Abstract
Purpose: To evaluate the in-vitro inhibition of xanthine oxidase (purified from bovine milk) by extracts of Lycium arabicum, as well as it is in vivo hypouricemic and renal protective effects. Methods: Four extracts of Lycium arabicum, methanol (CrE), chloroform (ChE), ethyl acetate (EaE) and aqueous (AqE) extracts, were screened for their total phenolics and potential inhibitory effects on purified bovine milk xanthine oxidase (XO) activity by measuring the formation of uric acid or superoxide radical. The mode of inhibition was investigated and compared with the standard drugs, allopurinol, quercitin and catechin. To evaluate their hypouricemic effect, the extracts were administered to potassium oxonate-induced hyperuricemic mice at a dose of 50 mg/kg body weight. Results: The results showed that EaE had the highest content of phenolic compounds and was the most potent inhibitor of uric acid formation (IC50 = 0.017 ± 0.001 mg/mL) and formation of superoxide (IC50 = 0.035 ± 0.001 mg/ml). Lineweaver-Burk analysis showed that CrE and EaE inhibited XO competitively, whereas the inhibitory activities exerted by ChE and AqE were of a mixed type. Intraperetoneal injection of L. arabicum extracts (50 mg/kg) elicited hypouricemic actions in hyperuricemic mice. Hyperuricemic mice presented a serum uric acid concentration of 4.71 ± 0.29 mg/L but this was reduced to 1.78 ± 0.11 mg/L by EaE, which was the most potent hyporuricemic extract. Conclusion: L. arabicum fractions have a strong inhibitory effect on xanthine oxidase and and also have a significantly lowering effect on serum and liver creatinine and urea levels in hyperuricemic mice.
Highlights
Hyperuricemia is the most cited pathology involving xanthine oxidase (XO)
Globularia alypum (GA) was extracted with solvent of varying polarity allowed its separation into four subtractions: crude extract (CrE) chloroform extract (ChE), ethyl acetate extract (AcE) and aqueous extracts (AqE)
The results showed that the extract (AcE) is the richest in polyphenols and flavonoids followed by CrE and AqE, whereas ChE is the poorest (Table 1)
Summary
It is a pathological state that arises from overproduction (by XO) or under excretion (renal tubule disorders) of uric acid. As a result of hyperuricemia, insoluble uric acid forms microscopic crystals in the capillary vessels of joints. These crystals cause inflammation and sharp pain, which is termed acute gouty arthritis or acute gout (Sachs et al, 2009). Xanthine oxidase (XO) catalyses the oxidation of hypoxanthine and xanthine to uric acid. XO inhibitors have been proposed as potential therapeutic agents for treating hyperuricemia as they could be used to block the biosynthesis of uric acid (Unno et al., 2004; Newcombe, 2013). There is an urgent need to develop new XO inhibitors from natural sources
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