This study was aimed at evaluating the hypouricemic effect of rape bee pollen from Qinghai province in China. Rape bee pollen crude extracts (RPCE) was obtained by n-butanol extraction and purified by polyamide resin and AB-8 resin respectively to generate five fractions (fraction 1–5). In vitro , fraction 5 had strongest inhibition on xanthine oxidase (XO) (IC 50 = 0.21 ± 0.02 mg mL −1 ) among five fractions and had reversible and mixed inhibitory effect on XO. Fraction 5 was further purified and then generated fraction 5′. In vivo , fraction 5′ had lower serum UA level and could reduce serum BUN, Cr levels and hepatic XO activity more effectively than RPCE in potassium oxonate-induced hyperuricemic mice . Moreover, fraction 5′ had higher CAT activity and content of GSH in hyperuricemic mice. Six compounds including quercetin-3-O-(2″-O-glucopyranosyl)-glucopyranoside (peak 1), quercetin-3-O-(2″-O-glucopyranosyl)-rhamnopyranoside (peak 2), kaempferol-3-O-(2″-O-glucopyranosyl)-glucopyranoside (peak 3) and N′, N″-di- p -coumaroylspermidine (peak 4–6) in RPCE were identified by using HPLC-ESI-QTOF-MS/MS, whereas only peak 4 to 6 were found in fraction 5′. This study shows that rape bee pollen has potential clinical application value as an effective anti-hyperuricemia bioactive drug or functional food.
Cyclocarya paliurus , as an important edible and medicinal plant, its effects and mechanisms on hyperuricemic nephropathy remain unclear. Herein, we investigated the hypouricemic and nephroprotective effects of the water extracts of C. paliurus leaves (CPE) in a hyperuricemic nephropathy rat model induced by adenine and ethambutol. The results showed that CPE could significantly decrease plasma uric acid (PUA) and urea nitrogen (PUN), as well as reduce renal fibrosis in the hyperuricemic nephropathy rat model. Plasma metabolomics indicated that CPE improved the disordered arachidonic acid metabolism. Meanwhile, CPE reduced renal inflammation via inhibition of COX--2. Moreover, CPE could improve disturbed purine metabolism by inhibiting the hepatic xanthine oxidase (XOD), reversing the renal urate transporter 1 (URAT1) and organic anion transporter 1 (OAT1). Collectively, this study demonstrated that CPE could exhibit hypouricemic effect by improving purine metabolism, and attenuate kidney injury by improving arachidonic acid metabolism and alleviating kidney inflammation.
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