中等负荷运动训练对心理应激大鼠行为和氧自由基的影响

目的研究中等负荷的运动训练对心理应激大鼠行为和外周血氧自由基的影响。方法健康的雄性SD大鼠32只,随机分为对照组、心理应激组、运动组和运动心理应激组,实验后测定大鼠的开场行为以及外周血自由基的变化情况。结果①心理应激组、运动组以及运动心理应激组(分别为64.37±16.90,59.63±13.45,54.88±10.68)与对照组(43.25±16.42)比较数都有显著的增加(P<0.05);伸高次数(分别为16.63±5.09,10.00±6.85,17.00±10.77)与对照组(23.88±6.79)相比较都有所降低,且心理应激组和运动组具有显著的统计学意义(P<0.05)②心理应激组、运动组(分别为78.13±18.10和56.48±19.21)与对照组(36.90±4.19)比较SOD的活性显著增强(P<0.05),运动心理应激组SOD的活性(36.90±4.19)降低;而MDA浓度的变化,心理应激组(8.63±3.18)与对照组(4.90±1.58)比较显著增加(P<0.01),运动组(2.76±1.60)显著降低(P<0.01),运动心理应激组下降但差异无显著性。结论中等负荷的运动训练可以通过降低心理应激反应的强度,拮抗心理应激对机体的损伤。     

中等负荷运动训练对心理应激大鼠行为和氧自由基的影响

目的研究中等负荷的运动训练对心理应激大鼠行为和外周血氧自由基的影响.方法健康的雄性SD大鼠32只,随机分为对照组、心理应激组、运动组和运动心理应激组,实验后测定大鼠的开场行为以及外周血自由基的变化情况.结果①心理应激组、运动组以及运动心理应激组(分别为64.37±16.90,59.63±13.45,54.88±10.68)与对照组(43.25±16.42)比较数都有显著的增加(P <0.05);伸高次数 (分别为16.63±5.09,10.00±6.85,17.00±10.77)与对照组(23.88±6.79)相比较都有所降低,且心理应激组和运动组具有显著的统计学意义(P <0.05)②心理应激组、运动组(分别为78.13±18.10和56.48±19.21)与对照组(36.90±4.19)比较SOD的活性显著增强(P <0.05),运动心理应激组SOD的活性(36.90±4.19)降低;而MDA浓度的变化,心理应激组(8.63±3.18)与对照组(4.90±1.58)比较显著增加(P <0.01),运动组(2.76±1.60)显著降低(P <0.01),运动心理应激组下降但差异无显著性.结论中等负荷的运动训练可以通过降低心理应激反应的强度,拮抗心理应激对机体的损伤.     

利心冲剂对心力衰竭大鼠模型的氧化应激和凋亡相关基因的影响

目的探讨利心冲剂调控心力衰竭大鼠模型氧化应激抗细胞凋亡的分子机制。方法实验分组：正常组、模型组、卡托普利治疗组、利心冲剂低剂量组、利心冲剂高剂量组。腹腔注射阿霉素（ADR）5mg/kg,每5天1次,共3次,复制大鼠心力衰竭模型,左心室插管术测定血流动力学指标;血清学检测氧化指标SOD1、MDA;Real time PCR检测氧化应激及凋亡相关基因SOD1、PGC-1α和Bcl-2、Bax。结果利心冲剂治疗组和模型组比较,形态学显示心肌细胞变性坏死明显减轻;左心室收缩内压显著升高;氧化应激相关指标SOD1、PGC-1α升高、MDA降低;凋亡相关基因Bcl-2升高、Bax/Bcl-2降低;均有显著性差异（P〈0.05）。 结论利心冲剂调控氧化应激相关基因SOD1、PGC-1α,降低凋亡相关基因Bax/ Bcl-2表达,减轻心肌细胞凋亡,改善心脏收缩与舒张功能。     

中药活血利湿方对酒精性肾损害大鼠抗氧化酶活性及丙二醛含量的影响

目的研究复方中药活血利湿方(HLP)对酒精性肾损害大鼠的抗氧化作用。方法 Wistar大鼠酒精灌胃造模,HLP灌胃处理,分别于第4、8、12周末检测大鼠肾组织谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的变化。结果随着造模时间的延长,中药组大鼠肾组织GSH-Px及SOD活性明显增强,MDA的含量显著降低(P<0.05,P<0.01)。结论酒精可诱发大鼠肾组织氧化应激的产生,HLP具有拮抗酒精性肾损害的作用,可能与其抗氧化应激功能有关。     

有氧运动对心理应激衰老大鼠行为和氧自由基的影响

目的:研究有氧运动对心理应激衰老大鼠行为和外周血氧自由基的影响. 方法:健康雌性SD大鼠28只,随机分为对照组、运动组、心理应激组、运动 心理应激组,实验后测定大鼠的开场行为和外周血自由基的变化情况. 结果: :①开场行为:在穿越格数上运动组、心理应激组、运动 心理应激组与对照组相比较均有显著的增加(P＜0.05),在站立次数上心理应激组、运动 心理应激组与对照组及运动组相比较有显著减少(P＜0.01).②血清中SOD活性、H2O2含量:各组间均无明显差异性;MDA含量:运动组、运动 心理应激组与对照组及心理应激组相比较有明显的减少(P＜0.05);过氧化氢酶(CAT)活性:运动组的CAT活性明显高于心理应激组(P＜0.05);GSH-px活性:与对照组相比较,运动组、运动 心理应激组的活性明显增加(P＜0.05),心理应激组则明显降低(P＜0.05).结论:不适宜的心理应激可对动物的自发行为和探究行为产生影响,并可诱发机体内自由基量的增加而导致机体损伤,而通过有氧运动可减轻心理应激对机体产生的影响.     

热应激预处理对大鼠肢体缺血再灌注后血清丙二醛、超氧化物歧化酶的影响

目的探讨热应激预处理对大鼠肢体缺血再灌注损伤的影响。方法制备大鼠缺血再灌注模型及热应激预处理模型。采用硫代巴比妥酸法测定大鼠丙二醛(MDA)浓度,采用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活力并与对照组比较。结果大鼠肢体缺血再灌注后血清中的MDA含量明显增高(P<0.01),并有随再灌时间延长不断升高的趋势,而SOD活性明显降低(P<0.01);热应激预处理后,血清中MDA含量明显降低(P<0.01),SOD活性明显增高(P<0.01)。结论热应激预处理可增强SOD清除细胞内氧自由基的水平。     

肝细胞糖原拮抗缺血肝脏肝细胞凋亡及相关机制

目的探讨增加肝细胞糖原含量能否拮抗缺血肝脏肝细胞凋亡及相关机制。方法制备糖原含量显著不同的3组兔肝脏模型（A组、B组及C组）,在各组肝脏缺血再灌注过程中,检测肝组织内肝细胞凋亡及SOD、MDA水平。结果 3组肝脏于再灌注1h,组织内可见明显的肝实质细胞凋亡现象,其凋亡细胞数量依次为,A组〉B组〉C组,且3组彼此间差异均具有统计学意义,并且此时各组肝组织中SOD活性及MDA含量也差异均有统计学意义。结论增加肝细胞内糖原含量可显著拮抗肝脏缺血再灌注过程中肝细胞凋亡。其间,肝细胞糖原可能是通过抑制肝组织内氧自由基的产生而达到拮抗肝实质细胞凋亡的发生。     

慢性应激对大鼠淋巴细胞DNA损伤机制的研究

目的:研究慢性应激对大鼠淋巴细胞DNA损伤机制.方法:选择Wistar成年雄性大鼠18只,建立慢性应激动物模型(实验组).测定大鼠血清皮质醇的含量;电镜观察海马超微结构改变;黄嘌啉氧化酶法测定大鼠血清和脏器中超氧化物歧化酶(Superoxide dismutase,SOD)活性;TBA法测定脂质过氧化物(Malondiasldehyde,MDA)含量;彗星实验评价大鼠外周血淋巴细胞DNA损伤情况.结果:实验组海马超微结构异常;血清SOD活性为(56.70±15.65)U/ml,低于对照组(P＜0.05),MDA含量为(9.21±2.75)nmol/ml,高于对照组(P＜0.05);SOD活性与皮质醇呈负相关(r=0.52,P＜0.05),MDA含量与皮质醇呈正相关(r=0.54,P＜0.05),彗星细胞发生率56.5%,高于对照组(P＜0.05);实验组淋巴细胞DNA损伤率较对照组明显增加(P＜0.05);DNA损伤与MDA含量呈正相关(r=0.53,P＜0.05).结论:慢性应激可损伤海马超微结构,可诱导机体产生过量的自由基,促进脂质过氧化,进而损伤外周血淋巴细胞DNA.     

氧化应激对COPD大鼠膈肌影响及N-乙酰半胱氨酸作用

[摘要] 目的 研究氧化应激对COPD大鼠膈肌萎缩的影响及机制;N-乙酰半胱氨酸对膈肌的保护机制。方法 24只SD雄性大鼠随机分为对照组、COPD组、N-乙酰半胱氨酸干预组(NAC组)。膈肌称重,透射电镜观察超微结构。检测各组大鼠膈肌中MDA含量、SOD活力、泛素蛋白表达及膈肌细胞凋亡指数（AI）。结果 较对照组COPD组大鼠膈肌重量、SOD活力、泛素平均灰度值均显著降低（P<0.01）;MDA含量、AI显著升高（P<0.01）;较COPD组NAC组大鼠膈肌重量、SOD活力、泛素平均灰度值均显著升高（P<0.01）;MDA含量、AI显著降低（P<0.01）;COPD组较对照组膈肌超微结构损害明显,NAC组较COPD组明显改善。结论 氧化应激水平升高使COPD大鼠膈肌萎缩,超微结构破坏,过多的氧自由基可通过使泛素蛋白及细胞凋亡增加致膈肌萎缩变薄、N-乙酰半胱氨酸可降低膈肌氧化应激水平从而起保护作用。     

热应激预处理对大鼠肢体缺血再灌注后血清丙二醛、超氧化物歧化酶的影响

目的：探讨热应激预处理对大鼠肢体缺血再灌注损伤的影响。方法：制备大鼠缺血再灌注模型及热应激预处理模型。采用硫代巴比妥酸法测定大鼠丙二醛（MDA）浓度，采用黄嘌呤氧化酶法测定超氧化物歧化酶（SOD）活力并与对照组比较。结果：大鼠肢体缺血再灌注后血清中的MDA含量明显增加（P＜0．01），并有随再灌注时间延长不断升高的趋势，而SOD活性明显降低（P＜0．01）；热应激预处理后，血清中MDA含量明显降低（P＜0．01），SOD活性明显增高（P＜0．01）。结论：热应激 预处理可增强SOD清除细胞内氧自由基的水平。     

锌对热应激大鼠SOD活性的影响

目的：探讨热应激时锌对超氧化物歧化酶（ＳＯＤ）活性的影响。方法：以ＳＤ大鼠制备热应激模型，测定以不同浓度的锌饲料喂养的大鼠在热应激的不同时间肝脏、大脑皮质ＳＯＤ活性。结果：热应激后大鼠ＳＯＤ活性升高，持续应激后ＳＯＤ活性下降；高、中锌组ＳＯＤ活性明显高于低锌组。结论：充足的锌能够通过增强ＳＯＤ活性而提高机体热耐受力。     

影响野生型Canton S果蝇睡眠时间的相关生理因素

目的分析和评价常规给药应激对大鼠和小鼠部分免疫指标的影响。方法采用Wistar大鼠建立经口灌胃、腹腔注射、肌肉注射应激模型,测定外周WBC和WSCR,以及血清IL-2、IL-4、IFN-γ水平,并计算IFN-γ／IL-4比值;采用ICR小鼠建立经口灌胃应激、腹腔注射应激模型,测定外周WBC、WSCR和血清IL-2水平：与空白对照组比较分析各指标的变化。结果所有应激大鼠血清IL-2和外周WBC降低,IFN-γ和IFN-γ／IL-4升高,腹腔注射应激和肌肉注射应激大鼠WSCR升高;所有应激小鼠血清IL-2降低,灌胃应激小鼠WBC和WSCR均降低,腹腔注射应激小鼠WBC升高。结论经口灌胃、腹腔注射、肌肉注射操作所引起的应激均可导致大鼠、小鼠的免疫部分指标发生变化,其主要特点是IL-2和WBC降低、IFN-γ升高以及Th1极化。     

补肾及健脾复方对皮质酮大鼠T细胞凋亡信号相关基因群调控模式的对比研究

目的:探讨补肾及健脾复方对皮质酮大鼠T细胞凋亡信号相关基因表达的调控模式.方法:采用TUNEL标记的流式细胞技术,对皮质酮大鼠模型及各治疗组激活诱导的T细胞凋亡进行定量分析;采用荧光实时定量PCR技术对各组大鼠T细胞凋亡信号相关基因群mRNA表达水平进行定量与比较;采用分光光度法检测caspase-8、caspase-3的活性.结果:(1)与正常组相比,模型组T细胞凋亡百分率明显增高;右归饮组及补肾益寿胶囊组T细胞凋亡百分率与皮质酮模型组相比明显降低;四君子汤与模型组相比T细胞凋亡百分率无显著性差异.(2)模型组促凋亡的Fas、FasL、TNR1、Bax基因表达上调,抗凋亡的TNFR2、Bcl-2、cIAP1、cIAP2基因表达下调;两个补肾复方均可下调FasL、TNFR1 mRNA表达水平,并可上调Bcl-2、cIAPl、cIAP2 mRNA表达水平;四君子汤仅对Bcl-2,cIAP2 mRNA表达水平有显著上调作用.(3)模型组caspase-8、caspase-3活性显著增高,两个补肾复方均可降低caspase-8、caspase-3的活性,四君子汤对caspase-8、caspase-3的活性无显著下调作用.结论:两个补肾复方下调促凋亡基因FasL、TNFR1的转录,上调抗凋亡基因Bcl-2、cIAPl、cIAP2的转录,并且降低caspase-8、caspase-3的活性,从而降低皮质酮大鼠过度的T细胞凋亡,是补肾法特有的对皮质酮大鼠T细胞凋亡相关基因群的调控模式.     

Increased hsp70 of glucocorticoid receptor complex induced by scald and heat stress and its possible effect on the affinity of glucocorticoid receptor

Background Glucocorticoid (GC) insensitivity/GC resistance is an important etiological and prognostic factor in multiple diseases and pathophysiological processes such as scald, shock and asthma. The function of GC was mediated by glucocorticoid receptor (GR). Scald not only decreased the expression of GR but also reduced the affinity of GR, which played an important role in GC resistance in scalded rats. Whereas the molecular mechanism responsible for the decrease of GR affinity resulted from scald remains unclear. Recent studies showed that the changes of heat shock proteins (hsp) especially hsp90 and hsp70 of GR heterocomplex were associated with GR low affinity in vitro. Methods The affinity of GR in hepatic cytosols and in the cytosols of SMMC-7721 cells were determined by radioligand binding assay and scatchard plot. GR heterocomplex in cytosols were captured by coimmunoprecipation and the levels of hsp90 and hsp70 of GR complex were detected by quantitative Western blotting.Results Similar with that of hepatic cytosol of scalded rats, a remarkable decrease of GR affinity was also found in the cytosol of heat stressed SMMC-7721 cells. The level of hsp70 of GR complex in hepatic cytosol of scalded rats (30% total body surface area immersion scald) and in cytosol of heat stressed human hepatocarcinoma cell line SMMC-7721 were both increased by 1.5 fold, whereas no change of hsp90 in GR heterocomplex was found. According to the correlation analysis, there may be a positive relationship between increased hsp70 of GR complex and decreased GR affinity in the cytosols.Conclusions The primary results indicated that the level of hsp70 of GR heterocomplex was increased in the hepatic cytosol of scalded rats and the cytosol of heat stressed SMMC-7721 cells. The increase of hsp70 of GR complex might be associated with the decrease of GR affinity.     

Increased hsp70 of glucocorticoid receptor complex induced by scald and heat stress and its possible effect on the affinity of glucocorticoid receptor

Background Glucocorticoid (GC) insensitivity/GC resistance is an important etiological and prognostic factor in multiple diseases and pathophysiological processes such as scald, shock and asthma. The function of GC was mediated by glucocorticoid receptor (GR). Scald not only decreased the expression of GR but also reduced the affinity of GR, which played an important role in GC resistance in scalded rats. Whereas the molecular mechanism responsible for the decrease of GR affinity resulted from scald remains unclear. Recent studies showed that the changes of heat shock proteins (hsp) especially hsp90 and hsp70 of GR heterocomplex were associated with GR low affinity in vitro. Methods The affinity of GR in hepatic cytosols and in the cytosols of SMMC-7721 cells were determined by radioligand binding assay and scatchard plot. GR heterocomplex in cytosols were captured by coimmunoprecipation and the levels of hsp90 and hsp70 of GR complex were detected by quantitative Western blotting.Results Similar with that of hepatic cytosol of scalded rats, a remarkable decrease of GR affinity was also found in the cytosol of heat stressed SMMC-7721 cells. The level of hsp70 of GR complex in hepatic cytosol of scalded rats (30% total body surface area immersion scald) and in cytosol of heat stressed human hepatocarcinoma cell line SMMC-7721 were both increased by 1.5 fold, whereas no change of hsp90 in GR heterocomplex was found. According to the correlation analysis, there may be a positive relationship between increased hsp70 of GR complex and decreased GR affinity in the cytosols.Conclusions The primary results indicated that the level of hsp70 of GR heterocomplex was increased in the hepatic cytosol of scalded rats and the cytosol of heat stressed SMMC-7721 cells. The increase of hsp70 of GR complex might be associated with the decrease of GR affinity.     

Analysis of Age Dependent Effects of Heat Stress on EEG Frequency Components in Rats

Objective To demonstrate changes in different frequencies of cerebral electrical activity or electroencephalogram （EEG） following exposure to high environmental heat in three different age groups of freely moving rats. Methods Rats were divided into three groups （i） acute heat stress - subjected to a single exposure for four hours at 38 ℃; （ii） chronic heat stress exposed for 21 days daily for one hour at 38 ℃, and （iii） handling control groups. The digital polygraphic sleep-EEG recordings were performed just after the heat exposure from acute stressed rats and on 22nd day from chronic stressed rats by simultaneous recording of cortical EEG, EOG （electrooculogram）, and EMG （electromyogram）. Further, power spectrum analyses were performed to analyze the effects of heat stress. Results The frequency analysis of EEG signals following exposure to high environmental heat revealed that in all three age groups of rats, changes in higher frequency components （β2） were significant in all sleep-wake states following both acute and chronic heat stress conditions. After exposure to acute heat, significant changes in EEG frequencies with respect to their control groups were observed, which were reversed partly or fully in four hours of EEG recording. On the other hand, due to repetitive chronic exposure to hot environment, adaptive and long-term changes in EEG frequency patterns were observed. Conclusion The present study has exhibited that the cortical EEG is sensitive to environmental heat and alterations in EEG frequencies in different sleep-wake states due to heat stress can be differentiated efficiently by EEG power spectrum analysis.     

热应激反应对IL-6所致中性粒细胞凋亡障碍的影响

目的观察体外诱导热应激反应对IL-6所致中性粒细胞凋亡障碍的影响。方法将14例健康人的中性粒细胞分成6份，其中1份作为对照组，其余5份应用热休克或氯化镉诱导热应激反应后与培养液或IL-6共同孵育，分为热休克组、氯化镉组、IL-6组、IL-6 热休克组及IL-6 氯化镉组。各组于热应激反应诱导后3、20h分别测定中性粒细胞热休克蛋白(HSP70)的表达及凋亡率。结果热休克与氯化镉均可诱导热应激反应，细胞内HSP70表达增加；热应激反应促进凋亡，IL-6导致中性粒细胞凋亡抑制，IL-6不影响热应激反应对中性粒细胞的促凋亡作用。结论热应激反应促进凋亡并可逆转IL-6对其凋亡的抑制作用，提示热应激反应可能参与机体的抗炎作用机制。     

金荞麦药酒对佐剂性关节炎大鼠氧自由基和免疫功能的影响

目的 研究金荞麦药酒对佐剂性关节炎模型大鼠的治疗效果,探讨其作用机制.方法 将大鼠随机分为正常组、模型组、阳性对照组(每天灌胃雷公藤多苷片混悬液0.03 g/kg),低、中、高剂量金荞麦组(每天灌胃金荞麦药酒0.54、1.08、2.16 g/kg).建立佐剂性关节炎模型12 d后给药21 d,观察大鼠左后足跖肿胀体积,检测血清肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)、丙二醛(MDA)和足跖软组织TNF-α、前列腺素E2(PGE2)、一氧化氮(NO)含量;流式细胞术分析脾脏淋巴细胞凋亡率,免疫组化法检测膝关节滑膜巨噬细胞密度.结果 与正常组比较,模型组足跖肿胀体积、血清TNF-α、MDA和足跖软组织TNF-α、PGE2、NO水平、膝关节滑膜巨噬细胞密度明显升高(P<0.01),血清SOD、脾脏淋巴细胞凋亡率明显降低(P<0.01).与模型组比较,金荞麦可明显降低足跖肿胀体积、TNF-α、PGE2、NO水平和膝关节滑膜巨噬细胞密度,升高脾脏淋巴细胞凋亡率(P<0.05或P<0.01),但SOD、MDA无明显变化(P>0.05).结论 金荞麦药酒治疗类风湿关节炎的机制可能与调节TNF-α、PGE2、NO水平、膝关节滑膜巨噬细胞密度、脾脏淋巴细胞凋亡率有关.     

Increased hsp70 of glucocorticoid receptor complex induced by scald and heat stress and its possible effect on the affinity of glucocorticoid receptor

Background Glucocorticoid （GC） insensitivity/GC resistance is an important etiological and prognostic factor in multiple diseases and pathophysiological processes such as scald, shock and asthma. The function of GC was mediated by glucocorticoid receptor （GR）. Scald not only decreased the expression of GR but also reduced the affinity of GR, which played an important role in GC resistance in scalded rats. Whereas the molecular mechanism responsible for the decrease of GR affinity resulted from scald remains unclear. Recent studies showed that the changes of heat shock proteins （hsp） especially hsp90 and hsp70 of GR heterocomplex were associated with GR low affinity in vitro. Methods The affinity of GR in hepatic cytosols and in the cytosols of SMMC-7721 cells were determined by radioligand binding assay and scatchard plot. GR heterocomplex in cytosols were captured by coimmunoprecipation and the levels of hsp90 and hsp70 of GR complex were detected by quantitative Western blotting. Results Similar with that of hepatic cytosol of scalded rats, a remarkable decrease of GR affinity was also found in the cytosol of heat stressed SMMC-7721 cells. The level of hsp70 of GR complex in hepatic cytosol of scalded rats （30% total body surface area immersion scald） and in cytosol of heat stressed human hepatocarcinoma cell line SMMC-7721 were both increased by 1.5 fold, whereas no change of hsp90 in GR heterocomplex was found. According to the correlation analysis, there may be a positive relationship between increased hsp70 of GR complex and decreased GR affinity in the cytosols. Conclusions The primary results indicated that the level of hsp70 of GR heterocomplex was increased in the hepatic cytosol of scalded rats and the cytosol of heat stressed SMMC-7721 cells. The increase of hsp70 of GR complex might be associated with the decrease of GR affinity.     

活血通腑方对术后腹腔粘连大鼠肠黏膜免疫屏障功能的影响

目的?观察活血通腑方对术后腹腔粘连早期肠道黏膜屏障的影响。方法?取SD雄性大鼠60只,随机分为对照组、模型组、活血通腑方组,除对照组外,其余动物均采用锉刀法构建腹腔粘连大鼠模型,分别于术后第3、6、12?h和24?h给予相应剂量的药物,术后48?h采血及组织样本,ELISA法测定血浆中TNF-α水平,免疫组化法检测肠黏膜sIgA的含量和CD4细胞数量,TUNEL法检测肠黏膜下淋巴细胞凋亡情况。结果?与对照组相比,6、12?h和24?h后模型组血浆中TNF-α水平具有统计学差异（P<0.05~0.01）;3、6?h模型组黏膜sIgA表达明显下降;肠黏膜下淋巴细胞凋亡明显（P<0.01）,12、24?h时sIgA的分泌量明显增多（P<0.05）;而模型组12、24?h与3、6?h相比,黏膜下淋巴细胞凋亡明显下降接近对照组水平;模型组3?h肠道黏膜CD4细胞数量明显下降（P<0.01）;6、12、24?h时CD4细胞数量3组比较未见明显异常（P>0.05）。活血通腑方在术后3?h可显著降低模型鼠血浆中TNF-α水平;增高肠道黏膜sIgA含量和CD4细胞数量;减弱黏膜下淋巴细胞凋亡。结论?活血通腑方组可通过降低血TNF-α的水平,减轻黏膜下淋巴细胞凋亡,增加肠道黏膜sIgA含量和CD4细胞数量,提高局部免疫水平,抑制炎症反应。