Title : Obesity Promotes Experimental Colitis by Increasing Oxidative Stress and Mitochondrial Dysfunction in the Colon.

Pub. Date : 2020 Oct

PMID : 32495128






4 Functional Relationships(s)
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1 After HCT116 cells were treated with palmitate acid (PA) and/or TNF-alpha for 24 h, the combination of PA and TNF-alpha increased ROS production, promoted mitochondrial dysfunction, and activated the pro-apoptotic pathway, but these effects were markedly attenuated by a ROS inhibitor. Reactive Oxygen Species tumor necrosis factor Homo sapiens
2 After HCT116 cells were treated with palmitate acid (PA) and/or TNF-alpha for 24 h, the combination of PA and TNF-alpha increased ROS production, promoted mitochondrial dysfunction, and activated the pro-apoptotic pathway, but these effects were markedly attenuated by a ROS inhibitor. Reactive Oxygen Species tumor necrosis factor Homo sapiens
3 After HCT116 cells were treated with palmitate acid (PA) and/or TNF-alpha for 24 h, the combination of PA and TNF-alpha increased ROS production, promoted mitochondrial dysfunction, and activated the pro-apoptotic pathway, but these effects were markedly attenuated by a ROS inhibitor. Reactive Oxygen Species tumor necrosis factor Homo sapiens
4 After HCT116 cells were treated with palmitate acid (PA) and/or TNF-alpha for 24 h, the combination of PA and TNF-alpha increased ROS production, promoted mitochondrial dysfunction, and activated the pro-apoptotic pathway, but these effects were markedly attenuated by a ROS inhibitor. Reactive Oxygen Species tumor necrosis factor Homo sapiens