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2016-01-01 - Article/Dans un journal avec peer-review - Anglais - 27 page(s)

Bunel Valérian , Antoine Marie-Hélène, Stévigny Caroline, Nortier Joëlle, Duez Pierre , "New in vitro insights on a cell death pathway induced by magnolol and honokiol in aristolochic acids tubulotoxicity" in Food & Chemical Toxicology, 87, 77-87, doi:10.1016/j.fct.2015.11.020

  • Edition : Elsevier Science, Exeter (United Kingdom)
  • Codes CREF : Chimie analytique (DI1314), Pharmacognosie (DI3410), Sciences pharmaceutiques (DI3400), Toxicologie pharmaceutique (DI3440)
  • Unités de recherche UMONS : Chimie thérapeutique et Pharmacognosie (M136)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
Texte intégral :

Abstract(s) :

(Anglais) Aristolochic acids (AA) are nephrotoxic agents found in Aristolochia species whose consumption leads to the onset of a progressive tubulointerstitial fibrosis. This AA-nephropathy was first reported during the Belgian outbreak of the 1990's in which more than a hundred patients consumed slimming pills containing an Aristolochia species and Magnolia officinalis. The patients developed an end-stage kidney disease requiring dialysis or transplantation. Magnolol and honokiol are bioactive compounds from M. officinalis known for their potent antioxidant activity. As they can alleviate oxidative stress, we investigated their respective effects on AA-mediated tubulotoxicity using HK-2 cells. Magnolol and honokiol were able to reduce the oxidative stress associated with AA-treatment. Cytotoxicity alleviation was further investigated and overall cell viability measurements unexpectedly revealed that both compounds worsened the survival of AA-treated cells. Flow cytometry analyses of annexin V/PI stained cells indicated that the lignans efficiently prevented AA-induced apoptosis; but favored necrosis. Microscopy observations highlighted extensive vacuolization; other types of cell death, including autophagy, paraptosis or accelerated senescence were excluded. Ki-67 index and cell cycle analysis indicated that both magnolol and honokiol inhibited proliferation by blocking the cell cycle at the G1 phase; they also prevented the AA-induced G2/M arrest.