variance found that the blood plasma motilin level of the CAG model group rats was higher than normal control group. After treated by Gastritis I, the blood plasma motilin level of the CAG model group rats was decreasing.
Gastritis I could improve the gastric mucosa damage of the CAG rats, and promote gastric mucosa plerosis, by raising the serum gastrin level and decreasing the blood plasma motilin level.
引文
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