Analysis of Hypouricemic Mechanism of Mangiferin Based on Intestinal Urate Transporter ABCG2

XU Xiang-wei; NIU Yan-fen; GAO Li-hui; LI Ling; LIN Hua

doi:10.13422/j.cnki.syfjx.20181733

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Analysis of Hypouricemic Mechanism of Mangiferin Based on Intestinal Urate Transporter ABCG2

更新时间：2024-01-04

- Analysis of Hypouricemic Mechanism of Mangiferin Based on Intestinal Urate Transporter ABCG2
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 17, Pages: 145-149(2018)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20181733
  CLC： R285.5
- Published：2018
- 稿件说明：
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XU Xiang-wei, NIU Yan-fen, GAO Li-hui, et al. Analysis of Hypouricemic Mechanism of Mangiferin Based on Intestinal Urate Transporter ABCG2[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(17): 145-149.
DOI：

XU Xiang-wei, NIU Yan-fen, GAO Li-hui, et al. Analysis of Hypouricemic Mechanism of Mangiferin Based on Intestinal Urate Transporter ABCG2[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(17): 145-149. DOI： 10.13422/j.cnki.syfjx.20181733.

摘要

目的：探讨芒果苷对尿酸诱导的高尿酸血症小鼠血尿酸、肠道尿酸转运体三磷酸腺苷结合盒转运蛋白G2[ATP-binding cassette superfamily G（White）member 2，ABCG2]mRNA及蛋白表达的影响，初步探讨芒果苷降尿酸的作用机制。方法：昆明种小鼠60只，随机分为6组，每组10只，分为正常组，模型组组，芒果苷（1.5，3.0，6.0 mg·kg-1）组和阳性药苯溴马隆（25.0 mg·kg-1）组，除正常组外，以腹腔注射的方式给予小鼠尿酸，诱导形成高尿酸血症模型，同时灌胃给予芒果苷及苯溴马隆，2周后磷钨酸法检测小鼠血尿酸，逆转录聚合酶链式反应（RT-PCR）及蛋白免疫印迹法（Western blot）检测小鼠空肠、回肠部ABCG2 mRNA和蛋白的表达，并采用苏木素-伊红（HE）染色观察小鼠回肠病理学变化。结果：与正常组比较，模型组小鼠血尿酸显著升高，小鼠的空部、回肠部ABCG2 mRNA明显降低，小鼠的空部、回肠部ABCG2蛋白明显升高（P<0.05，P<0.01），病理变化不明显；灌胃给药2周后，与模型组比较，芒果苷（3.0，6.0 mg·kg-1）组小鼠血尿酸明显下降（P<0.05，P<0.01），芒果苷（1.5，3.0，6.0 mg·kg-1）组小鼠的空部、回肠部ABCG2 mRNA表达均明显的上调，芒果苷（6.0 mg·kg-1）组小鼠空肠部ABCG2蛋白明显下调，而在小鼠回肠部，芒果苷（3.0，6.0 mg·kg-1）组的ABCG2蛋白表达明显下调（P<0.05）。结论：芒果苷可明显降低高尿酸血症小鼠的血尿酸水平，并能使小鼠肠道ABCG2 mRNA和蛋白表达改变恢复至正常水平。

Abstract

Objective:To research the effect of mangiferin on serum uric acid and intestinal urate transporter ATP-binding cassette superfamily G (White) member 2(ABCG2) gene and protein expressions in the hyperuricemic mice induced by urate. Method:A total of 60 Kunming mice were randomly divided into six groups

namely the normal group

the model group

the mangiferin (1.5

3.0

6.0 mg·kg-1) groups and the positive drug benzbromarone (25.0 mg·kg-1) group

with 10 mice in each group. Except for the normal group

the hyperuricemia model was induced by intraperitoneal injection with urate at a dosage of 150 mg·kg-1. Meanwhile

mangiferin and benzbromarone were administered intragastrically. Two weeks later

the phosphotungstic acid method was used to detect the uric acid of mice; reverse transcription PCR and Western blot were performed to detect jejunal and ileac ABCG2 mRNA and protein expressions of mice; and htoxylin eosin(HE) staining was adopted to observe the pathological change in ileum of mice. Result:Compared with the normal group

the model group showed a significant increase in blood uric acid

remarkable decrease in jejunal and ileac ABCG2 mRNA and protein expressions

and notable rise in jejunal and ileac ABCG2 (P<0.05

P<0.01)

without any significant pathological change; after 2 weeks of administration with mangiferin

mangiferin (3.0

6.0 mg·kg-1) significantly lowered the serum uric acid compared with hyperuricemic mice; after administration with mangiferin (1.5

3.0

6.0 mg·kg-1) to hyperuricemic mice

mangiferin significantly increased the ABCG2 mRNA expression in jejunum and ileum; However

mangiferin (1.5

3.0

6.0 mg·kg-1) significantly caused the down-regulation of ABCG2 protein in jejunum and ileum (P<0.05). Conclusion:Mangiferin can obviously decrease the serum uric acid levels in hyperuricemic mice induced by urate

and restore ABCG2 mRNA and protein expressions of jejunum and ileum in hyperuricemic mice.

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