Synthesis, characterization, toxicity evaluation and inhibitory effect of hesperitin-copper (Ⅱ) complex on xanthine oxidase

Li, Kai; Zeng, Ni; Pan, Junhui; Gong, Deming; Zhang, Guowen

doi:10.1016/j.molliq.2022.120812

Cited by 3 publications

(5 citation statements)

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“…Such as kaempferol-3 ′ -sulfonate, and chicory aqueous extract inhibited XO activity to reduce serum uric acid levels in HUA mice [58,59]. Similarly, in the present study, the high-dose Hsp-Cu(II) complex significantly inhibited liver XO and ADA activities in HUA mice, equivalent to the positive control allopurinol, which was consistent with the results in vitro [33]. The inhibition of XO by Hsp was weaker than that of the Hsp-Cu(II), and there was no significant inhibition on ADA.…”

Section: Discussionsupporting

confidence: 90%

“…However, the inhibition rate of XO by Hsp was only 10.9%. This was consistent with previous studies that the Hsp-Cu(II) complex exerted a significantly stronger inhibitory effect on XO in vitro than the ligand Hsp [33]. For the inhibition of ADA activity in the liver (Figure 4B), the Normal, Diseased, All, Hsp, and LHC groups exhibited fragile inhibitory ability, with no significant differences, but the MHC and HHC groups significantly inhibited ADA activity with inhibition rates of 18.4% and 23.2% (p < 0.05), respectively.…”

Section: Activities Of Xo and Adasupporting

confidence: 93%

“…To date, clinical drugs often cause adverse reactions. Our previous research demonstrated that the Hsp-Cu(II) complex was non-toxic and possessed a significantly higher inhibition ability against xanthine oxidase in vitro than the ligand Hsp [33]. However, the effect of uric acid-lowering by the complex in the body was unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Oteracil potassium was acquired from Macklin Biochemical Technology Co., Ltd. (Shanghai, China). The Hsp-Cu(II) complex was synthesized and characterized in our laboratory [33]. The biochemical assay kits of UA (C012-2-1), blood urea nitrogen (BUN, C013-2-1), creatinine (Cr, C011-2-1), XO (A002-1-1), ADA (A048-2-1), T-SOD (A001-1-1), CAT (A007-1-1), malondialdehyde (MDA, A003-1-2), interleukin-1β (IL-1β, H002), interleukin-6 (IL-6, H007-1-1), tumor necrosis factor-α (TNF-α, H052-1), and transforming growth factor-β(TGF-β, H034-1) were all bought from Nanjing Jiancheng Bioengineering Institute (Nanjing, China).…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

“…Cu(II) could bind to Chrysin to form a metal complex that showed stronger inhibitory activity on XO than that of the ligand chrysin [32]. Based on the abundant resources of Hsp and an edible trace element of copper that is essential to the human body, we synthesized and characterized Hsp-Cu(II) complex, and found that the complex was non-toxic and strongly inhibited XO with ten times and nearly twice the strengths of Hsp and the clinical drug allopurinol (Alp) [33], respectively, indicating that the complex may have a strong UA-lowering effect, and may be a potential new type of XO inhibitor. However, to our knowledge, whether the complex has a hypouricemic effect in vivo is not known.…”

Section: Introductionmentioning

confidence: 99%

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Hesperitin-Copper(II) Complex Regulates the NLRP3 Pathway and Attenuates Hyperuricemia and Renal Inflammation

Peng,

Liu,

et al. 2024

Foods

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Background: Hyperuricaemia (HUA) is a disorder of purine metabolism in the body. We previously synthesized a hesperitin (Hsp)-Cu(II) complex and found that the complex possessed strong uric acid (UA)-reducing activity in vitro. In this study we further explored the complex’s UA-lowering and nephroprotective effects in vivo. Methods: A mouse with HUA was used to investigate the complex’s hypouricemic and nephroprotective effects via biochemical analysis, RT-PCR, and Western blot. Results: Hsp-Cu(II) complex markedly decreased the serum UA level and restored kidney tissue damage to normal in HUA mice. Meanwhile, the complex inhibited liver adenosine deaminase (ADA) and xanthine oxidase (XO) activities to reduce UA synthesis and modulated the protein expression of urate transporters to promote UA excretion. Hsp-Cu(II) treatment significantly suppressed oxidative stress and inflammatory in the kidney, reduced the contents of cytokines and inhibited the activation of the nucleotide-binding oligomerization domain (NOD)-like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory pathway. Conclusions: Hsp-Cu(II) complex reduced serum UA and protected kidneys from renal inflammatory damage and oxidative stress by modulating the NLRP3 pathway. Hsp-Cu(II) complex may be a promising dietary supplement or nutraceutical for the therapy of hyperuricemia.

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Section: Discussionsupporting

confidence: 90%

Section: Activities Of Xo and Adasupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Chemicals and Reagentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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