参苓白术散对腹泻小鼠胃肠运动功能的影响及机制探讨

目的 通过对腹泻小鼠胃肠运动和腹泻大鼠结肠中胃肠肽蛋白表达影响的研究,探讨参苓白术散对腹泻的作用及其机制.方法 采用番泻叶泻下法复制模型,观察小鼠的排便次数、腹泻率、稀便级、稀便率、腹泻指数；用碳末推进法观测小肠碳末推进率的变化；免疫组织化学法检测结肠中P物质(SP)、血管活性肠肽(VIP)蛋白表达,观察参苓白术散对其干预作用.结果 经番泻叶泻下法复制模型后,小鼠的排便次数、腹泻率、稀便级、稀便率、腹泻指数升高；大鼠结肠中SP和VIP蛋白表达升高.参苓白术散治疗后,腹泻小鼠排便次数、腹泻率、稀便级、稀便率、腹泻指数降低,小肠推进被抑制；大鼠结肠中SP、VIP蛋白表达降低.结论 参苓白术散可以明显抑制胃肠运动,降低SP、VIP蛋白表达可能是其作用机制之一.     

玉米须对老年小鼠脾脏免疫细胞功能影响的实验研究

目的研究玉米须水煎剂及玉米须粗多糖对老年小鼠脾脏免疫细胞功能的影响。方法用称重法测定小鼠脾脏指数，中性红比色法测量脾脏中巨噬细胞的吞噬功能，MTT法测量脾脏B淋巴细胞增殖能力，以玉米须水煎剂及其粗多糖灌胃老年小鼠30d，观测其对老年小鼠上述指标的影响。结果老年组小鼠脾脏指数下降，脾脏中巨噬细胞的吞噬功能下降，脾脏B淋巴细胞增殖能力下降；与老年组比较，药物治疗组脾脏指数升高，脾脏中巨噬细胞的吞噬功能升高，脾脏B淋巴细胞增殖能力提高，且玉米须水煎剂与粗多糖对上述指标的影响无差别。结论玉米须水煎剂有提高老年小鼠脾脏免疫细胞免疫功能的作用，其功效成份为粗多糖。     

久泻灵对小鼠胸腺、脾脏重量及单核细胞吞噬功能影响的实验研究

目的研究久泻灵冲剂对慢性腹泻模型小鼠胸腺、脾脏熏量及单核细胞吞噬功能影响。方法建立对照组，检测小鼠免疫功能指标的变化。结果久泻灵冲剂可使模型小鼠脾脏重量明显增加，能显著提高小鼠单核细胞吞噬指数和吞噬系数。结论久泻灵冲剂能激活模型小鼠单核细胞的吞噬功能，使脾脏增重，从而增强机体非特异性抵抗能力。     

脾虚小鼠免疫功能的探讨

用大黄水煎剂灌胃制成脾虚模型小鼠，然后检测脾虚小鼠和正常小鼠的免疫功能。结果表明，脾虚小鼠的脾脏重量、脾重指数、胸腺重量、胸腺指数、巨噬细胞吞噬功能、抗体、IL－1及IL－2的产生能力，与正常组相比均显著降低，说明牌虚小鼠的免疫功能低下。     

脾虚小鼠免疫功能的探讨

用大黄水煎剂灌胃制成灌模型小鼠，然后检测脾虚小型和正常小鼠的免疫功能。结果表明，脾虚小鼠的脾脏重量、脾重指数、巨噬细胞吞噬功能，抗体ＩＬ－１及ＩＬ－２的产生能力，与正常组相比均显著降低，说明脾虚小鼠的免疫功能低下。     

四溴双酚A对小鼠免疫功能的影响

目的:探讨四溴双酚A(TBBPA)对小鼠免疫功能的影响。方法:通过给小鼠灌胃服用TBBPA粉末(2.5 mg/d)21 d,期间测定脾脏重量和生长指数、体外抗体形成细胞和腹腔巨噬细胞吞噬功能等,检测TBBPA对小鼠外周免疫器官脾脏生长、抗体生成及吞噬细胞功能的影响。结果:服用TBBPA组小鼠脾脏的重量、生长指数低于对照组(P0.05);服用TBBPA组小鼠巨噬细胞吞噬百分率为(25.8±2.1)%,吞噬指数为0.4±0.3,均显著低于对照组(40.4±2.1)%、0.9±0.3(均P0.05);服用TBBPA组小鼠1×106个脾细胞所含PFC数为223.4±19.2,显著低于对照组405.8±14.5(P0.01)。结论:TBBPA可致小鼠抗体介导的特异性免疫和吞噬细胞参与的非特异性免疫功能下降。     

枸杞和大蒜素对小鼠巨噬细胞功能的影响

用枸杞水提液及大蒜素和枸杞混合液,大蒜素胶囊液、鲜蒜提取液多次灌胃小鼠,均可提高小鼠巨噬细胞对鸡红细胞的吞噬率和吞噬指数,均能增强小鼠巨噬细胞的吞噬功能和细胞免疫功能。     

青黛颗粒对小鼠小肠推进运动的影响

[目的]通过青黛颗粒对正常小鼠小肠推进运动功能和对新斯的明所致小鼠小肠运动功能亢进作用的影响,探讨该药对小肠运动功能的作用机制.[方法]第1批小鼠50只,随机分为空白对照组,青黛高、中、低剂量组,阳性对照药组,每组10只.连续给药3 d,第4天给予含50%墨汁的0.85%氯化钠溶液灌胃,灌胃后7 min脱颈椎处死,取出小肠,计算墨汁推进率.第2批小鼠60只,随机分为空白对照组,模型对照组,青黛高、中、低剂量组,阳性对照药组,每组10只.连续给药4 d,禁食16 h后,末次给药30 min后,除空白对照组外均灌胃给予新斯的明.10 min后给予含50%墨汁的0.85%氯化钠灌胃,灌胃后5 min处死小鼠,测量小肠墨汁推进长度,计算推进率.[结果]两批小鼠青黛高、中、低剂量组和阳性对照药组的墨汁推进长度受到抑制,与空白对照组比较,均P＜0.01.[结论]青黛颗粒对正常小鼠小肠推进运动和新斯的明所致小肠运动亢进有显著抑制作用.     

沙棘叶水提物对小鼠非特异免疫功能的影响及抗凝血作用

目的 沙棘叶水提取物对小鼠非特异免疫功能的影响及抗凝血作用研究.方法 配制不同剂量的沙棘叶水提物,用12号灌胃针头对小鼠连续10 d灌胃.观察和测定沙棘叶水提物对小鼠的出血时间、凝血时间、白细胞指数、胸腺和脾免疫器官的指数及其对小鼠腹腔内巨噬细胞吞噬指数的影响.结果 沙棘叶水提取物能够延长小鼠的出血时间和凝血时间,明显增加小鼠体内的白细胞指数,能增加小鼠胸腺指数和脾指数,增强小鼠巨噬细胞吞噬功能.结论 沙棘叶水提物具有活血抗凝血的功能,同时能够提高小鼠的免疫能力.     

戴氏绿僵菌多糖对衰老小鼠免疫功能的影响

目的探讨戴氏绿僵菌多糖对衰老模型小鼠免疫功能的影响。方法建立D-半乳糖诱导的亚急性衰老模型小鼠,同时灌胃不同剂量的戴氏绿僵菌多糖,6 w后,观察模型小鼠体重变化,免疫器官(胸腺、脾脏)指数,腹腔巨噬细胞吞噬及血清中Ig G含量等免疫功能的影响。结果戴氏绿僵菌多糖能够改善模型小鼠体重;3种不同剂量的多糖均能提高模型小鼠T淋巴细胞的增殖能力,高剂量虫草多糖能提高B淋巴细胞增殖能力;同时能够显著提高小鼠脾脏、胸腺指数及腹腔巨噬细胞吞噬能力及显著提高血清中Ig G的含量。结论戴氏绿僵菌多糖可增强亚急性衰老模型小鼠的细胞和体液免疫功能。     

Effects of psychological stress on small intestinal motility and expression of cholecystokinin and vasoactive intestinal polypeptide in plasma and small intestine in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and expression of cholecystokinin (CCK) and vasoactive intestinal polypeptide (VIP) in plasma and small intestine, and to explore the relationship between small intestinal motor disorders and gastrointestinal hormones under psychological stress. METHODS: Thirty-six mice were randomly divided into psychological stress group and control group. A mouse model with psychological stress was established by housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. CCK and VIP levels in plasma and small intestine in mice were measured by radioimmunoassay (RIA). RESULTS: Small intestinal transit was inhibited (52.18±19.15% vs70.19±17.79%, P<0.01) in mice after psychological stress, compared to the controls. Small intestinal CCK levels in psychological stress mice were significantly lower than those in the control group (0.75±0.53 μg/g vs1.98±1.17 μg/g, P<0.01), whereas plasma CCK concentrations were not different between the groups. VIP levels in small intestine were significantly higher in psychological stress mice than those in the control group (8.45±1.09 μg/g vs7.03±2.36 μg/g, P<0.01), while there was no significant difference in plasma VIP levels between the two groups. CONCLUSION: Psychological stress inhibits the small intestinal transit, probably by down-regulating CCK and up-regulating VIP expression in small intestine.     

Effect of emodin on small intestinal peristalsis of mice and relevant mechanism

AIM: To investigate the effect of emodin on small intestinal peristalsis of mice and to explore its relevant mechanisms. METHODS: The effect of emodin on small intestinal peristalsis of mice was observed by charcoal powder propelling test of small intestine. The contents of motilin and somatostatin in small intestine of mice were determinated by radioimmunoassay. The electrical potential difference (PD) related to Na+ and glucose transport was measured across the wall of reverted intestinal sacs. Na+-K+-ATPase activity of small intestinal mucosa was measured by spectroscopic analysis. RESULTS: Different dosages of emodin can improve small intestinal peristalsis of mice. Emodin increased the content of motilin, while reduced the content of somatostatin in small intestine of mice significantly. Emodin 0.2, 0.4, 0.8, and 1.6 g/L decreased PD when there was glucose. However, emodin had little effect when glucose was free. The Na+-K+-ATPase activity of small intestinal mucosa of mice in emodin groups was inhibited obviously. CONCLUSION: Emodin can enhance the function of small intestinal peristalsis of mice by mechanisms of promoting secretion of motilin, lowering the content of somatostatin and inhibiting Na+-K+-ATPase activity of small intestinal mucosa.     

Oral Bifidobacterium modulates intestinal immune inflammation in mice with food allergy

Background and Aims: It is proposed that probiotics have a therapeutic effect on the treatment of immune disorders. However, the underlying mechanisms require clarification. The present study aimed to evaluate the effect of gavage‐feeding Bifidobacteria on suppression of T helper 2 (Th2) pattern inflammation in the intestines of mice with food allergy. Methods: Mice were sensitized to ovalbumin to induce the intestinal Th2 pattern inflammation. Allergic mice were treated with or without Bifidobacteria via gavage‐feeding. Th2 response, number of regulatory T cells (Treg) in the spleen and intestine, intestinal epithelial barrier function and bifidobacterial translocation were examined. Results: The results showed that serum‐specific immunoglobulin E antibody and interleukin 4 (IL‐4) were increased in allergic mice. Intestinal epithelial barrier function was impaired in allergic mice as shown by the increase in epithelial ion secretion and permeability to macromolecular protein horseradish peroxidase in Ussing chambers. Number of Treg was decreased in both spleen and intestines of allergic mice. Gavage‐feeding Bifidobacteria significantly suppressed the skewed Th2 response and increased the number of Treg. Transient bifidobacterial translocation was observed in allergic mice. Conclusions: Oral administration of Bifidobacteria has the capacity to suppress the skewed Th2 response in allergic mice, increasing the number of Treg and IL‐10‐positive cells and improve the impaired intestinal epithelial barrier function.     

脾虚证进程中小鼠特异性/非特异性免疫功能变化及中药的干预作用

目的 观察脾虚证进程中小鼠特异性/非特异性免疫功能的变化及中药敦煌大宝胶囊对其免疫功能的影响.方法 受试动物随机分为空白对照组、模型组、敦煌大宝胶囊大、中、小治疗组,阳性对照组,每组8只.建立脾虚证小鼠模型,中药干预后观测各组小鼠腹腔巨噬细胞吞噬率和吞噬指数;ConA,LPS诱导的T、B淋巴细胞增殖反应及NK细胞活性等指标.结果 脾虚证进程中小鼠特异性/非特异性免疫功能低下(P＜0.05).经中药干预后,与模型组比较,敦煌大宝胶囊治疗组小鼠腹腔巨噬细胞吞噬率和吞噬指数;ConA,LPS诱导的T、B淋巴细胞增殖反应及NK细胞活性显著升高,差异具有统计学意义(P<0.05).结论 脾虚证进程中小鼠特异性/非特异性免疫功能低下,敦煌大宝胶囊对脾虚证小鼠免疫功能紊乱具有明显改善作用.     

Regulation of mucosal immune responses by recombinant interleukin 10 produced by intestinal epithelial cells in mice

BACKGROUND & AIMS: Interleukin (IL)-10 is a cytokine with anti-inflammatory properties. The aim of this study was to explore the effect of a site-specific delivery of IL-10 on intestinal immune responses. METHODS: Transgenic mice were created in which IL-10 is expressed by the intestinal epithelial cells. RESULTS: Transgenic mice showed a marked increase in the number of intraepithelial lymphocytes in the small intestine. Mucosal lymphocytes of transgenic animals produced fewer T helper type 1 cytokines than wild-type lymphocytes. By contrast, the production of transforming growth factor beta was increased. Moreover, the epithelial layer in transgenic mice was significantly enriched for CD4(+)CD25(+) T cells. Furthermore, transgenic mice had increased numbers of immunoglobulin A-producing B cells in the small intestine. These effects were local because splenic lymphocytes were not affected. Studies in models of inflammatory bowel disease showed that transgenic IL-10 was able to attenuate the acute colitis induced by dextran sodium sulfate administration or by adoptive transfer of CD4(+)CD45RB(high) splenocytes, with a modest effect on the chronic intestinal inflammation arising spontaneously in IL-10(-/-) mice. CONCLUSIONS: These observations provide evidence for an in vivo lymphoepithelial cross talk, by which cytokines locally produced by epithelial cells can regulate immune responses in the intestine without systemic modifications.     

Intravital observation of adhesion of lamina propria lymphocytes to microvessels of small intestine in mice

BACKGROUND & AIMS: Although the recirculation of lymphocytes through the intestinal mucosa is important for the specific immune defense, the homing of lamina propria lymphocytes (LPLs) has not been clearly understood. The aim of this study is to compare, under an intravital microscope, the dynamic process of lymphocyte-endothelium recognition and binding in the murine intestinal mucosa of T lymphocytes from the lamina propria of intestine to that of T lymphocytes from the spleen. METHODS: LPLs isolated from nonlymphoid areas of the small intestine and spleen (SPL) were fluorescence-labeled and injected into a jugular vein of recipient mice. Microvessels of the villus mucosa and ileal Peyer's patches were observed under an intravital fluorescence microscope, and the effects of anti-adhesion-molecule antibodies on lymphocyte-endothelial interaction were investigated. RESULTS: LPLs accumulated abundantly in the microvessels of villus tips but not in the submucosal venules or postcapillary venules of Peyer's patches, where SPLs migrated selectively. The accumulation of LPLs in the villus tips was almost completely inhibited by anti-beta7-integrin and was significantly inhibited by anti-mucosal addressin cell-adhesion molecule 1 (MAdCAM-1) and anti-alpha4-integrin. Significant MAdCAM-1 expression was observed in the microvessels of the villus mucosa. Some SPLs adhered to the nonlymphoid mucosa, but most soon detached. CONCLUSIONS: It was shown in vivo for the first time that T lymphocytes from the lamina propria but not from the spleen adhere selectively, mostly via alpha4beta7 and MAdCAM-1, to the microvessels of villus tips of the intestine, but not to the postcapillary venules of Peyer's patches.     

The action of salt and captopril on blood pressure in mice with genetic hypertension

OBJECTIVE: Does captopril lower blood pressure in genetically hypertensive, normotensive and hypotensive mice under normal and salt-loaded conditions? DESIGN AND METHODS: Groups of inbred mice that were genetically hypertensive, normotensive or hypotensive were given one of the following treatments: (a) captopril in drinking water for 7 days; controls were given water. (b) 0.85% saline to drink for up to 14 days; controls were given water. (c) Water or saline followed by captopril/water or captopril/saline for 7 days. (d) In hypotensive mice only, 0.85% saline, 0.85% saline plus captopril, water or captopril in water. Systolic blood pressures (SBP) were measured by a computerized tail-cuff sphygmomanometer. Results were compared by analysis of variance (ANOVA). RESULTS: Captopril lowered SBP in all strains of mice. When saline was given with captopril, the fall in SBP was slower but the final SBP level was similar to that of mice given captopril in water. Hypotensive mice showed a transient rise in SBP on saline, which was abolished by concurrent treatment with captopril. CONCLUSION: Captopril lowers blood pressure in hypertensive, normotensive and hypotensive mice. Salt-loading retards the captopril-induced fall in SBP, but the final level of SBP achieved is similar to that in mice given captopril with water. The BPL1 strain of mouse was slightly salt-sensitive, and this was abolished by captopril.     

人胃癌原位移植模型中宿主脾虚证的探讨

目的：探讨人胃癌裸小鼠原位移植模型的脾虚证及该模型用于中药抗胃癌作用研究的可行性。方法：所有动物随机分为对照组,单纯造模组和健脾为主中药SRRS复方治疗组,建立人胃癌裸小鼠原位移植模型,观察肿瘤生长,转移及宿主体重、进食、自然杀伤（NK）细胞活性、红细胞免疫的变化,并观察健脾复方SRRS干预后肿瘤的进展情况,结果：经病理证实所有造模动物均形成腺胃部位的人胃癌移植瘤,单纯造模组出现较多肝脏、胰腺、横膈等脏器部位的肿瘤转移,动物进食量减少,体重明显下降,NK细胞活性降低,免疫复合物花环率较造模前显著增加,而在健脾为主中药SRRS复方治疗组,动物进食量稍减少,无体重下降,NK细胞活性较单纯造模组提高,原位肿瘤生长受到抑制,肿瘤转移灶少,结论：人胃癌裸小鼠原位移植可造成宿主消化,免疫功能低下等脾虚证表现。该模型作为病证结合的胃癌模型值得进一步研究,健脾为主SRRS复方对人胃癌原位移植瘤有抑瘤和改善其脾虚状态的作用。