Obesity and oxidative stress intensify psoriasis through activating IL-17/IL-23 pathway

被引:0
作者
Vikasari, Suci Nar [1 ,3 ]
Sukandar, Elin Yulinah [3 ]
Suciati, Tri [2 ]
Adnyana, I. Ketut [2 ]
机构
[1] Inst Teknol Bandung, Sch Pharm, Doctoral Program Pharm, Bandung, Indonesia
[2] Inst Teknol Bandung, Sch Pharm, Bandung, Indonesia
[3] Univ Jenderal Achmad Yani, Fac Pharm, Cimahi, Indonesia
来源
PHYSIOLOGY AND PHARMACOLOGY | 2024年 / 28卷 / 01期
关键词
Psoriasis; Autoimmune; Obese; Oxidative stress; IL-17/IL-23; pathway; PATHOPHYSIOLOGY; PATHOGENESIS; UPDATE;
D O I
10.61186/phypha.28.1.18
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Psoriasis is an autoimmune disease characterized by keratinocyte hyperproliferation and skin thickening. Psoriasis is caused by a complicated interaction between the innate and acquired immune systems. In the skin, this reaction produces abnormal T helper cell (Th1, Th17, and Th23) reactivation. Keratinocyte hyperproliferation is caused by increased cell (TNF-alpha), and interferon-gamma (INF-gamma). Obesity, free fatty acids, microorganisms in the skin and digestive tract, free radicals in the body, and the cardiovascular system are also essential variables in psoriasis. Several variables influence the cytokine activation of the IL17/IL-23 pathway. Obesity, which is marked by changes in lipid profile in psoriasis patients, is linked to increased oxidative stress and the generation of proinflammatory cytokines, both of which can potentially trigger psoriasis relapse. Antioxidant-rich diet and intake can be employed as one of the stages in preventing psoriasis recurrence.
引用
收藏
页码:18 / 26
页数:9
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