Vasoactive intestinal polypeptide (VIP) corrects chronic inflammatory response syndrome (CIRS) acquired following exposure to water-damaged buildings

Exposure in water-damaged buildings (WDB) to airborne bioaerosols including metabolic products of toxigenic fungi, bacteria and actinomycetes;and inflammagens, can lead to a persistent innate immune inflammatory illness. This illness, termed a chronic inflammatory response syndrome (CIRS-WDB), is systemic with symptoms acquired from multiple organ systems. Treatment of CIRS-WDB has progressed rapidly as a better understanding of the inflammatory pathophysiology has led to targeted, sequential therapies. The fundamental basis of uncontrolled innate immune responses, the humoral deficiency of regulatory neuropeptides melanocyte stimulating hormone (MSH) or vasoactive intestinal polypeptide (VIP), seen in over 98% of pa tients, has not consistently responded to any treatment modality. Use of replacement VIP has been attempted anecdotally;VIP replacement therapies show promise in short term studies but longer therapies have not been attempted. Here we report an open label trial of 20 patients with refractory CIRS-WDB illness who took replacement VIP in a nasal spray for at least 18 months with confirmation of durable efficacy and absence of significant side effects. These 20 patients were similar in symptoms and lab find- ings to three previously published cohorts in- volving 1829 patients and 169 controls. Dosage of VIP was titrated downwards from four to zero doses a day to determine minimum effective dose, and retitrated upwards for maximum improvement over time. The trial showed that VIP therapy safely 1) reduced refractory symptoms to equal controls;2) corrected inflammatory parameters C4a, TGF beta-1, VEGF, MMP9;3) corrected estradiol, testosterone and 25-OH Vitamin D;4) returned pulmonary artery systolic pressure (PASP) during exercise to normal;and 5) enhanced quality of life in 100% of trial patients. Subsequent identification of correction of T-regulatory cell levels supports the potential role of VIP in both innate and adaptive immune function.

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 fluoxetine on depression-induced changes in the expression of vasoactive intestinal polypeptide and corticotrophin releasing factor in rat duodenum

AIM: To investigate changes in vasoactive intestinal polypeptide (VIP) and corticotrophin releasing factor (CRF) in the plasma and duodenum of chronic stress- induced depressed rats and the effects of fluoxetine hydrochloride (fluoxetine) treatment on depression- induced changes in VIP and CRF. METHODS: A Sprague-Dawley rat model of chronic stress-induced depression was produced. Thirty experimental rats were randomly divided into the following groups: control group, saline-treated depressed group, and fluoxetine-treated depressed group. Open- f ield testing was performed to assess the rats’ behavior. VIP and CRF levels in plasma were measured by ELISA. Immunofluorescence techniques combined with laser scanning confocal microscopy (LSCM) were used to investigate VIP and CRF expression in the duodenum. RESULTS: The open-field behavior, both crossing and rearing, of depression model rats, decreased signif icantly compared with those of normal control rats over 5 min. Defecation times increased significantly. Compared to the control group, FITC fluorescence of duodenal CRF expression and plasma CRF levels in the depressed rats increased significantly (fluorescence intensity of duodenal CRF: 11.82 ± 2.54 vs 25.17 ± 4.63; plasma CRF: 11.82 ± 2.54 ng/L vs 25.17 ± 4.63 ng/L, P < 0.01), whereas duodenal VIP expression and plasma VIP levels decreased signif icantly (fluorescence intensity of duodenal VIP: 67.37 ± 18.90 vs 44.51 ± 16.37; plasmaVIP: 67.37 ± 18.90 ng/L vs 44.51 ± 16.37 ng/L, P < 0.01). Fluoxetine improved depressed behavior, increased VIP expression and decreased CRF expression in plasma and the duodenal tissue of depressed rats. CONCLUSION: Chronic stress can induce injury to the duodenum, accompanied by increasing CRF and decreasing VIP in the plasma and duodenum. Treatment with fluoxetine can ameliorate pathological changes in the duodenum of depressed rats, which suggests that antidepressants are an effective therapeutic agent for some duodenal diseases caused by chronic stress. VIP is a potential therapeutic strategy.

Study on vasoactive intestinal polypeptide receptor 1 gene translation in psoriatic epidermis with the topical treatment of capsaicin ointment

Objective To investigate the mechanism of capsaicin in treating active psoriasis vulgaris.Methods A total of 42 patients with active psoriasis vulgaris diagnosed by histology and clinical features were given either placebo or 0.025% capsaicin ointment four times daily for 30 days randomly by double-blind method.Vasoactive intestinal polypeptide receptor 1(VIPR1)gene translation in active psoriatic lesions before and after treatment with capsaicin ointment was detected by in situ hybridization.Results There was positive staining of VIPR1 gene in all the layers of psoriatic epidermis(95.5%)before the treatment with capsaicin ointment,but nearly no dyeing in epidermis(18.2%)after the treatment for 30 days.There was nearly no brown staining before and after treatment in control group.Conclusion VIPR1 gene translation in psoriatic epidermis is down-regulated after capsaicin treatment for 30 days.

VASOACTIVE INTESTINAL POLYPEPTIDE PREVENTS INJURY OF PULMONARY VASCULAR PERMEABILITY DUE TO XANTHINE WITH XANTHINE OXIDASE

Hyperpermeability is a crux of pathogenesis of sudden lung edema in many pulmonary disorders. especially in acute lung injury and adult respiratory distress syndrome(ARDS). Using our modified method for assessment of pulmonary vascular permeability. we observed the effects of xanthine with xanthine oxidase(X-XO) perfused in rat pulmonary artery and the protection of vasoactive intestinal polypeptide(VIP) against the injury of pulmonary vascular permeabilrty. After addition of xanthine oxidase in the perfusate reservoir containing xanthine￣(125) I-albumin leak index (￣(125)IALI)was remarkably increased while peak airway pressure(Paw) was not significantly increased, and perfusion pressure of pulmonary artery(Ppa)and lung wet/dry weight ratio(W/D) were only slightly increased. Xanthine plus xanthine oxidase also increased thromboxane B_2(TX B_2) and 6-keto-prostaglandin F_(1α)(6-keto -PGF_(1α)) in the perfusate. Treatment with VIP obviously reduced or totally prevented all signs of injury. Simultaneously, VIP also diminished or abolished the associated generation of arachidonate products. The results indicated that VIP has potent protective activity against injury of pulmonary vascular permeability and may be a physiological modulator of inflammatory damage to vascular endothelium associated with toxic oxygen metacolites.

Vasoactive Intestinal Peptide (VIP) and VIP Receptors-Elucidation of Structure and Function for Therapeutic Applications

Vasoactive intestinal peptide (VIP) is a 28-amino acid polypeptide first isolated from swine duodenum. VIP is a neurotransmitter that is extensively distributed in tissues. According to published reports, VPAC1 and VPAC2 act as VIP receptors and are widely present in the central nervous system and peripheral tissues. VIP exerts diverse actions on the cardiovascular system, pancreas, digestive tract, respiratory system, and urological system. Recent reports indicated that VIP has immunological and neuroprotective effects and also affects cell growth. While primary investigations for developing therapeutic applications for various pathological conditions and diseases are underway, the structure and function of VIP should be analyzed in more detail.

Distribution of Vasoative Intestinal Polypeptide in CranialParasym pathetic Ganglion of the Rat

Immunoreactivity (IR) for vasoactive intestinal polypeptide (VIP) of cranial parasympathetic ganglia of the rat was observed with indirect immunofluorescent method. It was found that there were VIP IR principal neurons in the ciliary, pterygopalatine, and otic ganglia. The highest positive ratio of VIP IR cells was located in the ciliary ganglia (34.8%), followed by that in the pterygopalatine ganglia(17.0%), and the lowest was found in the otic ganglia (15.4%). VIP IR small intensely fluorescent (SIF) cells and nerve fibers were not observed. Distributive characteristics of neuropeptides and functional significance of VIP in cranial parasympathetic ganglia were discussed.

RELAXANT EFFECTS OF VASOACTIVE INTESTINAL PEPTIDE ON PULMONARY ARTERY IN CHRONICALLY HYPOXIC RATS

The object of this study is to investigate the effect of VIP on pulmonary artery of chronically hypoxic rats. It was shown that chronic hypoxia depressed significantly pulmonary artery relaxation induced by VIP as compared with those of control (P<0. 001). The vascular relaxation of both groups was correlated with concentration of VIP. In addition, the relaxant effect of VIP on pulmonary arteries in rats was endothelium─independent, and was not prevented by indomethacin or nordihydroguaiaretic acid, but was abolished completely by methylene blue. These results suggest that the lower relaxation of pulmonary artery in rats might not be due to the endothelial injury caused by chronic hypoxia, and chronic hypoxia may inhibit directly the soluble guanylate cyclase in vascular smooth muscle cells invloved in synthesis of cGMP and thus reduced the sensitivity and reactivity of pulmonary artery to VIP.

THE AUTOCRINE REGULATORY EFFECT OF VASOACTVE INTESTINAL PEPTIDE ON THE GROWTH OF HUMAN PANCREATIC CARCINOMA CELLS

In the present study, the effects of VIP on the growth of two human pancreatic carcinoma cell lines PU-PAN-l and PANC-I were determined using tritiated thymidine incorporation. VIP receptors. intracellular cAMP and polyamines were investigated. The results indicated that VIP at a concentration of 10-8 mol/L to 10-7 mol/L can significantly stimulate the growth of PU-PAN-I cells but not PANC-1 cells. This effect is dose-dependent and abolished by VIP receptor antagonist, [4-C1-Phe6 . Leu17] VIP, suggesting VIP receptors in PU-PAN-I cells may mediate this effect. VIP can markedly elevate the levels of intracellular cAMP and polyamines in PU-PAN-I cells.indicating that the growth-promoting effect stimulated by VIP may be via a rapid increase in the biosyntheses of cAMP and polyamines. In addition, the VIP-antibody inhibited the growth of PU-PAN-I cells in serum-free culture mediurn. The results above suggested that VIP has an autocrine regulatory effect on this pancreatic carcinoma cell line (PU-PAN-1).

养荣润肠舒合剂对慢性传输型便秘SD大鼠结肠5-HT、VIP的影响

目的探讨慢性传输型便秘大鼠结肠黏膜5-羟色(5-hydroxytryptophan,5-HT)、血管活性肠多肽(vasoactive intestinal polypeptide,VIP)的含量,以明确中药制剂养荣润肠舒合剂对大鼠结肠5-HT、VIP表达的调节作用。方法将60只健康的SD大鼠随机分为空白组10只,造模组50只(模型组10只、莫沙必利组10只、养荣润肠舒合剂高、中、低剂量组各10只)。应用复方地芬诺酯灌胃(2 mL/200 g体质量)以复制慢性传输型便秘大鼠模型(每天1次,连续10 d)。期间记录大鼠首次排便时间,并收集粪便、测量粪便剂量、含水量以判断造模是否成功。复制模型成功后进行药物治疗,每天1次,连续10 d。然后采用间接酶联免疫吸附试验(Enzyme Linked Immunosorbent Assay,ELISA)观测大鼠结肠5-HT、VIP的光密度(optical density,OD)值。结果①与空白组比较,模型组SD大鼠的首次排便时间延后,且新鲜粪便的剂量、含水量减少,差异有显著统计学意义(P<0.01)。②与模型组比较,莫沙必利组和养荣润肠合剂低、中、高剂量组治疗后大鼠的首次排便时间均提前,且粪便的含水率、重量除使用养荣润肠低组外均有所增长(P<0.01)。③与莫沙必利组比较,养荣润肠舒合剂中组剂量组大鼠的一般状况最好,首次排便时间最接近莫沙必利组且较短于莫沙必利组,差异无统计学意义(P>0.05),新鲜粪便剂量最接近莫沙必利组且较重于莫沙必利组,差异无统计学意义(P>0.05),含水量明显优于莫沙必利组,差异有统计学意义(P<0.05);养荣润肠舒合剂高剂量组大鼠排便状况与莫沙必利组相差不大,差异无统计学意义(P>0.05);莫沙必利组大鼠排便状况明显优于养荣润肠舒合剂低剂量组,差异有显著统计学意义(P<0.01)。④养荣润肠舒合剂中剂量组的大鼠一般状况更佳,而低剂量组的大鼠状况较差,新鲜粪便的剂量、含水量较小。⑤与空白组比较,模型组大鼠近端结肠组织5-HT、VIP的含量显著降低,OD值缩小(P<0.01)。⑥治疗后与模型组比较,莫沙必利组及养荣润肠舒合剂低、中、高剂量SD大鼠结肠5-HT、VIP含量显著升高,OD值增加,差异有明显统计学意义(P<0.01)。⑦治疗后与莫沙必利组比较,养荣润肠舒合剂中剂量大鼠结肠的5-HT、VIP含量及OD值增加,最接近莫沙必利组且较高于莫沙必利组,差异无统计学意义(P>0.05);养荣润肠舒合剂高剂量组大鼠状况及大鼠结肠5-HT、VIP含量与莫沙必利组相差不大,差异无统计学意义(P>0.05)。⑧与养荣润肠舒合剂高剂量组比较,养荣润肠舒合剂中剂量组大鼠结肠5-HT、VIP含量更高,OD值差异无统计学意义(P>0.05),而养荣润肠舒合剂低剂量组大鼠结肠的5-HT、VIP含量相对较低,与养荣润肠舒合剂中剂量组相比OD值也较低,具有统计学意义(P<0.01)。结论5-HT作为脑—肠轴的关键神经递质,VIP作为存在于中枢神经和肠神经系统中的神经递质,在慢性传输型便秘的发病中起着重要的作用;中药方剂养荣润肠舒合剂能有效提高慢性传输型便秘大鼠结肠5-HT、VIP含量,增强5-HT、VIP的表达有关;因此,作者认为养荣润肠舒合剂可能是通过这一机制改善慢性传输型便秘的临床症状,从而达到“以补治秘”的目的。

肠易激综合征肠黏膜SP、VIP、CGRP变化的研究

目的 :探讨肠易激综合征 (IBS)患者结肠黏膜 P物质 (SP)、血管活性肠肽 (VIP)和降钙素基因相关肽 (CGRP)的变化 ,以及它们在 IBS中的可能作用和临床意义。 方法 :黏膜标本取自 17例正常人、16例腹泻型 IBS(D- IBS)患者和 12例便秘型 IBS(C- IBS)患者的回盲部、乙状结肠 ,应用免疫组织化学染色法和放射免疫测定法分别检测 SP、VIP、CGRP。结果 :IBS患者结肠黏膜 SP、VIP含量均较正常对照组显著升高 (P<0 .0 1) ;IBS患者结肠黏膜 SP、VIP免疫反应阳性神经纤维较正常对照组增多、增粗、阳性增强 (P<0 .0 1) ;IBS患者与正常对照组结肠黏膜的 CGRP含量和 CGRP免疫反应阳性神经纤维的强度、面积、密度差异无统计学意义 (P>0 .0 5 )。 结论 :SP、VIP可能参与了 IBS的病理生理过程。

血管活性肠肽对便秘大鼠排便及结肠组织中VIP-cAMP-PKA-AQP3信号通路的影响

目的:观察血管活性肠肽(vasoactive intestinal peptide,VIP)对便秘大鼠肠道水液代谢、环磷酸腺苷-蛋白激酶A信号通路(cyclic AMP protein kinase A signaling pathway,c AMP-PKA)和水通道蛋白3(water channel protein 3,AQP3)的影响,探讨VIP治疗便秘的作用及机制。方法:45只健康成年Sprague-Dawley大鼠随机分为空白对照组、模型组、模型+VIP组。给药4周后,墨汁灌胃法检测大鼠首粒黑便排出时间;根据大鼠粪便干湿重计算粪便含水率;HE染色观察各组大鼠结肠组织形态学变化;Western印迹检测各组大鼠结肠组织中VIP和AQP3蛋白表达水平;定量即时聚合酶链锁反应(quantitative real time polymerase chain reaction,q PCR)检测各组大鼠结肠组织中c AMP,PKA和AQP3 m RNA的表达水平。结果:与空白对照组比较,模型组大鼠首粒黑便出现时间延长,粪便含水率明显减少(均P<0.01);结肠黏膜上皮部分破坏,杯状细胞体积减小,数量明显减少;结肠组织中VIP和AQP3蛋白含量明显减少,AQP3,c AMP和PKA m RNA相对表达水平均有所降低(均P<0.05)。与模型组比较,模型+VIP组大鼠首粒黑便出现时间缩短,粪便含水率明显增加(均P<0.05);结肠黏膜上皮完整性明显改善,杯状细胞体积增大,数量增多;结肠组织中VIP和AQP3蛋白含量增多,CAMP,PKA和AQP3 m RNA相对表达水平升高(均P<0.05)。结论:VIP静脉注射能够调节肠道水液代谢,改善大鼠便秘症状,其机制可能与调节VIP-c AMP-PKA-AQP3信号通路有关。

冷应激大鼠血浆及回肠P物质和VIP的变化

采用放免法对冷束缚应激大鼠血浆及回肠始段P物质 (SP)、血管活性肠肽 (VIP)进行测定。发现与正常对照组相比 ,应激组回肠段SP含量无明显改变 ,VIP含量降低 (P <0 .0 5 ) ;应激组血浆中SP质量浓度明显增加 (P <0 .0 1 ) ,VIP质量浓度则明显降低 (P <0 .0 1 )。提示 :应激组大鼠回肠始段及血浆SP、VIP的改变 ,可能与其胃肠功能变化的调节有关。

特发性便秘患者乙状结肠粘膜VIP、NOS阳性神经的变化

目的:研究特发性便秘患者乙状结肠粘膜内VIP、NOS阳性神经的变化情况。方法:利用免疫组化技术研究了8例特发性便秘患者乙状结肠粘膜内VIP、NOS阳性神经的变化情况并与5例健康人相比较。结果:特发性便秘患者乙状结肠粘膜内NOS阳性神经较正常人明显增多(P<0.01)。结论:特发性便秘的发病可能与结肠内NO产生增多有关。

实验性脾虚证大鼠胃窦部SP、VIP、CGRP含量的研究

采用放射免疫分析方法（ＲＩＡ）观察了实验性脾虚证大鼠胃窦部Ｐ物质（ＳＰ）、血管活性肠肽（ＶＩＰ）、降钙素基因相关肽（ＣＧＲＰ）含量的变化。结果：脾虚组胃窦部ＳＰ、ＶＩＰ、ＣＧＲＰ免疫活性肽（ｉｒＳＰ、ｉｒＶＩＰ、ｉｒＣＧＲＰ）含量均明显降低，下降百分率为ｉｒＳＰ＞ｉｒＶＩＰ＞ｉｒＣＧＲＰ。自然恢复组ｉｒＳＰ含量无明显恢复，ｉｒＶＩＰ、ｉｒＣＧＲＰ含量均恢复正常。加味四君子汤治疗组ｉｒＳＰ含量有一定程度恢复，但与对照组相比仍有显著差异，ｉｒＶＩＰ、ｉｒＣＧＲＰ含量均恢复正常。结果提示：脾虚大鼠胃窦部ｉｒＳＰ、ｉｒＶＩＰ、ｉｒＣＧＲＰ含量的改变可能与脾虚证胃动力失调有一定关系。

Treg细胞在VIP治疗实验性类风湿性关节炎中的作用研究

目的:本研究探讨血管活性肠肽(VIP)治疗实验性类风湿性关节炎的免疫调节机制及Treg细胞参与的调节。方法:本研究以鸡Ⅱ型胶原(CCⅡ)诱导的Wistar大鼠实验性类风湿性关节炎(CIA)为动物模型,分析大鼠关节指数评分和关节病理变化,通过细胞因子检测分析Th1/Th2平衡关系;通过流式细胞术和功能实验分析Treg的变化,评价VIP的治疗作用和机制。结果:我们的研究显示体内经VIP治疗的CIA大鼠在临床和组织学水平均得到了保护和缓解。其抑制作用与下列因素有关:抑制致病性T细胞的增殖,免疫应答由Th1型应答向Th2型应答转换,以及上调了具有抑制T细胞活化和增殖作用的CD4+CD25+Treg细胞数量与功能。结论:本研究揭示了VIP可通过调节Th1/Th2平衡和上调Treg细胞来抑制致病性T细胞的活性,从而保护、缓解实验性关节炎。

胆囊结石形成时Calponin、VIP在胆囊平滑肌和Oddi括约肌中的表达及意义

目的探索血管活性肠肽(VIP)和调宁蛋白(Calponin)在胆囊平滑肌和Oddi括约肌中的表达,并评估二者在胆囊胆固醇结石形成机制中的作用。方法(1)动物模型:新西兰兔40只,随机分成对照组20只,喂普通饮食;结石组20只,饲喂含1.2g/d胆固醇的成石饮食4周。免疫组化法测定Calponin、VIP在胆囊平滑肌和Oddi括约肌中的表达。结果结石组16只出现胆囊结石,19只出现胆固醇结晶,对照组无结石及结晶出现;结石组胆囊平滑肌Calponin和VIP阳性产物与对照组相比较明显升高,差异有统计学意义(P<0.05),Oddi括约肌Calponin和VIP阳性产物与对照组相比较明显降低,差异有统计学意义(P<0.05)。Calponin阳性表达与VIP呈正相关。结论胆囊排空功能在胆囊结石形成中起重要作用,胆囊结石家兔胆囊排空障碍与Calponin、VIP明显相关。

模拟失重对大鼠血浆ghrelin、VIP和胃肠动力的影响

目的探讨模拟失重状态下胃肠激素ghrelin和VIP的改变以及对胃肠动力的影响。方法 32只Wistar大鼠,随机分为4组,每组8只,按模拟失重的时程分为14 d组和21 d组,并分别设立非悬吊14 d对照组和非悬吊21 d对照组。先后进行胃浆膜肌电的描记、葡聚糖蓝2000标记法测定胃残留率和小肠推进率,血浆ghrelin和VIP浓度分别用酶免法(ELISA)和放免法(RI)测定。结果悬吊14 d组与21 d组与相应对照组比较,ghrelin浓度下降VIP浓度升高,同时表现为胃肌电延缓,胃残留率增加;小肠推进率下降,差异均具有统计学意义(P<0.05)。结论模拟失重状态下血浆ghrelin下降和VIP升高可能是导致胃肠动力下降的重要因素之一。

A型肉毒毒素抑制大鼠变应性鼻炎鼻溢及VIP在鼻腔粘膜的免疫表达

目的 :确定A型肉毒毒素 (BTX A)对大鼠变应性鼻炎鼻溢是否具有治疗的作用 ,以及毒素使用前后血管活性肠肽 (VIP)免疫表达和组织学改变 .方法 :卵清蛋白 (Ovalbu min)致敏Wistar大鼠制作变应性鼻炎 (allergicrhinitis,AR)动物模型 ,16只大鼠随机分为 3组 ,即对照组 (n =6 ) ;致敏组 (n=10 ) ;致敏后A型肉毒毒素 (BTX A)用药组 (n =5 ) .观察给予BTX A前后大鼠鼻部症状和体征的变化 .采用组织学和免疫组织化学方法观察鼻腔粘膜形态学改变以及对VIP物质表达的影响 .结果 :①致敏组动物鼻分泌量明显增多 .组织学结果显示 :致敏组鼻腔粘膜水肿、腺体增生、嗜酸性粒细胞增多 .免疫组织化学结果显示 :致敏组腺体周围VIP纤维密集 ,呈束状 .②致敏后BTX A用药组 ,鼻分泌量明显减少 ,致敏后BTX A用药组与致敏组相比鼻分泌量差异有显著性(P 0 .0 5 ) ,但鼻痒及喷嚏症状无明显改变 .组织学结果示 :鼻粘膜上皮完整 ,腺体明显减少 ,腺管萎缩 .免疫组织化学结果示 :致敏组动物致敏后BTX A用药组腺体周围VIP纤维减少 ,未见束状VIP纤维 .结论 :BTX A能缓解变应性鼻炎流涕 ,VIP纤维密度和数量免疫阳性反应减少 ,能治疗变应性鼻炎的鼻溢症状 .

济川煎及其拆方对STC模型大鼠血清SP VIP水平的影响

目的:观察济川煎对慢传输型便秘模型大鼠血清SP、VIP水平的影响,探讨该方温肾润肠的作用机制及其组方配伍规律。方法:复制大鼠慢传输型便秘模型,检测济川煎及其拆方对模型大鼠粪便干、湿重和血清SP、VIP水平的影响。结果:与模型组相比,温肾润肠组粪便干湿比显著升高(P<0.01),其余各药物治疗组粪便干湿比显著降低(P<0.01)。济川煎及拆方各组血清SP升高,而VIP水平均显著低于模型对照组(P<0.01)。结论:济川煎及拆方各组可改善STC模型动物粪便性状,其作用机理与血清SP水平升高,以及异常升高的VIP的降低有关。