HP相关胃病脾胃湿热证胃粘膜IFN-γ、IL-12表达的研究
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摘要
研究目的：
通过检测幽门螺杆菌(Helicobacter pylori, Hp)相关胃病脾胃湿热证患者胃粘膜Hp感染程度、胃粘膜病理改变及干扰素-γ (interferon-γ, IFN-γ)、白细胞介素-12(interleukin-12, IL-12)的表达情况,并以脾气虚证为对照组,从局部的角度探讨脾胃湿热证的病理生理与Hp感染及上述两个炎症因子表达的内在联系,从现代医学角度诠释脾胃湿热证的本质。
研究方法：
1、收集中医证型属脾胃湿热证和脾气虚证的慢性胃炎及消化性溃疡患者114例,其中脾胃湿热证83例,脾气虚证组19例,并招募正常志愿者12名作为正常对照组。脾胃湿热证Hp阳性共44例,其中热重于湿12例,湿热并重15例,湿重于热17例,脾胃湿热证Hp阴性39例；脾气虚证Hp阳性8例,脾气虚证Hp阴性11例。由专人对合符要求的各组受试对象进行询问,对症状进行评分并填写临床观察表。
2、各组受试对象行胃镜检查后在胃窦钳取胃粘膜组织两块,其中一块行快速尿素酶试验；一块放入中性甲醛液固定,石蜡包埋。
3、采用美蓝染色法并结合快速尿素酶试验检测Hp感染；采用常规HE染色法观察胃粘膜炎症程度及其活动性。
4、采用ElivisionTM plus二步免疫组织化学标记法检测各组胃粘膜IFN-γ、 IL-12的表达。
研究结果：
1、一般资料
本实验中各组性别、年龄、疾病构成之间无显著性差异(P>0.05),具有可比性。
2、各组Hp感染率与Hp感染严重程度的比较
各组Hp感染率显示脾胃湿热证组有高于脾气虚组的趋势,经统计学检验,两组Hp感染率未发现显著性差异(P>0.05)。各组Hp感染严重程度未发现显著性差异(P>0.05)。
3、各组Hp感染与临床症状积分的关系
各组主要临床症状积分比较,11p阳性组与}1p阴性组之间未见显著性差异(P>0.05)。
4、各组胃粘膜炎症程度、炎症活动性的比较及其与11p感染的关系
无论是各组胃粘膜炎症程度,还是各组胃粘膜炎症活动性的比较,脾胃湿热证组均重于脾气虚证组,而脾胃湿热证纽和脾气虚证组均明显重于正常对照纽,呈现脾胃湿热证组>脾气虚证组的趋势：脾胃湿热证组及脾气虚证组Hp阳性组炎症程度和炎症活动度均重于同证型Hp阴性组,Hp感染程度与胃粘膜炎症程度及炎症活动度均呈正相关(P<0.001)。
5、各组胃粘膜IFN-γ、IL-12的表达
各组IFN-γ主要表达于腺体及固有膜细胞,主要定位在胞浆；IL-12主要表达于腺体、固有膜及上皮,主要定位在胞核,但在肠化、异型增生的病例中则定位在胞浆。
各组IFN-γ、 IL-12的表达情况,脾胃湿热证组均高于脾气虚证组,呈现脾胃湿热证组高于脾气虚证组的趋势。脾胃湿热证Hp阳性组三个亚型之间比较,IFN-γ、 IL-12表达存在湿热并重组>湿重于热组>热重于湿组的趋势。
脾胃湿热证组中,脾胃湿热证Hp阳性组IFN-γ表达高于脾胃湿热证Hp阴性组；而在脾气虚证组中,脾气虚证Hp阳性组IFN-γ表达则低于脾气虚证Hp阴性组。脾胃湿热证和脾气虚证中Hp阳性组中IL-12的表达,均高于同证型Hp阴性组,且具有显著性差异。
6、Hp感染与IFN-γ、IL-12表达的关系
与Hp阴性组比较,Hp阳性组IFN-γ、IL-12表达均高于Hp阴性组,均具有显著性差异。
研究结论：
1、Hp感染在脾胃湿热证的致病过程中起一定作用,Hp介导了脾胃湿热证胃粘膜局部炎症性病理改变。
2、IFN-γ、IL-12的表达与脾胃湿热证有一定的相关性,其在脾胃湿热证组中存在较高的表达,这可能在一定程度上反映了脾胃湿热证湿热之邪亢盛,而脾胃正气未衰,机体正邪交争剧烈的病理特点。
3、IFN-γ、IL-12在脾胃湿热证组三个亚型中有不同的表达趋势。脾胃湿热证的形成及IFN-γ、IL-12的表达,是湿邪与热邪共同作用的结果,两者在三个亚型中的表达趋势,说明湿热合邪之后,湿热相搏的状态可能导致局部胃粘膜炎症性病理改变更为严重。
4、Hp感染诱导下的IFN-γ、IL-12的不同表达,反映了Hp相关胃病脾胃湿热证细胞因子网络的紊乱,这在一定意义上提示了脾胃湿热证的本质。
Objective:
By detecting Helicobacter pylori infection、pathological changes of the Gastric mucosa、Interferon-γ、Interleukin-12expressions of the patients with the Splenogastric Hygropyrexia belonging to H. pylori-associated Gastropathy, and deficiency of spleen-QI Syndrome, to explore the deep relations of the pathophysiology of Splenogastric Hygropyrexia Syndrome, Helicobacter pylori infection and IFN-γ,IL-12from the local Angle, This is from the Angle of modern medicine interpretation of the nature of Splenogastric Hygropyrexia Syndrome.
Method:
1. Choose114cases with CSG and PU including83cases belonging to Splenogastric Hygropyrexia Syndrome(among them,12cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and heavy dampness impairing heat,15cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and simultaneous onset of dampness and heat,17cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and heavy heat impairing dampness,39cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(-)) and19cases belong to the group of Splenic deficiency Syndrome(among them,8cases belong to the group of the deficiency of spleen-QI Syndrome HP(+),11cases belong to the group of the deficiency of spleen-QI Syndrome HP(-).12cases of recruitment of healthy voluteers as normal control group. Subjects in each group were asked to complete the clinical observation of form and carried out the assessment of symptoms.
2. we collected two pieces of the tunica mucosa sinus ventriculi under the gastroscope. One of them used the fast urease test, the other one was placed in neutral buffered formalin and embedded by the paraffin.
3. Hp was detected by toluidine blue staining method and fast urease test.The inflammation of musosa was observed by common hematocylin-eosin staining method.
4. Take the two step of ElivisionTM plus immunoristochemical labeling method to detect the expression of gastric mucosal Interferon-γ and Interleukin-12.
Result:
1. Analysis of common materials:
There were no obvious difference for the groups on the sex, age, the course of disease and the rate of Hp(p>0.05). So the groups could be compared by each other.
2. The comparison of the Hp infective rate and the Hp infection level:
The comparison showed that the Hp infective rate of the Splenogastric Hygropyrexia Syndrome groups were slightly higher than the Splenic deficiency Syndrome groups. But there were no obvious difference of the Hp infective rate and the Hp infection level between the the Splenogastric Hygropyrexia Syndrome groups and the Splenic deficiency Syndrome groups (P>0.05)
3. The ralationship of the main clinical symption sore
The main clinical symption sore between the the Splenogastric Hygropyrexia Syndrome groups and the Splenic deficiency Syndrome group (P>0.05) were similar.
4. The comparison of the gastric mucosa inflammation level and the gastric mucosa inflammation activity in each group and the relationship with Hp infection.
No matter the Gastric mucosa inflammation leve or the gastric mucosa inflammation activity, Splenogastric Hygropyrexia Syndrome group are severer than deficiency spleen QI Syndrome group,and both of the above are significantly severer than the normal control group, on the whole, the result have the tendency that Splenogastric Hygropyrexia Syndrome group>deficiency spleen-QI Syndrome group; the Gastric mucosa inflammation leveland the gastric mucosa inflammation activity of the Splenogastric Hygropyrexia Syndrome group and deficiency spleen-QI Syndrome group are severer than the same type of Hp(-),the ralationship among the Hp infection and the Gastric mucosa inflammation leveland the gastric mucosa inflammation activity (P<0.001)
5. The expression of gastric mucosal interferon-γand interleukin-12in each group.
Interferon-γmainly Positioning in cytolymph, of the membranae propria and gland cell. Interleukin-12mainly Positioning in cell nucleus of the membranae propria, epithelium and gland cell, but some of the Interleukin-12Positioning in cytolymph which with inintestinal metaplasia or Atypical hyperplasia.
6. The expression of gastric mucosal interferon-γand interleukin-12
In each group is that Splenogastric Hygropyrexia Syndrome group and deficiency spleen-QI Syndrome group are significantly higher than the normal control group. There have the tendency that Splenogastri Hygropyrexia Syndrome group>deficiency spleen-QI Syndrome group.
7. The comparison of the three sub-divided groups of Splenogastric Hygropyrexia Syndrome Hp(+),have the tendency that simultaneous onset of dampness and heat group>heavy dampness impairing heat group>heavy heat impairing dampness group, and the expression of Interleukin-12of the three sub-divided groups are higher than the normal control group. So, there have the tendency that simultaneous onset of dampness and heat group>heavy dampness impairing heat group>heavy heat impairing dampness group.
6. The ralationship of the Hp infection and the expression of interferon-γ and interleukin-12.
Compare with the Hp(-) group, the expression of interferon-γ and interleukin-12are both higher than the Hp(+) group, there were obvious difference of them.
Conclusion:
1.Hp infection play a role in the pathogenic process of Splenogastric Hygropyrexia Syndrome. Hp infection result in the pathological changes of the Gastric mucosa.
2. There may exist the relativity to some extent between the expression of gastric mucosal interferon-γand interleukin12and Splenogastric Hygropyrexia Syndrome. The high expression of ginterferon-γand interleukin-12may reflect the connotation that dampness and heat is excessive and Quarrel with each other, but the upright qi is not deficiency.
3. The expression of interferon-γ and interleukin-12of the three sub-divided groups of Splenogastric Hygropyrexia Syndrome, has different tendency. The dampness and heat formate the Splenogastric Hygropyrexia Syndrome and and to help forward the expression of interferon-γ and interleukin-12. The tendency shows that, while the dampness and heat combine with each other the pathological changes of the Gastric mucosa may be more serious.
4. There may exist the relativity to some extent between the Hp infectionand the expression of interleukin-12, but not the interferon-γ, Hp infection may be played a role of inducing in the expression of interleukin-12.
通过检测幽门螺杆菌(Helicobacter pylori, Hp)相关胃病脾胃湿热证患者胃粘膜Hp感染程度、胃粘膜病理改变及干扰素-γ (interferon-γ, IFN-γ)、白细胞介素-12(interleukin-12, IL-12)的表达情况,并以脾气虚证为对照组,从局部的角度探讨脾胃湿热证的病理生理与Hp感染及上述两个炎症因子表达的内在联系,从现代医学角度诠释脾胃湿热证的本质。
研究方法：
1、收集中医证型属脾胃湿热证和脾气虚证的慢性胃炎及消化性溃疡患者114例,其中脾胃湿热证83例,脾气虚证组19例,并招募正常志愿者12名作为正常对照组。脾胃湿热证Hp阳性共44例,其中热重于湿12例,湿热并重15例,湿重于热17例,脾胃湿热证Hp阴性39例；脾气虚证Hp阳性8例,脾气虚证Hp阴性11例。由专人对合符要求的各组受试对象进行询问,对症状进行评分并填写临床观察表。
2、各组受试对象行胃镜检查后在胃窦钳取胃粘膜组织两块,其中一块行快速尿素酶试验；一块放入中性甲醛液固定,石蜡包埋。
3、采用美蓝染色法并结合快速尿素酶试验检测Hp感染；采用常规HE染色法观察胃粘膜炎症程度及其活动性。
4、采用ElivisionTM plus二步免疫组织化学标记法检测各组胃粘膜IFN-γ、 IL-12的表达。
研究结果：
1、一般资料
本实验中各组性别、年龄、疾病构成之间无显著性差异(P>0.05),具有可比性。
2、各组Hp感染率与Hp感染严重程度的比较
各组Hp感染率显示脾胃湿热证组有高于脾气虚组的趋势,经统计学检验,两组Hp感染率未发现显著性差异(P>0.05)。各组Hp感染严重程度未发现显著性差异(P>0.05)。
3、各组Hp感染与临床症状积分的关系
各组主要临床症状积分比较,11p阳性组与}1p阴性组之间未见显著性差异(P>0.05)。
4、各组胃粘膜炎症程度、炎症活动性的比较及其与11p感染的关系
无论是各组胃粘膜炎症程度,还是各组胃粘膜炎症活动性的比较,脾胃湿热证组均重于脾气虚证组,而脾胃湿热证纽和脾气虚证组均明显重于正常对照纽,呈现脾胃湿热证组>脾气虚证组的趋势：脾胃湿热证组及脾气虚证组Hp阳性组炎症程度和炎症活动度均重于同证型Hp阴性组,Hp感染程度与胃粘膜炎症程度及炎症活动度均呈正相关(P<0.001)。
5、各组胃粘膜IFN-γ、IL-12的表达
各组IFN-γ主要表达于腺体及固有膜细胞,主要定位在胞浆；IL-12主要表达于腺体、固有膜及上皮,主要定位在胞核,但在肠化、异型增生的病例中则定位在胞浆。
各组IFN-γ、 IL-12的表达情况,脾胃湿热证组均高于脾气虚证组,呈现脾胃湿热证组高于脾气虚证组的趋势。脾胃湿热证Hp阳性组三个亚型之间比较,IFN-γ、 IL-12表达存在湿热并重组>湿重于热组>热重于湿组的趋势。
脾胃湿热证组中,脾胃湿热证Hp阳性组IFN-γ表达高于脾胃湿热证Hp阴性组；而在脾气虚证组中,脾气虚证Hp阳性组IFN-γ表达则低于脾气虚证Hp阴性组。脾胃湿热证和脾气虚证中Hp阳性组中IL-12的表达,均高于同证型Hp阴性组,且具有显著性差异。
6、Hp感染与IFN-γ、IL-12表达的关系
与Hp阴性组比较,Hp阳性组IFN-γ、IL-12表达均高于Hp阴性组,均具有显著性差异。
研究结论：
1、Hp感染在脾胃湿热证的致病过程中起一定作用,Hp介导了脾胃湿热证胃粘膜局部炎症性病理改变。
2、IFN-γ、IL-12的表达与脾胃湿热证有一定的相关性,其在脾胃湿热证组中存在较高的表达,这可能在一定程度上反映了脾胃湿热证湿热之邪亢盛,而脾胃正气未衰,机体正邪交争剧烈的病理特点。
3、IFN-γ、IL-12在脾胃湿热证组三个亚型中有不同的表达趋势。脾胃湿热证的形成及IFN-γ、IL-12的表达,是湿邪与热邪共同作用的结果,两者在三个亚型中的表达趋势,说明湿热合邪之后,湿热相搏的状态可能导致局部胃粘膜炎症性病理改变更为严重。
4、Hp感染诱导下的IFN-γ、IL-12的不同表达,反映了Hp相关胃病脾胃湿热证细胞因子网络的紊乱,这在一定意义上提示了脾胃湿热证的本质。
Objective:
By detecting Helicobacter pylori infection、pathological changes of the Gastric mucosa、Interferon-γ、Interleukin-12expressions of the patients with the Splenogastric Hygropyrexia belonging to H. pylori-associated Gastropathy, and deficiency of spleen-QI Syndrome, to explore the deep relations of the pathophysiology of Splenogastric Hygropyrexia Syndrome, Helicobacter pylori infection and IFN-γ,IL-12from the local Angle, This is from the Angle of modern medicine interpretation of the nature of Splenogastric Hygropyrexia Syndrome.
Method:
1. Choose114cases with CSG and PU including83cases belonging to Splenogastric Hygropyrexia Syndrome(among them,12cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and heavy dampness impairing heat,15cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and simultaneous onset of dampness and heat,17cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(+) and heavy heat impairing dampness,39cases belong to the group of Splenogastric Hygropyrexia Syndrome Hp(-)) and19cases belong to the group of Splenic deficiency Syndrome(among them,8cases belong to the group of the deficiency of spleen-QI Syndrome HP(+),11cases belong to the group of the deficiency of spleen-QI Syndrome HP(-).12cases of recruitment of healthy voluteers as normal control group. Subjects in each group were asked to complete the clinical observation of form and carried out the assessment of symptoms.
2. we collected two pieces of the tunica mucosa sinus ventriculi under the gastroscope. One of them used the fast urease test, the other one was placed in neutral buffered formalin and embedded by the paraffin.
3. Hp was detected by toluidine blue staining method and fast urease test.The inflammation of musosa was observed by common hematocylin-eosin staining method.
4. Take the two step of ElivisionTM plus immunoristochemical labeling method to detect the expression of gastric mucosal Interferon-γ and Interleukin-12.
Result:
1. Analysis of common materials:
There were no obvious difference for the groups on the sex, age, the course of disease and the rate of Hp(p>0.05). So the groups could be compared by each other.
2. The comparison of the Hp infective rate and the Hp infection level:
The comparison showed that the Hp infective rate of the Splenogastric Hygropyrexia Syndrome groups were slightly higher than the Splenic deficiency Syndrome groups. But there were no obvious difference of the Hp infective rate and the Hp infection level between the the Splenogastric Hygropyrexia Syndrome groups and the Splenic deficiency Syndrome groups (P>0.05)
3. The ralationship of the main clinical symption sore
The main clinical symption sore between the the Splenogastric Hygropyrexia Syndrome groups and the Splenic deficiency Syndrome group (P>0.05) were similar.
4. The comparison of the gastric mucosa inflammation level and the gastric mucosa inflammation activity in each group and the relationship with Hp infection.
No matter the Gastric mucosa inflammation leve or the gastric mucosa inflammation activity, Splenogastric Hygropyrexia Syndrome group are severer than deficiency spleen QI Syndrome group,and both of the above are significantly severer than the normal control group, on the whole, the result have the tendency that Splenogastric Hygropyrexia Syndrome group>deficiency spleen-QI Syndrome group; the Gastric mucosa inflammation leveland the gastric mucosa inflammation activity of the Splenogastric Hygropyrexia Syndrome group and deficiency spleen-QI Syndrome group are severer than the same type of Hp(-),the ralationship among the Hp infection and the Gastric mucosa inflammation leveland the gastric mucosa inflammation activity (P<0.001)
5. The expression of gastric mucosal interferon-γand interleukin-12in each group.
Interferon-γmainly Positioning in cytolymph, of the membranae propria and gland cell. Interleukin-12mainly Positioning in cell nucleus of the membranae propria, epithelium and gland cell, but some of the Interleukin-12Positioning in cytolymph which with inintestinal metaplasia or Atypical hyperplasia.
6. The expression of gastric mucosal interferon-γand interleukin-12
In each group is that Splenogastric Hygropyrexia Syndrome group and deficiency spleen-QI Syndrome group are significantly higher than the normal control group. There have the tendency that Splenogastri Hygropyrexia Syndrome group>deficiency spleen-QI Syndrome group.
7. The comparison of the three sub-divided groups of Splenogastric Hygropyrexia Syndrome Hp(+),have the tendency that simultaneous onset of dampness and heat group>heavy dampness impairing heat group>heavy heat impairing dampness group, and the expression of Interleukin-12of the three sub-divided groups are higher than the normal control group. So, there have the tendency that simultaneous onset of dampness and heat group>heavy dampness impairing heat group>heavy heat impairing dampness group.
6. The ralationship of the Hp infection and the expression of interferon-γ and interleukin-12.
Compare with the Hp(-) group, the expression of interferon-γ and interleukin-12are both higher than the Hp(+) group, there were obvious difference of them.
Conclusion:
1.Hp infection play a role in the pathogenic process of Splenogastric Hygropyrexia Syndrome. Hp infection result in the pathological changes of the Gastric mucosa.
2. There may exist the relativity to some extent between the expression of gastric mucosal interferon-γand interleukin12and Splenogastric Hygropyrexia Syndrome. The high expression of ginterferon-γand interleukin-12may reflect the connotation that dampness and heat is excessive and Quarrel with each other, but the upright qi is not deficiency.
3. The expression of interferon-γ and interleukin-12of the three sub-divided groups of Splenogastric Hygropyrexia Syndrome, has different tendency. The dampness and heat formate the Splenogastric Hygropyrexia Syndrome and and to help forward the expression of interferon-γ and interleukin-12. The tendency shows that, while the dampness and heat combine with each other the pathological changes of the Gastric mucosa may be more serious.
4. There may exist the relativity to some extent between the Hp infectionand the expression of interleukin-12, but not the interferon-γ, Hp infection may be played a role of inducing in the expression of interleukin-12.
引文
[1]王洪京,黄海量,赵明等,消化性溃疡脾胃湿热证临床流行病学调查研究[J],山东中医药大学学报2010,34(5)：417-420.
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