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Dendrobium huoshanense Leaf Flavonoid Extract Ameliorates Hyperuricemia in Mice
Shuo Han1, Chengwang Li2, Jie Zhang2
1School of Pharmacy, Anhui Medical University, Hefei, People's Republic of China; Medical & Health Test and Detect Center, Anhui Academy of Medical Sciences, Anhui Institute of Medicine, Hefei, Anhui, People's Republic of China; Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Background:
Hyperuricemia is a chronic metabolic disorder posing serious health risks. Dendrobium huoshanense stems are widely used as medicine and functional food ingredients, but the leaves remain underutilized, and their health potential remains unexplored.
Objectives:
In this research, the antihyperuricemic efficacy and mechanism of D. huoshanense leaf flavonoid extract (DLFE) are investigated.
Methods:
Hyperuricemia was induced in male Kunming mice (20-25 g, n = 6 per group) by yeast extract. Mice were treated with benzbromarone (positive control) or DLFE [100 (L), 200 (M), 400 (H) mg/kg/d] for 14 consecutive days. The antihyperuricemic effects of DLFE were assessed by measuring serum uric acid (UA), blood urea nitrogen (BUN), serum creatinine (Cr), and hepatic xanthine oxidase (XOD) activity. Renal histology, kidney injury markers [kidney injury molecule-1 (Kim-1)], neutrophil gelatinase-associated lipocalin (NGAL), inflammatory cytokines (IL-1β and TNF-α), and urate transporters [urate anion transporter 1 (URAT1), glucose transporter 9 (GLUT9), ATP-binding cassette transporter G2 (ABCG2)] were assessed. Additionally, the underlying mechanisms were elucidated using network pharmacology and subsequently verified in vivo and in vitro.
Results:
DLFE significantly reduced serum UA [M, 136.99 μmol/L and H, 121.99 μmol/L compared with hyperuricemia (HUA), 228.06 μmol/L, P < 0.01], creatinine [M, 115.75 μmol/L and H, 99.58 μmol/L compared with HUA, 161.90 μmol/L, P < 0.01 and P < 0.001, respectively], BUN (M, 9.82 μmol/L and H, 3.46 μmol/L compared with HUA, 13.21 μmol/L, P < 0.01 and P < 0.001), and hepatic XOD activity (M, 25.80 U/L and H, 18.63 U/L compared with HUA, 37.59 U/L, P < 0.01 and P < 0.001), mitigated renal injury and decreased Kim-1, NGAL, IL-1β, and TNF-α concentrations. Moreover, DLFE downregulated URAT1 and GLUT9 expression and upregulated ABCG2 expression. Network pharmacology predicted that DLFE alleviates hyperuricemia primarily by targeting the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, which was confirmed by reduced PI3K and Akt phosphorylation in mouse renal tissue and HK-2 cells.
Conclusions:
These findings show that DLFE alleviates hyperuricemia not only by inhibiting hepatic XOD activity to reduce UA production, but, more importantly, by accelerating renal UA excretion via inhibiting the PI3K/Akt pathway to regulate renal UA transporters. Thus, DLFE shows promise as a potential functional food or dietary supplement for hyperuricemia prevention.