【摘要】：目的觀察涼血解毒方對咪喹莫特(imiquimod,IMQ)誘導(dǎo)的銀屑病樣小鼠模型中活化的樹突狀細(xì)胞(dendritic cells,DCs)的干預(yù)作用。方法將小鼠采用數(shù)字表法隨機(jī)分為正常對照組,模型組,涼血解毒方高(Liangxue Jiedu groups with high,LXJD-H)、中(medium,LXJD-M)、低(low,LXJD-L)劑量組和甲氨蝶呤(methotrexate,MTX)組,觀察小鼠背部皮損變化。采用銀屑病皮損面積和疾病嚴(yán)重程度評分(psoriasis area and severity index,PASI)標(biāo)準(zhǔn)進(jìn)行評分,光鏡下觀察皮膚組織形態(tài)學(xué)變化,測量表皮厚度;免疫熒光及組織化學(xué)法檢測皮損中Ki67、CD3、CD11c的表達(dá)情況;流式細(xì)胞術(shù)檢測脾臟中DCs數(shù)量;酶聯(lián)免疫法(enzyme linked immunosorbent assay,ELISA)檢測細(xì)胞上清液中細(xì)胞因子的量;采用RT-PCR法檢測皮損組織中DCs相關(guān)受體基因水平;Western blotting法檢測小鼠皮損中TLR7/TLR8通路相關(guān)蛋白表達(dá)。結(jié)果涼血解毒方明顯降低皮損PASI評分及表皮厚度、減少炎性反應(yīng)細(xì)胞的浸潤;抑制皮損中TLR7通路相關(guān)蛋白的表達(dá);體內(nèi)外降低白細(xì)胞介素-23(interleukin-23,IL-23)、Toll樣受體(Toll-like receptors,TLR7)、TLR8及IL~(-1)2p40 mRNA表達(dá)及下調(diào)IL-23、IL~(-1)β細(xì)胞因子分泌水平。結(jié)論涼血解毒方可以改善IMQ誘導(dǎo)的銀屑病樣小鼠皮損,且可以改善皮損中T淋巴細(xì)胞及DCs的浸潤,同時(shí)抑制DCs的活化。
[Abstract]:Aim to observe the intervention effect of Liangxue jiedu recipe on activated dendritic cells (dendritic cells,DCs) induced by imiquimod (imiquimod,IMQ) in silver chip-like mice. Methods the mice were randomly divided into normal control group, model group, high (Liangxue Jiedu groups with high,LXJD-H group, middle dose group (medium,LXJD-M), low dose group (low,LXJD-L) and methotrexate (methotrexate,MTX) group. The changes of the skin lesions in the back of mice were observed. The psoriasis lesion area and disease severity score (psoriasis area and severity index,PASI) was used to evaluate the histological changes of the skin and the thickness of the skin under light microscope. Immunofluorescence and histochemistry were used to detect the expression of Ki67,CD3,CD11c, flow cytometry was used to detect the number of DCs in spleen, enzyme-linked immunosorbent assay (enzyme linked immunosorbent assay,ELISA) was used to detect the amount of cytokines in the supernatant. RT-PCR method was used to detect the level of DCs-associated receptor gene in the lesions.; Western blotting method was used to detect the expression of TLR7/TLR8 pathway-related proteins in the lesions of mice. Results Liangxuejiedu recipe significantly decreased the PASI score and epidermal thickness, decreased the infiltration of inflammatory response cells, and inhibited the expression of TLR7 pathway-related proteins in the lesions. It decreased the expression of interleukin-23,IL-23), Toll-like receptor (Toll-like receptors,TLR7), TLR8 and IL~ (- 1) 2p40 mRNA and down-regulated the secretion of IL-23,IL~ (- 1) 尾 cytokines in vitro and in vivo. Conclusion Liangxuejiedu recipe can improve the IMQ-induced lesions of psoriasis-like mice, improve the infiltration of T lymphocytes and DCs in the lesions, and inhibit the activation of DCs at the same time.
【作者單位】： 首都醫(yī)科大學(xué)附屬北京中醫(yī)醫(yī)院;銀屑病中醫(yī)臨床基礎(chǔ)研究北京市重點(diǎn)實(shí)驗(yàn)室北京市中醫(yī)研究所;北京中醫(yī)藥大學(xué);
【基金】：國家自然科學(xué)基金青年科學(xué)基金(81403410) 北京市科技計(jì)劃課題“十病十藥”研發(fā)(Z141100002214015)~~
【分類號】：R285.5;R-332

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