Abnormal Homeostasis in the Redox State and Related Signaling Pathways, in Irritable Bowel Syndrome

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ABSTRACT Background IBS is multifactorial; however, elucidating its underlying mechanisms is crucial for advancing in its diagnosis and management. Aims Evaluate molecular processes related to oxidative stress (OS) and inflammation in IBS and its subtypes. Methods Thirty Rome III‐IBS outpatients and 30 controls were studied for OS biomarkers, including malondialdehyde (MDA), protein carbonyls (PC), reduced glutathione (GSH), and oxidized glutathione (GSSG). Also, serum interleukins (IL‐10, IL‐4, TNF‐α, IL‐6), and the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), nuclear factor erythroid 2‐related factor 2 (Nrf2), and nicotinamide‐adenine‐dinucleotide phosphate (NADPH) catalytic subunit gp91 phox . Results In IBS vs. controls there were higher MDA: 4.44 ± 1.76 vs. 2.42 ± 0.5 nmol/mg/protein ( p < 0.01); GSSG: 57.17 ± 17.49 vs. 42.73 ± 14.26 μM ( p < 0.01); and lower GSH: 26.17 ± 12.36 vs. 38.47 ± 16.71 μM ( p < 0.01). Also, an imbalance in pro‐ and anti‐inflammatory interleukins ( p < 0.01); and higher NF‐κB: 5.33 ± 3.39 vs. 3.08 ± 1.19 ( p = 0.01); gp91 phox : 4.28 ± 1.81 vs. 3.29 ± 1.03 ( p < 0.05); and lower Nrf2: 3.87 ± 2.9 vs. 7.56 ± 2.59 ( p < 0.05). Additionally, there were no significant differences between the IBS subtypes, nor according to severity. Finally, in IBS‐C, MDA correlated with IL‐4, TNF‐α with IL‐10; and in IBS‐D, GSH correlated with IL‐4 and no differences in transcription factors. Conclusions The data demonstrate an alteration in the homeostasis of the cellular redox state in IBS. Also, in IBS‐D, the antioxidant effect counteracts the low‐grade inflammation, whereas in IBS‐C, it is mainly driven by interleukins.

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