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纸质出版日期:2018
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徐象威, 牛艳芬, 高丽辉, 等. 基于肠道尿酸转运体ABCG2的芒果苷降尿酸作用机制分析[J]. 中国实验方剂学杂志, 2018,24(17):145-149.
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.
徐象威, 牛艳芬, 高丽辉, 等. 基于肠道尿酸转运体ABCG2的芒果苷降尿酸作用机制分析[J]. 中国实验方剂学杂志, 2018,24(17):145-149. DOI: 10.13422/j.cnki.syfjx.20181733.
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.
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。
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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