| Objective: Psoriasis is one of the most common chronic inflammatory proliferative skin disease with its characteristic manifests as erythema of different sizes,covered with thin white mica-like scales.At present,the specific mechanism of the pathogenesis of psoriasis is not yet clear,and there is no cure method.Finding new psoriasis therapeutic drugs is very important for the treatment of psoriasis.Curcumin is extracted from the plant turmeric,which is the most important part of turmeric.Extensive research over the past few decades has shown that curcumin is a highly pleiotropic molecule with anti-inflammatory,antioxidant,Anti-inflammatory and anti-oxidation.Because of the potential economic prospect of curcumin,various disciplines have been focused on the study of curcumin and its use.And a lot of studies have found that curcumin can significantly reduce the PASI value of psoriasis patients without any side effect.Therefore,in this study,the model of mouse psoriasis induced by imiquimod was further investigated on the basis of the mechanism of curcumin in the treatment of psoriasis,thus providing a theoretical basis for the treatment of psoriasis by curcumin.Methods: 1.Modeling:45 mice were randomly and equally divided into three groups.There are 15 mice in each group.The three group are called blank control group,model control group and experimental group.The three groups of mice were shaved in the same part of the back,with an area of about 2 cm x 3 cm.In the experiment,the mice in the model group were treated with double distilled water daily,and imiquimod cream was applied to the exposed skin of the mice's back to construct a psoriasis-like mouse model for 6 consecutive days.The mice in the experimental group were given intragastric administration of curcumin daily,and the same amount of imiquimod cream was applied on the same part of the back for 6 consecutive days.The mice in the control group were given an equal amount of white petrolatum on the exposed skin of the back.At the sametime,they were given daily double-distilled water for 6 days.At the end of modeling,changes in the appearance of the back skin of mice were recorded.2.The mice were sacrificed by dislocation.The skin of the mouse's back was removed and histopathological examination was performed to observe the pathological changes of the mouse skin lesions.RT-PCR was used to detect the m RNA expression of NLRP3 and ASC in the lesions.Immunohistochemistry were used to detect the expression and distribution of NLRP3 in lesions.Results: 1.After 6 days' continuous use of Imiquimod cream,it is observed that there was thick,scaly,well-defined plaque on the back of model control group mice,while the back of experimental group is slightly roughened and thickened.The skin of control group was as smooth as before.2.HE staining results showed that epidermal hyperkeratosis with hypokeratosis,spinous hypertrophy,epidermode extension,visible dermis superficial dilatation of small blood vessels could be observed in the model group.The experimental group showed acanthosis,but the degree was significantly lower than that of the model group.There was no obvious abnormality in the control group.RT-PCR results showed that the expression levels of NLRP3 and ASC in the model group were significantly higher than those in the control group.There was a statistically significant difference between the two groups(P<0.05).Compared with the mice in the model group,RT-PCR results showed that the expression levels of NLRP3 and ASC in the skin lesions of the experimental group were significantly reduced.There was a statistically significant difference between the two groups(P<0.05).Compared with the mice in the control group,RT-PCR results showed that the expression of NLRP3 and ASC in the skin lesions of the experimental group increased.There was a statistically significant difference between the two groups(P<0.05).The results of immunohistochemistry showed that NLRP3 was highly expressed in epidermal keratinocytes in the mouse skin of the model group,with yellow or brown particles visible.Compared with the mice in the model group,the expression level of NLRP3 in the skin lesions of the experimental group was significantly decreased.There was a statistically significant difference between the twogroups(P<0.05).Compared with the control group,the expression level of NLRP3 was significantly higher in the model group.There was a statistically significant difference between the two groups(P<0.05).Moreover,compared with the control group,the expression level of NLRP3 in the skin lesions of the experimental group was significantly higher,and there was a statistically significant difference between the two groups(P< 0.05).Conclusion: 1.NLRP3 inflammasome may be an important link in the pathogenesis of psoriasis.2.Curcumin may reduce the psoriasis condition by inhibiting the activity of NLRP3 inflammasome and achieve therapeutic effect. |
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