芩珠凉血合剂抗炎止痒作用的实验研究

目的研究中药芩珠凉血合剂对湿疹动物模型抗炎、止痒作用机制。方法①观察二甲苯引起小鼠耳廓肿胀，计算肿胀度、肿胀抑制率、病理变化，及芩珠凉血合剂抗炎作用。②观察磷酸组胺引起豚鼠背部创面瘙痒反应，计算豚鼠回头舔创面时磷酸组胺的总量，与芩珠凉血合剂止痒作用。结果发现芩珠凉血合剂具有抗炎作用；并能够提高磷酸组胺致痒阈。结论中药芩珠凉血合剂通过对抗炎症反应、提高磷酸组胺致痒阈影响，从而发挥对变态反应性疾病治疗作用。     

昆明山海棠霜抗炎止痒作用及皮肤毒性的实验研究

目的为了探讨昆明山海棠外用的药效及安全性,对昆明山海棠霜进行了止痒、抗炎作用及皮肤毒性的实验研究。方法二甲苯致小鼠耳廓肿胀法,磷酸组织胺致痒法,皮肤急毒、刺激及过敏等实验方法。结果昆明山海棠霜外用能明显提高豚鼠致痒阈,对二甲苯致小鼠耳廓肿胀无明显抑制作用,昆明山海棠霜外用未发现急性毒性及皮肤过敏反应。浓度较高时对家兔破损皮肤及完整皮肤有轻度刺激性,停药后皮肤刺激性反应可完全消退。结论昆明山海棠霜外用具有止痒作用且比较安全。     

甘草酸软膏治疗豚鼠慢性湿疹模型的实验研究

目的 观察甘草酸软膏抗炎、止痒和对豚鼠慢性湿疹的治疗作用。方法 雄性昆明种小鼠、雌雄昆明种小鼠、白色豚鼠各60只,分别随机分为模型对照组（10只）、基质对照组（10只）、醋酸地塞米松乳膏组（10只）、甘草酸软膏高（10只）、中（10只）、低（10只）剂量组,各组分别建立二甲苯致小鼠耳廓肿胀模型,右旋糖酐40致小鼠搔抓模型,以及2,4-硝基氯苯反复刺激的慢性湿疹豚鼠模型,分别观察甘草酸软膏对小鼠耳廓肿胀和搔抓反应以及慢性湿疹豚鼠耳廓肿胀的影响。结果 甘草酸软膏高、中剂量可以抑制二甲苯致小鼠耳廓肿胀（P < 0.05或0.01）;甘草酸软膏高剂量可以延长右旋糖酐致小鼠搔抓的潜伏期,甘草酸软膏高、中、低剂量可减少搔抓次数（P < 0.05或0.01）,减轻慢性湿疹豚鼠模型耳廓的肿胀（P < 0.05或0.01）,并对耳廓皮肤的病理改变有一定的改善作用。结论 甘草酸软膏对慢性湿疹豚鼠模型有一定的治疗作用。     

甘草酸软膏治疗豚鼠慢性湿疹模型的实验研究北大核心CSCD

目的观察甘草酸软膏抗炎、止痒和对豚鼠慢性湿疹的治疗作用。方法雄性昆明种小鼠、雌雄昆明种小鼠、白色豚鼠各60只,分别随机分为模型对照组（10只）、基质对照组（10只）、醋酸地塞米松乳膏组（10只）、甘草酸软膏高（10只）、中（10只）、低（10只）剂量组,各组分别建立二甲苯致小鼠耳廓肿胀模型,右旋糖酐40致小鼠搔抓模型,以及2,4-硝基氯苯反复刺激的慢性湿疹豚鼠模型,分别观察甘草酸软膏对小鼠耳廓肿胀和搔抓反应以及慢性湿疹豚鼠耳廓肿胀的影响。结果甘草酸软膏高、中剂量可以抑制二甲苯致小鼠耳廓肿胀（P〈0．05或o．01）;甘草酸软膏高剂量可以延长右旋糖酐致小鼠搔抓的潜伏期,甘草酸软膏高、中、低剂量可减少搔抓次数（P〈0．05或0．01）,减轻慢性湿疹豚鼠模型耳廓的肿胀（P〈0．05或0．01）,并对耳廓皮肤的病理改变有一定的改善作用。结论甘草酸软膏对慢性湿疹豚鼠模型有一定的治疗作用。     

除湿止痒软膏抗炎及止痒作用研究

目的 探讨除湿止痒软膏的抗炎及止痒作用。 方法 用2,4-二硝基氟苯（DNFB）腹部致敏和背部反复激发建立BALB/c小鼠特应性皮炎模型。实验动物分为正常对照组（未致敏也未治疗）、模型对照组（致敏但未治疗）、氢化可的松乳膏组（致敏 + 氢化可的松）、除湿止痒软膏组（致敏 + 除湿止痒软膏）。连续用药14 d,末次给药12 h后取背部皮肤,测定皮肤厚度及质量,进行HE染色和甲苯胺蓝染色,ELISA法检测皮损组织中干扰素（IFN）γ、肿瘤坏死因子（TNF）α、白细胞介素（IL）-4、IL-5含量。利用磷酸组胺诱发Hartley豚鼠局部皮肤瘙痒模型,观察除湿止痒软膏对豚鼠致痒阈的影响。 结果 用药后第15天,与模型对照组相比,氢化可的松乳膏和除湿止痒软膏均可明显减少小鼠的背部皮肤厚度和质量（P < 0.01）,减少淋巴细胞和肥大细胞浸润（P < 0.01）以及降低皮损组织中IFN-γ、TNF-α、IL-4及IL-5水平（P < 0.05或P < 0.01）。与正常对照组相比,氢化可的松乳膏组小鼠背部皮肤厚度和质量减小（P < 0.01）,除湿止痒软膏组无明显变化。此外,除湿止痒软膏也可显著提高豚鼠耐受磷酸组胺的致痒阈（P < 0.01）。 结论 除湿止痒软膏可明显抑制DNFB引起的小鼠特应性皮炎,其抗炎机制可能与恢复体内Th1/Th2型细胞因子平衡有关。除湿止痒软膏可明显减轻磷酸组胺所致豚鼠皮肤瘙痒反应。     

金花舒肤胶囊的主要药效学研究

为研究金花舒肤胶囊主要药效学，将Wister大鼠100只，雌雄各半，随机分成5组，分别给予金花舒肤胶囊高、中、低剂量、湿毒清胶囊、生理盐水灌胃给药，1次／d，连续5d。分别观察其透明质酸酶致大鼠足跖肿胀、大鼠毛细血管通透性、豚鼠磷酸组胺致痒阈、小鼠免疫功能的影响及体外抑菌作用。结果：金花舒肤胶囊可使透明质酸酶所致大鼠足跖肿胀度显著减轻（P〈0．01）；显著抑制组胺所致大鼠毛细血管通透性（P〈0．01）；显著提高磷酸组胺对豚鼠的致痒阈（P〈0．01）；对金黄色葡萄球菌等细菌具有显著的抑制作用；促使大鼠胸腺和脾脏萎缩（P〈0．05）；抑制单核巨噬细胞系统对血清中异物的吞噬功能；金花舒肤胶囊对急、慢性炎症有显著抑制作用，可显著抑制瘙痒，抑制机体的免疫功能。证明该制剂可以用于治疗湿疹。     

联苯苄唑乳膏体内外抗真菌活性及体内抗炎作用研究

目的 探讨1%联苯苄唑乳膏体内外抗真菌活性及体内抗炎作用。方法 采用豚鼠癣病模型、真菌体外药敏试验及小鼠二甲苯耳廓肿胀法评价1%联苯苄唑乳膏体内外抗真菌活性及体内抗炎作用。结果 1%联苯苄唑乳膏能有效治愈豚鼠须毛癣菌感染；体外抗皮肤癣菌和念珠菌最小抑菌浓度范围为 0.016 ～ 0.5 mg/L，最小杀菌浓度范围为0.063 ～ 2.0 mg/L；该药能显著抑制二甲苯所致的小鼠耳廓肿胀。结论 1%联苯苄唑乳膏具有明显抗皮肤癣菌、抗念珠菌和抗炎作用。     

复方苦参止痒霜治疗湿疹的实验研究

目的研究复方苦参止痒霜治疗亚急性、慢性湿疹的作用机制.方法①观察复方苦参止痒霜对二甲苯致小鼠耳廓肿胀的影响;②观察复方苦参止痒霜对4-氨基吡啶(4-AP)1 mg/kg颈背部皮下注射诱发小鼠舔体反应是否有抑制作用;③采用二硝基氯苯(DNCB)将豚鼠先致敏后多次激发,建立右耳部亚急性接触性湿疹模型,随后观察复方苦参止痒霜与其中药提取液对实验模型是否有实验治疗作用.结果复方苦参止痒霜与其中药提取液对二甲苯致小鼠耳廓肿胀急性炎症没有明显的抑制作用;对4-AP所致小鼠皮肤瘙痒有显著的抑制作用;中药提取液组豚鼠的接触性湿疹较基质组明显好转,与丁酸氢化可的松组相近似.结论复方苦参止痒霜具有抗迟发型变态反应、止痒作用.     

舒利通颗粒治疗慢性前列腺炎／盆腔疼痛综合征的临床与实验研究

目的:研究舒利通颗粒治疗阴虚湿热夹瘀型慢性前列腺炎的临床疗效,并探讨其机制。方法:用舒利通颗粒治疗80例阴虚湿热夹瘀型慢性前列腺炎3个月,观察临床疗效及治疗前后患者慢性前列腺炎症状评分(NIH-CPSI)变化情况。动物实验研究采用二甲苯、醋酸等致炎剂,观察舒利通颗粒对由此产生的小鼠耳廓肿胀及扭体的镇痛作用、大鼠棉球肉芽肿形成的影响。结果:舒利通颗粒治疗80例阴虚湿热夹瘀型慢性前列腺炎,痊愈14例,显效52例,有效9例,总有效率93·8%。治疗后患者NIH-CPSI评分明显低于治疗前(P<0·01)。实验研究:舒利通颗粒对小鼠醋酸扭体反应次数有显著性降低(P<0·01);舒利通颗粒对二甲苯的致炎作用有显著性减轻(P<0·05);舒利通颗粒对大鼠棉球肉芽肿形成有显著的抑制作用(P<0·01)。结论:舒利通颗粒对阴虚湿热夹瘀型慢性前列腺炎有较好的治疗效果。     

不同中医治法对豚鼠亚急性-慢性湿疹模型疗效实验研究

目的观察6种中医治法对豚鼠亚急性-慢性湿疹的疗效,探讨其可能的作用机制,为临床中医治疗湿疹提供可靠的理论依据。方法采用2,4-二硝基氯苯(2,4-dinitro-1-chlorobenzene,DNCB)诱导豚鼠耳廓亚急性-慢性湿疹模型,以祛风止痒-清热燥湿解毒法(A)、清热解毒法(B)、祛风止痒法(C)、清热燥湿法(D)、清热燥湿解毒法(E)、收敛解毒法(F)6种治法的中药制剂皮肤给药2次/d,连续2周,并与生理盐水(normal saline,NS)组对照。结果与NS组比A组减轻豚鼠耳廓肿胀最为明显,C组最低;A组脾脏系数和胸腺系数与NS组相比有明显降低(P0.05);各组组织切片真皮炎性细胞计数,与NS组相比均降低(P0.05),其中以E组最低,A组其次。结论祛风止痒、清热燥湿解毒法(A)能明显减轻豚鼠湿疹模型耳廓炎症肿胀、减少真皮炎细胞浸润、降低免疫器官比重系数,该治法可作为临床治疗亚急性-慢性湿疹的基本治法;其机制可能与抗迟发型变态反应、抗炎、免疫调节等作用有关。     

Superoxide production by eosinophils: activation by histamine

Both guinea pig peritoneal exudate and human peripheral blood eosinophils produce large amounts of superoxide anion when stimulated by preopsonized zymosan or phorbol myristate acetate (PMA). Superoxide production is also activated by histamine but not the histamine metabolite, imidazole acetic acid. Supernatants from degranulated rat mast cells stimulate superoxide production. In studies of both human and guinea pig eosinophils, the H1-antagonist, chlorpheniramine (10-3 M and 10-4 M), preopsonized zymosan histamine) production of superoxide anion but the H2-antagonist, cimetidine, only modestly inhibited superoxide anion production (zymosan, PMA), These studies provide direct evidence for the influence of histamine on the oxidative metabolism of eosinophils. These results are consistent with the hypothesis that histamine interacts with eosinophils predominantly via an H1 receptor site. Furthermore, they suggest that eosinophils may participate in immediate hypersensitivity reactions by the release of superoxide anion in response to stimulation by histamine.     

Response of skin to ammonium persulphate.

In order to investigate the histamine liberating actions of ammonium persulphate, skin slices from three species (guinea pig, rat and monkey) were incubated in vitro with concentrations of ammonium persulphate ranging from 1 to 1000 microgram/ml. None of these concentrations released significant amounts of histamine in guinea pig or monkey skin. In the rat the highest concentration (1000 microgram/ml) released 20-24% of the histamine content of the skin, but the intensitivity of this response to cooling indicates a non-specific "toxic" action on mast cells. By contrast a known chemical histamine liberator, compound 48/80, released significant amounts of histamine from skin at much lower concentrations in all three species. Ammonium persulphate is clearly not a potent histamine liberator. Ammonium persulphate dermatitis is presumably a result of increased sensitivity of skin mast cells, due to immunological or other factors, in susceptible individuals.     

Pharmacological studies on nonimmunologic contact urticaria in guinea pigs

Summary In the present study we examined the effects of chlorpheniramine and ranitidine, indomethacin, BW755C (an inhibitor of cyclo-oxygenase and lipooxygenase enzymes of arachidonic acid metabolism), dexamethasone, and capsaicin on nonimmunologic contact urticaria (NICU) induced in the guinea pig ear by benzoic acid, cinnamic acid, cinnamic aldehyde, methyl nicotinate, diethyl fumarate, or dimethyl sulfoxide. The intensity of edema in the urticarial reaction was quantified by measuring the ear thickness. Antihistamines inhibited reactions to intradermal histamine but not to agents causing NICU. Indomethacin and dexamethasone inhibited reactions to cinnamic acid and cinnamic aldehyde but not to other NICU agents. BW 755C and capsaicin had no effect on reactions to any of the NICU agents. Mast cell degranulation during the reaction was not seen in histologic sections. Histamine and capsaicin-sensitive nerves did not seem to be essential for the development of NICU in the guinea pig ear. The details of the inhibitory effects of indomethacin and dexamethasone are not clear, but it seems probable that more than one mechanism is involved in NICU due to different agents.     

Induction of formaldehyde contact sensitivity: dose response relationship in the guinea pig maximization test

The sensitizing potential of aqueous formaldehyde was evaluated with the guinea pig maximization test (GPMT) in two laboratories (Copenhagen and Stockholm) using different guinea pig strains. Six intradermal (0.01%-3%), and 6 topical (0.5%-20%) concentrations were used for induction, and formaldehyde 1% and 0.1% was used for challenge. The incidence of contact sensitivity depended on the intradermal, but not on the topical induction dose. Statistical analyses showed a non-monotonous (non-linear) dose response relationship. The estimated maximal sensitization rate in Copenhagen was 80% after intradermal induction with 0.65% formaldehyde; in Stockholm it was 84% after induction with 0.34%. The data from the two laboratories could be described by parallel displaced dose response curves suggesting that the guinea pig strain used in Stockholm was significantly more susceptible to formaldehyde than the strain used in Copenhagen. The EC50 (formaldehyde concentration at which 50% of the guinea pigs were sensitized) at the 72 h scoring and a 1% challenge concentration, was 0.061% in Copenhagen and 0.024% in Stockholm.     

Species specificity of nonimmunologic contact urticaria: guinea pig, rat, and mouse

In order to find the most suitable animal species for studies on nonimmunologic contact urticaria (NICU), human NICU agents: 20% benzoic acid (BA), 10% sorbic acid (SA), 15% cinnamic acid (CA), 20% cinnamic aldehyde (CAL), 1.0% diethyl fumarate (DEF), 0.2% methyl nicotinate (MN), all in absolute ethyl alcohol, and 100% dimethyl sulfoxide (DMSO) were each applied to the earlobes of guinea pigs, rats, and mice. Guinea pig ear reacted with swelling to all agents tested. The mean maximal increase in thickness of the guinea pig ear, measured with a micrometer, was 114 +/- 46%. No response to BA, SA, CA, DEF, or MN was noted in the rat or mouse ear. However, DMSO and CAL caused significant ear swelling both in the mouse and the rat. Thus, the guinea pig ear is more sensitive to a variety of human NICU agents than is rat or mouse ear. The striking differences in species reactivity to NICU agents suggest the possibility that there are several mechanisms (mediators) involved in reactions to different substances. The guinea pig ear swelling test remains the best quantitative animal method available for screening human NICU agents.     

Microdialysis of histamine in the skin of patients with mastocytosis

Mastocytosis represents a group of disorders characterized by the proliferation and accumulation of mast cells in tissue. The aim of the present study was to examine whether the interstitial histamine concentration in the skin is increased in mastocytosis patients and whether it correlates with the number of mast cells, the amount of metabolite N-methyl-imidazole acetic acid in the urine and the tryptase in serum. In 7 mastocytosis patients on a standardized diet, the analysis of histamine was performed on microdialysates obtained from catheters positioned intracutaneously in involved and uninvolved skin. N-methyl-imidazole acetic acid in the urine was collected for 24 h. Biopsies for analyses of mast cells were taken from skin adjacent to the microdialysis catheters. The histamine concentrations were 42+/-14, 12+/-3 (P<0.05) and 8+/-2 nmol/l (mean+/-SEM, n=7) in skin eruptions, non-lesional skin and plasma respectively. Mean N-methyl-imidazole acetic acid in the urine (9.7+/-3.5 mmol/mol creatinine) and mean tryptase (124+/-54 microg/l) had increased in all patients. In the present study, no linear correlation was found between these parameters and interstitial histamine in lesional skin. This finding corresponds to the fact that the concentration of histamine metabolites and tryptase derives from the entire mast-cell population, while interstitial histamine in the dermis represents the local tissue concentration before metabolic transformation. The microdialysis of histamine in the skin of mastocytosis patients could be used as a tool to investigate the effects of dermal mast-cell histamine release in different kinds of treatment regimen.     

刺山柑软膏抗炎止痒作用评价

目的：评价刺山柑软膏的抗炎、止痒作用。方法：昆明小鼠50只,随机分为基质组（10只）、丙酸氯倍他索组（10只）、刺山柑软膏组（低、中剂量各10只）,通过对二甲苯致鼠耳肿胀和冰醋酸致小鼠腹腔毛细血管通透性增高的影响评价刺山柑软膏抗炎作用,通过对右旋糖酐致小鼠全身瘙痒的影响评价刺山柑软膏止痒作用。结果：刺山柑乳膏可抑制鼠耳肿胀和腹腔毛细血管通透性增高．减轻小鼠全身瘙痒,且呈剂量依赖性。结论：刺山柑软膏具有抗炎、止痒作用。     

Studies on photosensitivity caused by sulfa drugs. Part 6. Sensitization with p-hydroxylaminobenzene sulfonamide and histamine metabolism

Repeated cutaneous applications of p-hydroxylaminobenzene sulfonamide (PHABSA), which is a photo-oxidation product of sulfanilamide (SNAm), sensitizes the guinea pig. By challenge with the substance, a marked cutaneous inflammatory reaction and an elevation of histamine level in the lesions are observed, although a single application of PHABSA to the non-sensitized animals elicits neither a cutaneous reaction nor changes of histamine content. In addition, the cutaneous changes and elevation of histamine level induced by challenge in the sensitized animals are markedly suppressed by pretreatment with either histamine liberator or antihistaminic. Thus, it is presumed that PHABSA plays an important role in the photoallergic reaction caused by SNAm and that one of the mediators in this process is histamine.