npj Science of Food
·
2026
·
IF 9.7
Zhi Dandan,He Xiying,Yang Linfu,Gong Xueyang,Xue Yunfei,Wang Shuang,Wen Xin,Guan Zhibin,Zhao Hongmu,Dong Kun,Tian Yakai
The incidence of hyperlipidemia, a lipid metabolic disorder, continues to increase globally, but current pharmacological therapies are often limited by adverse effects. Royal jelly acid, a unique monounsaturated fatty acid (MUFA) derived from royal jelly, shows therapeutic promise against hyperlipidemia; however, its direct targets and regulatory mechanisms remain unclear. In a diet-induced rat model of hyperlipidemia, royal jelly acid exhibited favorable safety and significantly improved body weight, serum lipid indices, hepatic enzyme activity, and antioxidant capacity, while alleviating hepatic lipid droplet accumulation. Royal jelly acid significantly increased the abundance of short-chain fatty acid (SCFA)-producing intestinal microorganisms, promoted SCFA production, and restored hyperlipidemia-associated intestinal microbial imbalance. Liver transcriptomic and plasma metabolomic analyses demonstrated that royal jelly acid regulated genes involved in glycolipid metabolism, oxidative stress, and inflammatory responses, as well as multiple key metabolites. Integrated multi-omics analysis and molecular docking confirmed that the glycerophospholipid metabolic pathway represents the core metabolic axis mediating these protective effects. Royal jelly acid mainly alleviates hyperlipidemia by enhancing antioxidant and anti-inflammatory defense through the gut–liver axis–mediated SCFAs–glycerophospholipid pathway. These findings support the use of royal jelly acid as a promising MUFA-based therapeutic strategy for hyperlipidemia and provide a scientific basis for its application.
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DOI
高影响因子
MOLECULAR NUTRITION & FOOD RESEARCH
·
2024
·Vol. 68
·期 19
·2400098
·
IF 4.5
Xinqi Huang,Lu Xiu,Yumei An,Yuan Gong,Sunao Li,Xueshi Chen,Chao Liu,Jianghuiwen Lu,Haiyan Shan,Jie Chang,Mingyang Zhang
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.
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2025
·
IF 4.7
Dan-dan Zhi,Xi-ying He,Lin-fu Yang,Yun-fei Xue,Yi-qiu Liu,Dan Yue,Yi-nan Feng,Kun Dong,Ya-kai Tian
Royal jelly acid is a unique unsaturated fatty acid isolated from royal jelly. Recently, royal jelly acid was proposed to have potential therapeutic effects on hyperlipidemia. However, its effect on hyperlipidemia and the underlying molecular mechanism remains unclear. Therefore, in this study, we analyzed the mechanism of anti-hyperlipidemia of royal jelly acid through animal experiments and plasma metabolomics in conjunction with human network pharmacology and molecular docking analyses. We found that royal jelly acid could significantly decrease the serum lipid levels, ameliorate hepatic pathological injury, and reduce the level of oxidative stress in the experimental rats. A total of 41 key metabolites and 10 hub targets played key roles in the exertion of anti-hyperlipidemic effects, including tumor necrosis factor (TNF), insulin (INS) and epidermal growth factor receptor (EGFR). A total of 24 pathways, including tryptophan, citrate cycle, and arachidonic acid metabolisms, were identified as the key pathways involved in royal jelly acid-alleviated hyperlipidemia. The present findings provide new insights into the pathogenesis, diagnosis, and treatment targets of hyperlipidemia as well as contribute to the development and utilization of royal jelly acid related products.
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DOI
PubMed
高影响因子