2. Academic Validation
  3. Zinc gluconate improves atopic dermatitis by modulating CXCL10 release of keratinocytes via PPARα activation

Zinc gluconate improves atopic dermatitis by modulating CXCL10 release of keratinocytes via PPARα activation

  • Biomed Pharmacother. 2024 Aug:177:117129. doi: 10.1016/j.biopha.2024.117129.
Yujia Wei 1,  Xiaomei Zhu 2,  Shan Lin 3,  Wei Yang 4,  Tingmei Wang 5,  Xiaoqi Nie 6,  Zeqi Shi 7,  Zhong Liu 8,  Ri Zhang 9,  Dong Li 10
Affiliations

Affiliations

  • 1 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: m202176167@hust.edu.cn.
  • 2 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: zhuxiaomei@tjh.tjmu.edu.cn.
  • 3 Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Nutrition and Food Hygiene and MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: d202081512@hust.edu.cn.
  • 4 Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Nutrition and Food Hygiene and MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: yw8278@hust.edu.cn.
  • 5 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: dwtm198935@126.com.
  • 6 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: 1625712361@qq.com.
  • 7 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: zeqishi_2022@tjh.tjmu.edu.cn.
  • 8 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: doctorliuz@126.com.
  • 9 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: zr080130@163.com.
  • 10 Department of Dermatology, Huazhong University of Science and Technology Tongji Medical College Tongji Hospital, Wuhan, China. Electronic address: lidong_2022@hust.edu.cn.
PMID: 39018874 DOI: 10.1016/j.biopha.2024.117129
Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin condition with complex causes involving immune factors. The presence of essential trace elements that support immune system function can influence the development of this condition. This study investigated how serum trace elements impact the pathogenesis of atopic dermatitis. Upon analyzing serum microelements in AD patients and control subjects, it was observed that patients with AD had notably lower zinc levels. Genomic analysis of AD skin revealed distinct gene expression patterns, specifically the increased expression of CXCL10 in the epidermis. The heightened levels of CXCL10 in AD skin lesions were found to correlate with reduced serum zinc levels. Treatment with zinc gluconate showed reduced chemotactic response and CXCL10 release, suggesting its potential to regulate CXCL10 expression of keratinocytes in AD. The mechanism behind this involved the downregulation of STAT phosphorylation through activating PPARα. In the AD-like dermatitis mouse model, zinc gluconate therapy decreased serum IgE levels, alleviated skin lesion severity, reduced skin thickness, and lowered CXCL10 expression, demonstrating its efficacy in managing AD-like skin conditions. These findings indicate that zinc gluconate can reduce inflammation in keratinocytes by activating PPARα, inhibiting STAT signaling, and decreasing CXCL10 release, thus highlighting its potential as a therapeutic target for AD.

Keywords

Atopic dermatitis; CXCL10; Inflammation; PPARα; STAT; Zinc.

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