Phytochemicals from Tradescantia albiflora Kunth extracts reduce serum uric acid levels in oxonate-induced rats

Abstract

Background:Tradescantia albiflora (TA) Kunth (Commelinaceae) has been used for treating gout and hyperuricemia as folklore remedies in Taiwan. Therefore, it is worthwhile to study the effect of TA extracts on lowering uric acid activity. The hypouricemic effects of TA extracts on potassium oxonate (PO)-induced acute hyperuricemia were investigated for the first time.Materials and Methods:All treatments at the same volume (1 ml) were orally administered to the abdominal cavity of PO-induced hyperuricemic rats. One milliliter of TA extract in n-hexane (HE), ethyl acetate (EA), n-butanol (BuOH), and water fractions has 0.28, 0.21, 0.28, and 1.03 mg TA, respectively; and the plasma uric acid (PUA) level was measured for a consecutive 4 h after administration.Results:All four fractions' extracts derived from TA were observed to significantly reduce PUA compared with the PO group. The EA-soluble fraction (TA-EA) exhibited the best xanthine oxidase (XO) inhibitory activity. Following column chromatography, 12 phytochemicals were isolated and identified from the EA fraction. The IC50 values of isolated phytochemicals indicated that bracteanolide A (AR11) showed the remarkable XO inhibitory effect (IC50 value of 76.4 μg/ml). These findings showed that the in vivo hypouricemic effect in hyperuricemic rats was consistent with in vitro XO inhibitory activity, indicating that TA extracts and derived phytochemicals could be potential candidates as hypouricemic agents.SUMMARY Tradescantia albiflora extracts possess in vivo hypouricemic action in hyperuricemic ratsT. albiflora extracts exhibited strong inhibitory activity against xanthine oxidase (XO)Butenolide may play an important role in XO inhibitionThe extract bracteanolide A was demonstrated potent XO inhibitory activity in vitro. Abbreviations used: TA: Tradescantia albiflora, PO: potassium oxonate, HE: n-hexane, EA: ethyl acetate, BuOH: n-butanol, PUA: plasma uric acid, XO: xanthine oxidase, MeOH: methanol, IP: intraperitoneal

Hypouricemic and Nephroprotective Effects of an Active Fraction from <b><i>Polyrhachis Vicina Roger</i></b> On Potassium Oxonate-Induced Hyperuricemia in Rats

“…Potassium oxonate is most frequently employed to develop an animal model of hyperuricemia by inhibiting uricase that converts uric acid to allantoin [37, 49]. In the present study, serum uric acid levels were significantly increased 8 and 12 weeks after potassium oxonate administration, suggesting the successful establishment of hyperuricemia model.…”

“…Therefore, the searches for more effective and less toxic agents against hyperuricemia are highly warranted. Natural products devoid of such disadvantages offer a great opportunity [32-37]. …”

Hypouricemic Effect of Ethanol Extract of Aster glehni Leaves in Potassium Oxonate-Induced Hyperuricemic Rats

“…A number of attempts have been made to find effective compounds that inhibit XO without side effects from traditional medicines and plants. Potential therapeutic agents for treating gout have been reported from soy sauce [ 6 ], Phyllanthus niruri methanol extract and lignans isolated from P. niruri [ 7 ], phytochemicals from Tradescantia albiflora Kunth extracts including bracteanolide A and butenolide [ 8 ], and astilbin [ 9 ].…”

Bracteanolide A abrogates oxidative stress‐induced cellular damage and protects against hepatic ischemia and reperfusion injury in rats

“…Given the increasing prevalence of liver illness on a global scale that ultimately requires liver transplantation or other surgical operations, which is largely susceptible to hepatic ischemia and reperfusion injury, we choose to investigate new compounds with the potential to reduce I/R damage to the liver. Bracteanolide A, whose structure is shown in Figure 1, is the major active compound of Tradescantia albiflora Kunth, a herb used to treat gout, edema, nephritis, enteritis, and diarrhea (Wang et al., 2016). However, evidence‐based medical efficacy of bracteanolide A is limited.…”