Diosgenin Modulates Oxidative Stress and Inflammation in High-Fat Diet-Induced Obesity in Mice

被引:12
|
作者
Khateeb, Sahar [1 ]
Albalawi, Aishah [2 ]
Alkhedaide, Adel [3 ]
机构
[1] Fayoum Univ, Biochem Div, Dept Chem, Fac Sci, Al Fayyum, Egypt
[2] Univ Tabuk, Fac Sci, Biol Dept, Tabuk, Saudi Arabia
[3] Taif Univ, Turabah Univ Coll, Dept Med Lab, POB 11099, Taif 21944, Saudi Arabia
关键词
obesity; diosgenin; adipose tissue; oxidative stress; proinflammatory cytokines; METABOLIC SYNDROME; OSTEOARTHRITIS; EXPRESSION; APOPTOSIS; CELLS; RISK;
D O I
10.2147/DMSO.S355677
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Introduction: Obesity is a chronic metabolic disorder that results in excessive energy accumulated in adipose tissue causing dysfunction of adipocytes, inflammation, and oxidative stress. Diosgenin (DG), a steroidal saponin produced by several plants, has been reported to have antioxidant activity. This study aimed to evaluate the effects of diosgenin on oxidative stress and inflammation in mice fed with a high-fat diet (HFD). Methods: Thirty adult male mice were divided into three groups including the control group, mice fed with a normal diet; the HFD group, mice fed with a high-fat diet for 6 weeks; and the HFD+DG group, mice fed with a high-fat diet and diosgenin daily for 6 weeks. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), malondialdehyde (MDA), and total antioxidant capacity (TAC) activities were evaluated. Histopathological changes in the adipose tissues have been investigated. Results: Data showed that diosgenin increased TAC activities with a concomitant decrease in MDA levels. As well, DG reduces the TNF and IL-6 levels. The histopathological changes in the adipose tissues due to high-fat consumption were restored upon DG supplementation. Conclusion: Our results suggested that diosgenin is a promising agent for regulating obesity by increasing the levels of antioxidants, modifying oxidative stress and pro-inflammatory cytokines, which might prevent the onset of many diseases.
引用
收藏
页码:1589 / 1596
页数:8
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