目的 考察白頭翁皂苷B₄對咪喹莫特誘導(dǎo)的銀屑病模型小鼠的炎癥及免疫相關(guān)指標(biāo)的影響，探討其對小鼠銀屑病的治療作用及其機(jī)制。方法 將56只BALB/c小鼠隨機(jī)分成對照組，模型組，阿維A膠囊組（6 mg/kg），白頭翁皂苷B₄低、中、高劑量（5、10、20 mg/kg）組，白頭翁皂苷B₄乳膏組（20 mg/kg），每組各8只。通過局部涂抹5%咪喹莫特乳膏誘導(dǎo)小鼠銀屑病模型，各組小鼠口服或涂抹相應(yīng)藥物，14 d后通過銀屑病皮損面積及嚴(yán)重程度評分（PASI）評價小鼠皮損程度；HE染色觀察皮膚組織病理學(xué)形態(tài)；血常規(guī)檢測血液中免疫細(xì)胞的變化；酶聯(lián)免疫吸附試劑（ELISA）檢測小鼠皮膚中白細(xì)胞介素（IL）-6、IL-12、IL-17、IL-1β的水平。結(jié)果 與模型組相比，阿維A膠囊組，白頭翁皂苷B₄ 5、10、20 mg/kg組，白頭翁皂苷B₄乳膏組小鼠皮損組織棘層厚度減小，真皮層炎癥細(xì)胞浸潤減少，PASI評分、血液中的免疫細(xì)胞及皮膚組織中IL-6、IL-12、IL-17、IL-1β的表達(dá)水平均顯著降低。結(jié)論 白頭翁皂苷B₄對5%咪喹莫特誘導(dǎo)小鼠銀屑病皮損具有明顯的治療作用，其機(jī)制可能是通過抑制IL-6、IL-12、IL-17、IL-1β等細(xì)胞因子表達(dá)發(fā)揮治療作用。

Objective To investigate the effects of anemoside B₄ on inflammation and immune-related indexes in imiquimote-induced mouse psoriasis model mice, and to explore its therapeutic effect and mechanism. Methods A total of 56 BALB/c mice were randomly divided into control group, model group, Avirin Capsule group (6 mg/kg), anemoside B₄ low-dose, medium-dose and high-dose groups (5, 10, 20 mg/kg), Anemoside B₄ Cream group (20 mg/kg), with 8 mice in each group. The psoriasis model of mice was induced by topical application of 5% imiquimod cream, and the psoriasis degree of mice was evaluated by psoriasis area and severity score (PASI) 14 days later. The histopathological morphology of skin was observed by HE staining. Blood routine tests to detect changes in immune cells in the blood. The levels of IL-6, IL-12, IL-17, and IL-1β in mice skin were determined by enzyme-linked immunosorbent assay (ELISA). Results Compared with model group, the thickness of spinous layer of skin lesion tissue of mice in avitra capsule group, anemoside B₄ 5, 10, 20 mg/kg groups and Anemoside B₄ Cream group decreased, and inflammatory cell infiltration in dermis decreased. PASI score, the expression levels of IL-6, IL-12, IL-17, and IL-1β in blood immune cells and skin tissue were significantly decreased. Conclusion Anemoside B4 has obvious therapeutic effect on 5% imiquimod-induced psoriasis in mice, and its therapeutic mechanisms may be through by inhibiting the expression of cytokines such as IL-6, IL-12, IL-17, IL-1β and other cytokines.

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廣西創(chuàng)新驅(qū)動發(fā)展項目（桂科AA19254024）；廣西科技計劃項目（桂科AB20025002）