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氨甲环酸可改善银屑病样皮肤炎症:来自体内和体外研究的证据。

Tranexamic acid improves psoriasis-like skin inflammation: Evidence from in vivo and in vitro studies.

机构信息

Department of Dermatology, China Medical University Hospital, Taichung 404327, Taiwan.

Institute of Nutrition, College of health Care, China Medical University, Taichung 406040, Taiwan.

出版信息

Biomed Pharmacother. 2023 Oct;166:115307. doi: 10.1016/j.biopha.2023.115307. Epub 2023 Aug 11.

Abstract

The chronic disease psoriasis is associated with severe inflammation and abnormal keratinocyte propagation in the skin. Tranexamic acid (TXA), a plasmin inhibitor, is used to cure serious bleeding. We investigated whether TXA ointment mitigated Imiquimod (IMQ)-induced psoriasis-like inflammation. Furthermore, this study investigated the effect of noncytotoxic concentrations of TXA on IL-17-induced human keratinocyte (HaCaT) cells to determine the status of proliferative psoriatic keratinocytes. We found that TXA reduced IMQ-induced psoriasis-like erythema, thickness, scaling, and cumulative scores (erythema plus thickness plus scaling) on the back skin of BALB/c mice. Additionally, TXA decreased ear thickness and suppressed hyperkeratosis, hyperplasia, and inflammation of the ear epidermis in IMQ-induced BALB/c mice. Furthermore, TXA inhibited IMQ-induced splenomegaly in BALB/c mouse models. In IL-17-induced HaCaT cells, TXA inhibited ROS production and IL-8 secretion. Interestingly, TXA suppressed the IL-17-induced NFκB signaling pathway via IKK-mediated IκB degradation. TXA inhibited IL-17-induced activation of the NLRP3 inflammasome through caspase-1 and IL1β expression. TXA inhibited IL-17-induced NLRP3 inflammasome activation by enhancing autophagy, as indicated by LC3-II accumulation, p62/SQSTM1 expression, ATG4B inhibition, and Beclin-1/Bcl-2 dysregulation. Notably, TXA suppressed IL-17-induced Nrf2-mediated keratin 17 expression. N-acetylcysteine pretreatment reversed the effects of TXA on NFκB, NLRP3 inflammasomes, and the Nrf2-mediated keratin 17 pathway in IL-17-induced HaCaT cells. Results further confirmed that in the ear skin of IMQ-induced mice, psoriasis biomarkers such as NLRP3, IL1β, Nrf2, and keratin 17 expression were downregulated by TXA treatment. TXA improves IMQ-induced psoriasis-like inflammation in vivo and psoriatic keratinocytes in vitro. Tranexamic acid is a promising future treatment for psoriasis.

摘要

慢性疾病银屑病与皮肤中的严重炎症和异常角质形成细胞增殖有关。氨甲环酸(TXA)是一种纤溶酶抑制剂,用于治疗严重出血。我们研究了 TXA 软膏是否减轻了咪喹莫特(IMQ)诱导的银屑病样炎症。此外,本研究还研究了非细胞毒性浓度的 TXA 对 IL-17 诱导的人角质形成细胞(HaCaT)的影响,以确定增殖性银屑病角质形成细胞的状态。我们发现 TXA 减少了 BALB/c 小鼠背部皮肤 IMQ 诱导的银屑病样红斑、厚度、鳞屑和累积评分(红斑加厚度加鳞屑)。此外,TXA 减少了耳厚度,并抑制了 IMQ 诱导的 BALB/c 小鼠耳表皮的过度角化、增生和炎症。此外,TXA 抑制了 BALB/c 小鼠模型中 IMQ 诱导的脾肿大。在 IL-17 诱导的 HaCaT 细胞中,TXA 抑制了 ROS 产生和 IL-8 的分泌。有趣的是,TXA 通过 IKK 介导的 IκB 降解抑制了 IL-17 诱导的 NFκB 信号通路。TXA 通过抑制 caspase-1 和 IL1β 的表达,抑制了 IL-17 诱导的 NLRP3 炎性小体的激活。TXA 通过增强自噬抑制了 IL-17 诱导的 NLRP3 炎性小体的激活,如 LC3-II 积累、p62/SQSTM1 表达、ATG4B 抑制和 Beclin-1/Bcl-2 失调所示。值得注意的是,TXA 抑制了 IL-17 诱导的 Nrf2 介导的角质蛋白 17 的表达。N-乙酰半胱氨酸预处理逆转了 TXA 对 IL-17 诱导的 HaCaT 细胞中 NFκB、NLRP3 炎性小体和 Nrf2 介导的角质蛋白 17 途径的影响。结果进一步证实,在 IMQ 诱导的小鼠耳皮肤中,TXA 处理下调了 NLRP3、IL1β、Nrf2 和角质蛋白 17 的表达等银屑病生物标志物。TXA 改善了体内 IMQ 诱导的银屑病样炎症和体外银屑病角质形成细胞。氨甲环酸是一种有前途的未来银屑病治疗方法。

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