Format

Send to

Choose Destination
Fitoterapia. 2016 Sep;113:1-5. doi: 10.1016/j.fitote.2016.06.015. Epub 2016 Jun 28.

Hypouricemic effect of allopurinol are improved by Pallidifloside D based on the uric acid metabolism enzymes PRPS, HGPRT and PRPPAT.

Author information

1
Tianjin Key Laboratory on Technologies Enabling Development of Clinical, Therapeutics and Diagnostics, College of Pharmacy, Tianjin Medical University, Tianjin 300070, China.
2
Tang Center for Herbal Medicine Research, University of Chicago, Chicago, IL 60637, USA.
3
Tianjin Key Laboratory on Technologies Enabling Development of Clinical, Therapeutics and Diagnostics, College of Pharmacy, Tianjin Medical University, Tianjin 300070, China; Tang Center for Herbal Medicine Research, University of Chicago, Chicago, IL 60637, USA. Electronic address: longhui804@163.com.

Abstract

Allopurinol is a commonly used medication to treat hyperuricemia and its complications. Pallidifloside D, a saponin glycoside constituent from the total saponins of Smilax riparia, had been proved to enhanced hypouricemic effect of allopurinol based on uric acid metabolism enzyme XOD. In this study, we evaluated whether Pallidifloside D (5mg/kg) enhanced hypouricemic effect of allopurinol (5mg/kg) related to others uric acid metabolism enzymes such as PRPS, HGPRT and PRPPAT. We found that, compared with allopurinol alone, the combination of allopurinol and Pallidifloside D significantly up-regulated HGPRT mRNA expression and down-regulated the mRNA expression of PRPS and PRPPAT in PC12 cells (all P<0.01). These results strongly suggest that hypouricemic effect of allopurinol are improved by Pallidifloside D via numerous mechanisms and our data may have a potential value in clinical practice in the treatment of gout and other hyperuricemic conditions.

KEYWORDS:

Allopurinol; HGPRT; Hyperuricemia; PRPPAT; PRPS; Pallidifloside D

PMID:
27370097
DOI:
10.1016/j.fitote.2016.06.015
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center