**5. Conclusions**

Hydroxychloroquine has a significant protective impact on endothelial function acting via the suppression of NOX-induced oxidative stress; it is unable to mitigate all of the e ffects of preeclamptic sera-induced injury in vitro or to mitigate ex vivo placental injury. Further evaluation is warranted to determine other molecular pathways by which hydroxychloroquine may prevent endothelial dysfunction in preeclampsia. The results of this study strongly sugges<sup>t</sup> that hydroxychloroquine seems likely to be clinically effective as adjuvant therapy in women diagnosed with preeclampsia.

**Author Contributions:** All authors have read and agree to the published version of the manuscript. Conceptualization, R.A.R., P.M., and E.M.W.; methodology, R.A.R. and P.M.; software, B.L.; validation, H.S. and P.M.; formal analysis, R.A.R., H.M., and P.M.; investigation, R.L.; data curation, S.G.; writing and editing—original draft preparation, R.A.R.; writing—review and editing, P.M. and E.M.W.; visualization, H.M.; supervision, P.M. and E.M.W.; project administration, E.M.W.; funding acquisition, E.M.W.

**Funding:** R.A.R. was supported by The Ministry of Higher Education of Malaysia.

**Acknowledgments:** We would like to acknowledge all mothers who donated their placenta and the staff at Monash Medical Centre, Clayton, Australia, for their assistance with collecting these tissue samples. Monash Health is supported by the Victorian Government's Operational Infrastructure Support Program.

**Conflicts of Interest:** The authors declare no conflict of interest.
