Psoriasis is an autoregulated immune and inflammation-based skin disease affecting approximately 3-4% of the worldwide population. Pinitol, conservatively used in ayurvedic medicine, has been shown to disclose an antiinflammatory effect, hold back the T-helper cells, and postpone cardiovascular diseases. In the present study we aimed to reveal the effect of D-pinitol on imiquimod (IMQ)-induced psoriasis-like skin inflammation in a mouse model via the nuclear factor-κB (NF-κB) pathway genes. In the current study, we found that D-pinitol ameliorated the skin abrasion and abridged epithelial thickness, inflammation numbers, and collagen-occupied regions in IMQ-induced psoriasis-like mice. The same results (epithelial thickness, inflammation numbers, and collagen-occupied regions) we achieved in dorsal skin regions. In addition, D-pinitol modified the lipid profile and antioxidant enzyme levels, which means that the IMQ-induced group showed elevated malondialdehyde when compared to D-pinitol. Downregulated expression of glutathione, superoxide dismutase, and catalase in the IMQ-induced group was incomparable with D-pinitol, control, and standard group. Additionally, inflammatory and NF-kB pathway gene levels in the psoriatic mouse skin, which includes tumor necrosis factor-α, interleukin [IL]-6, IL-17A, IL-23,TRAF3, NIK, IKKα, and RelB, were dramatically increased or decreased by treatment with D-pinitol. Histological and morphometric studies disclose the efficiency of D-pinitol. Finally, we found that D-pinitol reserved the TRAF3, NIK, IKKα, and RelB in the psoriatic skin, signifying that it restrains the commencement of NF-κB signaling pathways. The present results suggest that D-pinitol could prove to have tremendous preventive potential against the treatment and prevention of inflammatory disease.

中文翻译：

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D-山梨醇通过NF-κB途径改善了小鼠模型中的咪喹莫特诱导的牛皮癣样皮肤炎症。

牛皮癣是一种可自动调节的基于免疫和炎症的皮肤病，约占全球人口的3-4％。松果糖醇，保守地用于阿育吠陀医学中，已显示出具有抗炎作用，抑制T辅助细胞并延缓心血管疾病。在本研究中，我们旨在通过核因子-κB（NF-κB）通路基因揭示D-松醇对咪喹莫特（IMQ）诱导的牛皮癣样皮肤炎症的作用。在当前的研究中，我们发现在IMQ诱导的牛皮癣样小鼠中，D-松醇改善了皮肤磨损和上皮厚度，炎症数以及胶原蛋白占据的区域。我们在背部皮肤区域获得了相同的结果（上皮厚度，炎症数目和胶原蛋白占据的区域）。此外，D-松糖醇修饰了脂质谱和抗氧化酶水平，这意味着与D-松糖醇相比，IMQ诱导组的丙二醛水平升高。IMQ诱导组中谷胱甘肽，超氧化物歧化酶和过氧化氢酶的表达下调与D-松醇，对照组和标准组无可比拟。此外，银屑病小鼠皮肤中的炎症和NF-kB途径基因水平显着升高，其中包括肿瘤坏死因子-α，白介素[IL] -6，IL-17A，IL-23，TRAF3，NIK，IKKα和RelB。 D-松醇治疗可增加或减少。组织学和形态计量学研究揭示了D-松醇的功效。最后，我们发现D-松醇在牛皮癣皮肤中保留了TRAF3，NIK，IKKα和RelB，这表明它抑制了NF-κB信号通路的启动。