Abstract
Bisdemethoxycurcumin is one of the three curcuminoids of turmeric and exhibits good antioxidant activity in animal models. This study is aimed at investigating the effect of bisdemethoxycurcumin on small intestinal mitochondrial dysfunction in lipopolysaccharide- (LPS-) treated broilers, especially on the mitochondrial thioredoxin 2 system and mitochondrial biogenesis. A total of 320 broiler chickens were randomly assigned into four experimental diets using a 2 × 2 factorial arrangement with diet (0 and 150 mg/kg bisdemethoxycurcumin supplementation) and stress (saline or LPS challenge) for 20 days. Broilers received a dose of LPS (1 mg/kg body weight) or sterile saline intraperitoneally on days 16, 18, and 20 of the trial. Bisdemethoxycurcumin mitigated the mitochondrial dysfunction of jejunum and ileum induced by LPS, as evident by the reduced reactive oxygen species levels and the increased mitochondrial membrane potential. Bisdemethoxycurcumin partially reversed the decrease in the mitochondrial DNA copy number and the depletion of ATP levels. Bisdemethoxycurcumin activated the mitochondrial antioxidant response, including the prevention of lipid peroxidation, enhancement of manganese superoxide dismutase activity, and the upregulation of the mitochondrial glutaredoxin 5 and thioredoxin 2 system. The enhanced mitochondrial respiratory complex activities in jejunum and ileum were also attributed to bisdemethoxycurcumin treatment. In addition, bisdemethoxycurcumin induced mitochondrial biogenesis via transcriptional regulation of proliferator-activated receptor-gamma coactivator-1alpha pathway. In conclusion, our results demonstrated the potential of bisdemethoxycurcumin to attenuate small intestinal mitochondrial dysfunction, which might be mediated via activating the mitochondrial antioxidant system and mitochondrial biogenesis in LPS-treated broilers.
Highlights
Chickens suffer from a high prevalence of small intestinal mucosal injury, which poses a major threat to the health of poultry [1]
Did we examine the mitochondrial morphology, reactive oxygen species (ROS) production, mitochondrial membrane potential, mitochondrial redox system, and mitochondrial respiratory complex activity but we discussed the transcriptional regulation of the mitochondrial antioxidant system and mitochondrial biogenesis by bisdemethoxycurcumin treatment
The severely damaged mitochondrial architecture in jejunum and ileum was partially attenuated by dietary bisdemethoxycurcumin treatment in broilers
Summary
Chickens suffer from a high prevalence of small intestinal mucosal injury, which poses a major threat to the health of poultry [1]. Oxidative damage and the subsequent mitochondrial dysfunction are common characteristic features of small intestinal mucosal injury. The inactivation of the mitochondrial redox system induced by excessive reactive oxygen species (ROS) acts causally in mitochondrial dysfunction. Under a sustained high ROS level, nonenzymatic antioxidants are depleted, and antioxidant enzymatic activities are inhibited, resulting in the disruption of redox balance within mitochondria [4]. Several antioxidant and redox systems, such as the glutathione (GSH)-glutaredoxin (Grx) and thioredoxin (Trx) system, participate in ROS elimination and maintaining mitochondrial function in a redox-dependent manner [5]. The Trx system plays an important role in maintaining mitochondrial proteins in their reduced state, which is essential for the modification of mitochondrial function [8]
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