Affiliations 

  • 1 The Ritchie Centre, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton 3168, Melbourne, VIC, Australia; Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton 3168, Melbourne, VIC, Australia; Department of Obstetrics and Gynaecology, Faculty of Medicine, National University of Malaysia, Jalan Yaacob Latiff, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia
  • 2 Department of Medicine, School of Clinical Sciences, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton 3168, Melbourne, VIC, Australia
  • 3 The Ritchie Centre, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton 3168, Melbourne, VIC, Australia
  • 4 The Ritchie Centre, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton 3168, Melbourne, VIC, Australia; Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton 3168, Melbourne, VIC, Australia
  • 5 The Ritchie Centre, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton 3168, Melbourne, VIC, Australia; Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton 3168, Melbourne, VIC, Australia. Electronic address: euan.wallace@monash.edu
Pregnancy Hypertens, 2016 Oct;6(4):259-262.
PMID: 27939463 DOI: 10.1016/j.preghy.2016.09.001

Abstract

Hydroxychloroquine is an anti-malarial drug which, due to its anti-inflammatory and immunomodulatory effects, is widely used for the treatment of autoimmune diseases. In a model of systemic lupus erythematosus hydroxychloroquine has been shown to exert protective endothelial effects. In this study, we aimed to investigate whether hydroxychloroquine was endothelial protective in an in vitro model of TNF-α and preeclamptic serum induced dysfunction. We showed that hydroxychloroquine significantly reduced the production of TNF-α and preeclamptic serum induced endothelin-1 (ET-1). Hydroxychloroquine also significantly mitigated TNF-α induced impairment of angiogenesis. These findings support the further assessment of hydroxychloroquine as an adjuvant therapy in preeclampsia.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.