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Curative effect of BCG-polysaccharide nuceic acid on atopic dermatitis in mice

机译:卡介苗多糖核酸对小鼠特应性皮炎的治疗作用

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摘要

Objective:To explore the effect of bacilli Galmette-Gurin (BCG)-polysaccharide nuceic acid on atopic dermatitis in mice and its mechanism. Methods: Forty NC/Nga mice were selected and randomly divided into Group A (model group), Group B (dexamethasone treatment group), Group C (BCG polysaccharide nucleic acid treatment group) and Group D (control group) with 10 mice in each group. Atopic dermatitis model were constructed by applying 2, 4-dinitrochlorobenzene on the skin of the mice. Mice in Group D were treated with acetone solution (100μL) on the foot pad and abdomen after hair removal at the age of 7 weeks, then on ear skin at the age of 8-13 weeks. For mice in A, B and C groups, 100μL of acetone solution containing 2, 4-dinitrochlorobenzene was applied to the foot pad and the abdomen at the age of 7 weeks, then on ear skins at the age of 8 to 13 weeks. At the age of 7-13 weeks, mice in Group A and Group D were treated with 100μL saline (i.p.);mice were given dexamethasone (0.1 mL/kg, i.p.) every other day for 7 weeks in Group B;mice were treated with BCG polysaccharide nucleic acid (0.5 mg/kg, i.p.) every other day for 7 weeks in Group C. The ear thickness was measured every week and the scratching frequency was recorded 1 times for 10 min a week. The mice were sacrificed after the last administration of drugs. IgE, IL-4, IL-10, IL-12 and IFN-γin the plasma were detected using ELISA, and RT-PCR method was employed to detect the concentrations of IL-4, IL-10, IL-12 and IFN-γproteins. After HE staining, the lesion degree of inflammation in ear tissue was observed microscopically. Results:The ear thickness and scratching frequency of Group A were significantly higher than those in group B, C and D (P<0.05), and there was no significant difference between Group B and C (P>0.05);the concentrations of IgE, IL-4 and IL-10 in the plasma and the expression of IL-4, IL-10 mRNA in the spleen tissues of Group A, B and C were all significantly higher than those of Group D (P<0.05);the concentrations of plasma IL-12 and IFN-γ, and spleen protein expression of IL-12 and IFN-γin Group C mice were significantly higher than those of Group A (P<0.05). Histological observation showed obvious ear tissue exudation, erythema, swelling, desquamation of skin, and scabbing in Group A. Histopathology of the skin lesion also showed hyperkeratosis, focal-parakeratosis, stratum spinosum hypertrophy, mild sponge-like edema, a large number of lymphocytes along with plasma cell infiltration in dermis, angiectasis and hyperemia in Group A, while degree of ear skin lesion in Group B and D mice was significantly lighter than that of Group A. Conclusions:BCG polysaccharide nucleic acid can significantly reduce the serum IgE concentrations, increase the expression of IL-12, IFN-γprotein, correct the imbalance of Thl/Th2 in atopic dermatitis mice, and has obvious inhibitory effect on atopic dermatitis in NC/Nga mice.
机译:目的:探讨细菌性加尔米特-古林杆菌多糖多糖对小鼠特应性皮炎的作用及其机制。方法:选择NC / Nga小鼠40只,随机分为A组(模型组),B组(地塞米松治疗组),C组(BCG多糖核酸治疗组)和D组(对照组),每组10只组。通过在小鼠皮肤上施用2,4-二硝基氯苯来构建特应性皮炎模型。 D组的小鼠在脱毛后的7周龄时在足垫和腹部用丙酮溶液(100μL)处理,然后在8-13周龄时在耳朵皮肤上用丙酮溶液处理。对于A,B和C组的小鼠,在7周龄时将100μL含2,4-二硝基氯苯的丙酮溶液施于脚垫和腹部,然后在8至13周龄时施用于耳朵皮肤。在7-13周龄时,A组和D组的小鼠接受100μL盐水(ip)治疗; B组每隔一天对小鼠给予地塞米松(0.1 mL / kg,ip)治疗,B组持续7周;对小鼠进行治疗在C组中,每隔一天用BCG多糖核酸(0.5 mg / kg,腹腔注射)治疗7周。每周测量一次耳厚度,并记录抓痒频率,每周10分钟1次。最后一次给药后将小鼠处死。 ELISA法检测血浆中IgE,IL-4,IL-10,IL-12和IFN-γ,采用RT-PCR法检测血浆中IL-4,IL-10,IL-12和IFN-γ的浓度。 γ蛋白。 HE染色后,在显微镜下观察耳朵组织中炎症的损害程度。结果:A组的耳朵厚度和抓挠频率明显高于B,C和D组(P <0.05),B和C组之间的差异无统计学意义(P> 0.05); IgE的浓度血浆中IL-4,IL-10,A,B,C组脾脏组织中IL-4,IL-10 mRNA的表达均明显高于D组(P <0.05); C组小鼠血浆IL-12和IFN-γ的浓度,IL-12和IFN-γ的脾蛋白表达均明显高于A组(P <0.05)。组织学观察显示,A组有明显的耳部组织渗出,红斑,肿胀,皮肤脱屑和擦伤。皮肤病变的组织病理学还显示出角化过度,局灶性角化不全,棘状棘层肥大,轻度海绵样水肿,大量淋巴细胞A组的真皮细胞,血管扩张和充血伴随浆细胞浸润,而B组和D组小鼠的耳部皮肤病变程度明显轻于A组。结论:BCG多糖核酸可显着降低血清IgE浓度,增加特应性皮炎小鼠中IL-12,IFN-γ蛋白的表达,纠正Th1 / Th2失衡,对NC / Nga小鼠特应性皮炎有明显的抑制作用。

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  • 来源
    《亚太热带医药杂志(英文版)》 |2014年第011期|913-917|共5页
  • 作者单位

    Dermatology Department, Children’s Hospital of Fudan University, Shanghai-200032, China;

    Dermatology Department, Children’s Hospital of Fudan University, Shanghai-200032, China;

    Traditional Chinese Medicine Department, Children’s Hospital of Fudan University, Shanghai-200032, China;

    Dermatology Department, First Affiliated Hospital of University of South China, Hengyang-421001, Hunan, China;

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