【摘要】：目的探討5種治療銀屑病的常用藥物對咪喹莫特誘導(dǎo)的銀屑病樣模型皮損形成的影響。方法 Balb/c雄性小鼠,隨機(jī)分為正常對照組、模型組、阿維A組、地塞米松組、甲氨蝶呤組、雷公藤多苷組、環(huán)孢素組。采用銀屑病皮損面積和疾病嚴(yán)重程度(PASI)評分標(biāo)準(zhǔn)觀察銀屑病樣小鼠模型皮損變化情況。光鏡下觀察皮損組織形態(tài)學(xué)變化、測量表皮層厚度;免疫組織化學(xué)法檢測增殖細(xì)胞核抗原(PCNA)反映表皮角質(zhì)形成細(xì)胞增殖程度;檢測皮損中CD3反映T淋巴細(xì)胞浸潤程度。結(jié)果阿維A組、地塞米松組、甲氨蝶呤組、雷公藤多苷組小鼠皮損與同期模型組相比,皮損癥狀明顯改善,各項(xiàng)指標(biāo)PASI評分都低于同期模型組小鼠。環(huán)孢素對該模型皮損的形成呈現(xiàn)一個(gè)先抑制后促進(jìn)的作用。環(huán)孢素組PASI積分高峰出現(xiàn)的時(shí)間比模型組晚2～3d。HE染色顯示:與模型組小鼠比較,阿維A組、地塞米松組、甲氨蝶呤組、雷公藤多苷組小鼠皮膚表皮層較平整,角化不全的細(xì)胞明顯減少,表皮層厚度明顯低于模型組。而環(huán)孢素組與模型組小鼠皮損組織學(xué)表現(xiàn)相似,表皮層厚度與模型組相比差異無統(tǒng)計(jì)學(xué)意義(P0.05)。免疫組織化學(xué)染色顯示:阿維A組、地塞米松組、甲氨蝶呤組、雷公藤多苷組皮損組織中PCNA及CD3表達(dá)均顯著低于模型組,差異有統(tǒng)計(jì)學(xué)意義(P0.01或0.05)。環(huán)孢素組與模型組相比差異無統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論臨床治療銀屑病藥物阿維A、地塞米松、甲氨蝶呤、雷公藤多苷可有效干預(yù)咪喹莫特誘導(dǎo)的小鼠銀屑病樣皮損的形成,以上藥物對銀屑病樣皮損的表皮細(xì)胞增殖及T淋巴細(xì)胞浸潤均有抑制作用,因此該模型可作為進(jìn)行研究銀屑病藥物研究的藥理模型。但環(huán)孢素A對由咪喹莫特誘導(dǎo)的銀屑病樣小鼠模型的反應(yīng)不敏感。
[Abstract]:Objective to investigate the effects of five common drugs for psoriasis on the formation of psoriasis-like model induced by Imiquimod. Methods Balb/c male mice were randomly divided into normal control group, model group, avea group, dexamethasone group, methotrexate group, tripterygium wilfordii polyglycoside group and cyclosporine group. The area of psoriatic lesions and the severity of psoriasis were measured by (PASI) score. Histomorphologic changes were observed under light microscope and the thickness of epidermis was measured. Proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry to reflect the degree of proliferation of epidermal keratinocytes and CD3 was detected to reflect the degree of infiltration of T lymphocytes in skin lesions. Results the skin lesions of Avera group, dexamethasone group, methotrexate group and Tripterygium wilfordii polyglycoside group were significantly improved compared with the model group, and the PASI scores of each indexes were lower than those of the model group. Cyclosporine showed a first inhibition and then a promotion effect on the formation of skin lesions in the model. The peak time of PASI score in cyclosporine group was longer than that in model group. Compared with model group, the skin epidermis of Avera group, dexamethasone group, methotrexate group and tripterygium wilfordii polyglycoside group was more smooth than that of model group. The cells with hypokeratosis decreased significantly, and the thickness of epidermis was significantly lower than that of the model group. However, the skin lesions in the cyclosporine group and the model group were similar, and the thickness of the epidermis was not significantly different from that in the model group (P0.05). Immunohistochemical staining showed that the expressions of PCNA and CD3 in the lesions of Avera group, dexamethasone group, methotrexate group and tripterygium wilfordii group were significantly lower than those in the model group (P0.01 or 0.05). There was no significant difference between the cyclosporine group and the model group (P0.05). Conclusion Avera, dexamethasone, methotrexate, tripterygium wilfordii polyglycosides can effectively interfere with the formation of psoriatic lesions induced by Imiquimod in mice. The above drugs can inhibit the proliferation of epidermal cells and the infiltration of T lymphocytes in psoriatic lesions, so this model can be used as a pharmacological model for the study of psoriasis drugs. But cyclosporine A was insensitive to the model of psoriasis induced by Imiquimod.
【作者單位】： 北京市中醫(yī)研究所;
【基金】：國家自然科學(xué)基金資助項(xiàng)目(No.81072810)
【分類號(hào)】：R758.63

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本文編號(hào)：2319021