Planta Med 2017; 83(17): 1335-1341
DOI: 10.1055/s-0043-111012
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Salvia plebeia Extract Inhibits Xanthine Oxidase Activity In Vitro and Reduces Serum Uric Acid in an Animal Model of Hyperuricemia

Jin Kyu Kim1, *, Woo Jung Kim1, *, Jung Mi Hyun1, Jong Suk Lee1, Jin Gwan Kwon1, Changon Seo1, Myung-Jin Song1, Chun Whan Choi1, Seong Su Hong1, Kyuhee Park1, Pansoo Kim1, Hachang Sung2, Jin Koo Lee3, Yongmun Choi1
  • 1Biocenter, Gyeonggido Business and Science Accelerator, Suwon, Korea
  • 2Pharmaceutical development center, CJ HealthCare, Icheon, Korea
  • 3Department of Pharmacology, College of Medicine, Dankook University, Cheonan, Korea
Further Information

Publication History

received 04 April 2017
revised 02 May 2017

accepted 07 May 2017

Publication Date:
18 May 2017 (eFirst)


Hyperuricemia is a clinical condition characterized by an elevated level of serum uric acid and is a key risk factor for the development of gout and metabolic disorders. The existing urate-lowering therapies are often impractical for certain patient populations, providing a rationale to explore new agents with improved safety and efficacy. Here, we discovered that Salvia plebeia extract inhibited the enzyme activity of xanthine oxidase, which is a key enzyme generating uric acid in the liver. In an animal model of hyperuricemia, S. plebeia extract reduced serum urate to the levels observed in control animals. The urate-lowering effect of S. plebeia extract in vivo was supported by the identification of compounds that inhibit xanthine oxidase enzyme activity in vitro. Nepetin, scutellarein, and luteolin contributed significantly to S. plebeia bioactivity in vitro. These compounds showed the highest potency against xanthine oxidase with IC50 values of 2.35, 1.74, and 1.90 µM, respectively, and were present at moderate quantities. These observations serve as a basis for further elaboration of the S. plebeia extracts for the development of new therapeutics for hyperuricemia and related diseases.

* These authors contributed equally to this work.

Supporting Information