Preventive Effect of Royal Jelly and 10-HDA on Skin Damage in Diabetic Mice through Regulating Keratinocyte Wnt/β-Catenin and Pyroptosis Pathway.
Xinqi HuangLu XiuYumei AnYuan GongSunao LiXueshi ChenChao LiuJianghuiwen LuHaiyan ShanJie ChangMingyang ZhangPublished in: Molecular nutrition & food research (2024)
The objective of this study is to elucidate how Royal jelly (RJ) and 10-hydroxy-2-decanoic acid (10-HDA) prevents diabetic skin dysfunction by modulating the pyroptosis pathway. Type 2 diabetes models are induced by fat diet consumption and low dose of streptozotocin (STZ) in C57BL/6J mice and treated with RJ (100 mg kg -1 day -1 ) and 10-HDA, the major lipid component of royal jelly (100 mg kg -1 day -1 ) for 28 weeks. The results show that serum concentrations of glucose and triglyceride are significantly lower in the RJ group or 10-HDA than diabetes mellitus (DM) group. Compared to the control group, pyroptosis proteins, GSDMD, ASC, Caspase-1, and IL-1β are increased in the skin of the diabetic model, accompanied by the activation of the Wnt/β-catenin signal pathway. Further evaluations by RJ exhibit superior improvement of skin damage, repress activation of the Wnt/β-catenin pathway, and attenuate keratinocyte pyroptosis, but 10-HDA cannot completely suppress the activation of Wnt/β-catenin pathway and pyroptosis, which shows a relatively weak protective effect on skin damage which shows that RJ is a better effect on skin injury after DM.
Keyphrases
- wound healing
- type diabetes
- cell proliferation
- soft tissue
- nlrp inflammasome
- low dose
- stem cells
- oxidative stress
- histone deacetylase
- glycemic control
- epithelial mesenchymal transition
- umbilical cord
- high fat diet
- cell death
- cardiovascular disease
- adipose tissue
- weight loss
- blood pressure
- diabetic rats
- signaling pathway
- insulin resistance
- metabolic syndrome
- bone marrow
- skeletal muscle
- induced apoptosis
- endoplasmic reticulum stress
- wild type