• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Secoemestrin C 通过抑制 TNF-α/NF-κB 信号通路改善小鼠银屑病样皮肤炎症。

Secoemestrin C Ameliorates Psoriasis-like Skin Inflammation in Mice by Suppressing the TNF-α/NF-κB Signaling Pathway.

机构信息

Department of Stomatology, Chengdu Seventh People's Hospital, Chengdu, 610044, China.

Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

出版信息

Curr Med Sci. 2024 Feb;44(1):232-240. doi: 10.1007/s11596-024-2828-8. Epub 2024 Feb 23.

DOI:10.1007/s11596-024-2828-8
PMID:38393530
Abstract

OBJECTIVE

Secoemestrin C (SC), an epitetrathiodioxopiperazine isolated from Aspergillus nidulans, has been previously reported to have immunomodulatory and hepatoprotective effects against acute autoimmune hepatitis. However, the effect of SC on regulating the inflammation and its underlying mechanisms in the pathogenesis of psoriasis remain unclear. This study aimed to evaluate the effects of SC on inflammatory dermatosis both in vitro and in vivo.

METHODS

In vitro, HaCaT cells were induced with tumor necrosis factor-alpha (TNF-α, 10 ng/mL) to establish an inflammatory injury model, and the expression of nuclear transcription factor-κB (NF-κB) pathway components was measured using qRT-PCR and Western blotting. An in vivo mouse model of imiquimod (IMQ)-induced psoriasis-like skin inflammation was used to evaluate the effectiveness of SC in alleviating psoriasis.

RESULTS

SC significantly blocked the activation of NF-κB signaling in TNF-α-stimulated HaCaT cells. In addition, systemic and local administration of SC improved psoriatic dermatitis in the IMQ-induced mouse model. SC reduced skin scale and significantly inhibited the secretion of inflammatory factors in skin lesions.

CONCLUSION

The protective effect of SC against psoriatic-associated inflammation reveals its potential therapeutic value for treating psoriasis.

摘要

目的

Secoemestrin C(SC)是从构巢曲霉中分离得到的一种表硫代二氧哌嗪,具有免疫调节和肝保护作用,可对抗急性自身免疫性肝炎。然而,SC 对调节银屑病发病机制中的炎症及其潜在机制的影响尚不清楚。本研究旨在评估 SC 在体内和体外对炎症性皮肤病的作用。

方法

体外,用肿瘤坏死因子-α(TNF-α,10ng/ml)诱导 HaCaT 细胞建立炎症损伤模型,并用 qRT-PCR 和 Western blot 测定核转录因子-κB(NF-κB)途径成分的表达。采用咪喹莫特(IMQ)诱导的银屑病样皮肤炎症小鼠模型评价 SC 减轻银屑病的效果。

结果

SC 显著阻断了 TNF-α 刺激的 HaCaT 细胞中 NF-κB 信号的激活。此外,SC 的全身和局部给药改善了 IMQ 诱导的小鼠模型中的银屑病样皮炎。SC 减少了皮肤鳞屑,显著抑制了皮肤病变中炎症因子的分泌。

结论

SC 对银屑病相关炎症的保护作用表明其在治疗银屑病方面具有潜在的治疗价值。

相似文献

1
Secoemestrin C Ameliorates Psoriasis-like Skin Inflammation in Mice by Suppressing the TNF-α/NF-κB Signaling Pathway.Secoemestrin C 通过抑制 TNF-α/NF-κB 信号通路改善小鼠银屑病样皮肤炎症。
Curr Med Sci. 2024 Feb;44(1):232-240. doi: 10.1007/s11596-024-2828-8. Epub 2024 Feb 23.
2
Tryptanthrin ameliorates imiquimod-induced psoriasis in mice by suppressing inflammation and oxidative stress via NF-κB/MAPK/Nrf2 pathways.靛玉红通过NF-κB/MAPK/Nrf2途径抑制炎症和氧化应激,从而改善咪喹莫特诱导的小鼠银屑病。
J Nat Med. 2023 Jan;77(1):188-201. doi: 10.1007/s11418-022-01664-9. Epub 2022 Nov 15.
3
Glycyrrhizin ameliorates imiquimod-induced psoriasis-like skin lesions in BALB/c mice and inhibits TNF-α-induced ICAM-1 expression via NF-κB/MAPK in HaCaT cells.甘草酸可改善咪喹莫特诱导的BALB/c小鼠银屑病样皮肤损伤,并通过NF-κB/MAPK途径抑制肿瘤坏死因子-α诱导的HaCaT细胞中细胞间黏附分子-1的表达。
Cell Physiol Biochem. 2015;35(4):1335-46. doi: 10.1159/000373955. Epub 2015 Feb 12.
4
Ginsenoside Rg1 abolish imiquimod-induced psoriasis-like dermatitis in BALB/c mice via downregulating NF-κB signaling pathway.人参皂苷 Rg1 通过下调 NF-κB 信号通路来消除咪喹莫特诱导的 BALB/c 小鼠银屑病样皮炎。
J Food Biochem. 2019 Nov;43(11):e13032. doi: 10.1111/jfbc.13032. Epub 2019 Sep 9.
5
Eupatilin inhibits keratinocyte proliferation and ameliorates imiquimod-induced psoriasis-like skin lesions in mice via the p38 MAPK/NF-κB signaling pathway.灯盏乙素通过p38丝裂原活化蛋白激酶/核因子κB信号通路抑制角质形成细胞增殖并改善咪喹莫特诱导的小鼠银屑病样皮肤损伤。
Immunopharmacol Immunotoxicol. 2023 Apr;45(2):133-139. doi: 10.1080/08923973.2022.2121928. Epub 2022 Oct 28.
6
Daphnetin inhibits proliferation and inflammatory response in human HaCaT keratinocytes and ameliorates imiquimod-induced psoriasis-like skin lesion in mice.瑞香素抑制人 HaCaT 角质形成细胞增殖和炎症反应,并改善咪喹莫特诱导的小鼠银屑病样皮肤损伤。
Biol Res. 2020 Oct 20;53(1):48. doi: 10.1186/s40659-020-00316-0.
7
L. Ameliorates Imiquimod-Induced Psoriasis-Like Dermatitis and Inhibits Inflammatory Cytokines Production through TLR7/8-MyD88-NF-κB-NLRP3 Inflammasome Pathway.L. 通过 TLR7/8-MyD88-NF-κB-NLRP3 炎性小体途径改善咪喹莫特诱导的银屑病样皮炎并抑制炎症细胞因子的产生。
Molecules. 2019 Jun 7;24(11):2157. doi: 10.3390/molecules24112157.
8
Selenium-Rich Yeast Peptide Fraction Ameliorates Imiquimod-Induced Psoriasis-like Dermatitis in Mice by Inhibiting Inflammation via MAPK and NF-κB Signaling Pathways.富硒酵母肽通过抑制 MAPK 和 NF-κB 信号通路改善咪喹莫特诱导的小鼠银屑病样皮炎。
Int J Mol Sci. 2022 Feb 14;23(4):2112. doi: 10.3390/ijms23042112.
9
Increased βTrCP are associated with imiquimod-induced psoriasis-like skin inflammation in mice via NF-κB signaling pathway.βTrCP的增加通过NF-κB信号通路与咪喹莫特诱导的小鼠银屑病样皮肤炎症相关。
Gene. 2016 Oct 30;592(1):164-171. doi: 10.1016/j.gene.2016.07.066. Epub 2016 Jul 28.
10
Khasianine ameliorates psoriasis-like skin inflammation and represses TNF-α/NF-κB axis mediated transactivation of IL-17A and IL-33 in keratinocytes.卡西亚宁可改善银屑病样皮肤炎症,并抑制角质形成细胞中 TNF-α/NF-κB 轴介导的 IL-17A 和 IL-33 的反式激活。
J Ethnopharmacol. 2022 Jun 28;292:115124. doi: 10.1016/j.jep.2022.115124. Epub 2022 Feb 17.

引用本文的文献

1
PIEZO1 promotes psoriasis-like skin inflammation in mice via NF-κB/IL-17 signaling pathway activation.PIEZO1通过激活NF-κB/IL-17信号通路促进小鼠银屑病样皮肤炎症。
Mol Med. 2025 Jun 10;31(1):225. doi: 10.1186/s10020-025-01279-2.

本文引用的文献

1
Khasianine ameliorates psoriasis-like skin inflammation and represses TNF-α/NF-κB axis mediated transactivation of IL-17A and IL-33 in keratinocytes.卡西亚宁可改善银屑病样皮肤炎症,并抑制角质形成细胞中 TNF-α/NF-κB 轴介导的 IL-17A 和 IL-33 的反式激活。
J Ethnopharmacol. 2022 Jun 28;292:115124. doi: 10.1016/j.jep.2022.115124. Epub 2022 Feb 17.
2
The Cytokine Mediated Molecular Pathophysiology of Psoriasis and Its Clinical Implications.细胞因子介导的银屑病分子病理生理学及其临床意义。
Int J Mol Sci. 2021 Nov 26;22(23):12793. doi: 10.3390/ijms222312793.
3
Sortilin regulates keratinocyte proliferation and apoptosis through the PI3K-AKT signaling pathway.
Sortilin 通过 PI3K-AKT 信号通路调节角质形成细胞的增殖和凋亡。
Life Sci. 2021 Aug 1;278:119630. doi: 10.1016/j.lfs.2021.119630. Epub 2021 May 15.
4
New Treatment Addressing the Pathogenesis of Psoriasis.新型疗法直击银屑病发病根源。
Int J Mol Sci. 2020 Oct 11;21(20):7488. doi: 10.3390/ijms21207488.
5
Secoemestrin C inhibits activation of NKT/conventional T cells and protects against concanavalin A-induced autoimmune hepatitis in mice.异欧前胡素C抑制NKT/传统T细胞的活化,并对小鼠刀豆蛋白A诱导的自身免疫性肝炎具有保护作用。
Am J Transl Res. 2020 Jul 15;12(7):3389-3401. eCollection 2020.
6
Risk Factors for the Development of Psoriasis.银屑病发病的危险因素。
Int J Mol Sci. 2019 Sep 5;20(18):4347. doi: 10.3390/ijms20184347.
7
Malignancy and mortality rates in patients with severe psoriatic arthritis requiring tumour-necrosis factor alpha inhibition: results from the British Society for Rheumatology Biologics Register.严重银屑病关节炎患者使用肿瘤坏死因子-α抑制剂的恶性肿瘤和死亡率:来自英国风湿病学会生物制剂登记处的结果。
Rheumatology (Oxford). 2019 Jan 1;58(1):80-85. doi: 10.1093/rheumatology/key241.
8
A Critical Role of the IL-1β-IL-1R Signaling Pathway in Skin Inflammation and Psoriasis Pathogenesis.IL-1β-IL-1R 信号通路在皮肤炎症和银屑病发病机制中的关键作用。
J Invest Dermatol. 2019 Jan;139(1):146-156. doi: 10.1016/j.jid.2018.07.025. Epub 2018 Aug 16.
9
Psoriasis: Which therapy for which patient: Psoriasis comorbidities and preferred systemic agents.银屑病:哪种疗法适合哪种患者:银屑病合并症和首选的系统药物。
J Am Acad Dermatol. 2019 Jan;80(1):27-40. doi: 10.1016/j.jaad.2018.06.057. Epub 2018 Jul 11.
10
Indirect co-cultures of healthy mesenchymal stem cells restore the physiological phenotypical profile of psoriatic mesenchymal stem cells.健康间充质干细胞的间接共培养可恢复银屑病间充质干细胞的生理表型特征。
Clin Exp Immunol. 2018 Aug;193(2):234-240. doi: 10.1111/cei.13141. Epub 2018 May 31.