<p>This study aimed at determining the effects of type II collagen (CII)-induced arthritis (CIA) on cardiac homeostasis in the contexts of a laboratory chow (LC) and a Western diet (WD). The influence of dietary docosahexaenoic acid (DHA) was also examined. Sixty female Wistar rats were assigned to five groups. The first two groups were fed the LC and were treated or not with CII (LC + CIA and LC); the third and fourth groups were fed a WD with or without CII treatment (WD + CIA and WD); and the fifth group was treated with CII and it was fed the WD whose 2.5% of the lipid fraction was replaced by DHA (DHA + CIA). Ionic homeostasis, redox status, inflammation markers, and mitochondrial stress were analysed in the heart. CIA reduced the body weight and favoured wasting of the lipid and protein stores. It also reduced cardiac cell density. The CIA subgroups, particularly the WD + CIA rats, showed higher cardiac calcium and lower reduced glutathione to oxidized glutathione ratio. In the LC + CIA rats, no oxidative/nitrosative stress (ONS) was noticed and the mitochondrial extraction yield (MEY) was similar to that measured in the LC subgroup. In contrast, the ONS was higher and the MEY was lower in the WD + CIA subgroup compared to the WD one. The observed differences were not due to inflammation. DHA had little effect on the cardiac consequences of CIA. In conclusion, the WD amplified the deleterious effects of CIA on cardiac homeostasis by weakening the mitochondria via an increased ONS.</p>

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A western diet amplified the deleterious consequences of collagen-induced arthritis on cardiac homeostasis in female rats

  • Chrystèle Jouve,
  • Jean-Paul Rigaudiere,
  • Véronique Patrac,
  • Frédéric Capel,
  • Luc Demaison,
  • Anne Tournadre

摘要

This study aimed at determining the effects of type II collagen (CII)-induced arthritis (CIA) on cardiac homeostasis in the contexts of a laboratory chow (LC) and a Western diet (WD). The influence of dietary docosahexaenoic acid (DHA) was also examined. Sixty female Wistar rats were assigned to five groups. The first two groups were fed the LC and were treated or not with CII (LC + CIA and LC); the third and fourth groups were fed a WD with or without CII treatment (WD + CIA and WD); and the fifth group was treated with CII and it was fed the WD whose 2.5% of the lipid fraction was replaced by DHA (DHA + CIA). Ionic homeostasis, redox status, inflammation markers, and mitochondrial stress were analysed in the heart. CIA reduced the body weight and favoured wasting of the lipid and protein stores. It also reduced cardiac cell density. The CIA subgroups, particularly the WD + CIA rats, showed higher cardiac calcium and lower reduced glutathione to oxidized glutathione ratio. In the LC + CIA rats, no oxidative/nitrosative stress (ONS) was noticed and the mitochondrial extraction yield (MEY) was similar to that measured in the LC subgroup. In contrast, the ONS was higher and the MEY was lower in the WD + CIA subgroup compared to the WD one. The observed differences were not due to inflammation. DHA had little effect on the cardiac consequences of CIA. In conclusion, the WD amplified the deleterious effects of CIA on cardiac homeostasis by weakening the mitochondria via an increased ONS.