Essential Site Maintenance: Authorea-powered sites will be updated circa 15:00-17:00 Eastern on Tuesday 5 November.
There should be no interruption to normal services, but please contact us at [email protected] in case you face any issues.

loading page

Allicin Ameliorates IMQ-induced psoriasis-like Skin Inflammation Via Disturbing the Interaction of Keratinocytes with IL-17A
  • +8
  • Lu Zhang,
  • Xuehong Ma,
  • Rongmei Shi,
  • Libo Zhang,
  • Ruolin Zhao,
  • Ran Duan,
  • Yuanyuan Qin,
  • Sijia Gao,
  • Xinxia Li,
  • Jingjing Duan,
  • Jianguang Li
Lu Zhang
Xin Jiang Medical University

Corresponding Author:[email protected]

Author Profile
Xuehong Ma
Xin Jiang Medical University
Author Profile
Rongmei Shi
Xin Jiang Medical University
Author Profile
Libo Zhang
China Pharmaceutical University
Author Profile
Ruolin Zhao
China Pharmaceutical University
Author Profile
Ran Duan
China Pharmaceutical University
Author Profile
Yuanyuan Qin
China Pharmaceutical University
Author Profile
Sijia Gao
China Pharmaceutical University
Author Profile
Xinxia Li
Xin Jiang Medical University
Author Profile
Jingjing Duan
China Pharmaceutical University
Author Profile
Jianguang Li
Xin Jiang Medical University
Author Profile

Abstract

Background and Purpose: Psoriasis is an inflammatory skin disease of chronic recurrence mediated by the interaction between IL-17 and keratinocytes, which sustains a vicious circle of inflammation. Currently, there is no safe and effective natural medicine for the clinical treatment of psoriasis. Given its prominent anti-proliferative and anti-inflammatory properties, we investigated the mechanism of allicin improving psoriasis. Experimental Design: Pharmacodynamics and toxicology experimental studies were estimated after topical administration of allicin on the skin of mice. Changes in inflammatory factors expression were analyzed by qPCR and immunohistochemistry after topical treatment with allicin in mice with psoriasis-like lesions induced by imiquimod. The impacts of allicin on proliferation and apoptosis of keratinocytes were analyzed by CCK8 assay and flow cytometry. The interaction between IL-17A and keratinocytes was studied using HaCaT cells, and the mechanism of action of allicin was explored by Western Blot. Transcriptomic changes following the action of allicin were probed by RNA-seq. Key Results: Our study demonstrated that allicin significantly improved the epidermal structure by inhibiting excessive proliferation and evasion of apoptosis of keratinocytes. Furthermore, allicin reduced the secretion of inflammatory cytokines (IL-17A/F, IL-22, IL-12, IL-20), chemokines (CXCL2, CXCL5, CCL20), and antibacterial peptides (S100A8/9). Mechanistically, allicin directly inhibited the IL-17-induced TRAF6/MAPK/NF-κB and STAT3/NF-κB signaling cascades in keratinocytes, thus breaking the positive inflammation feedback and alleviating imiquimod-induced psoriasis-like dermatitis in mice. Importantly, topical administration of allicin did not cause skin allergy, and the safety and adaptability of long-term application were verified.
11 May 2022Submitted to British Journal of Pharmacology
17 May 2022Submission Checks Completed
17 May 2022Assigned to Editor
19 May 2022Reviewer(s) Assigned
04 Jul 2022Review(s) Completed, Editorial Evaluation Pending
05 Jul 2022Editorial Decision: Revise Minor
31 Aug 20221st Revision Received
14 Sep 2022Submission Checks Completed
14 Sep 2022Assigned to Editor
16 Sep 2022Reviewer(s) Assigned
09 Oct 2022Review(s) Completed, Editorial Evaluation Pending
20 Oct 2022Editorial Decision: Accept
30 Nov 2022Published in British Journal of Pharmacology. 10.1111/bph.15983