Redox imbalance is resulted from the destruction of balance between oxidants and antioxidants. The dominant oxidants are reactive oxygen species (ROS), which are involved in multiple cellular processes by physiologically transporting signal as a second messenger or pathologically oxidizing DNA, lipids, and proteins. Generally speaking, low concentration of ROS is indispensable for cell survival and proliferation. However, high concentration of ROS is cytotoxic. Additionally, ROS are now known to induce the oxidative modification of macromolecules especially proteins. The redox modification of proteins is involved in numerous biological processes related to diseases including CRC. Herein, we attempt to afford an overview that highlights the crosstalk between redox imbalance and CRC.

We investigated the effect of 1.4% isoflurane (ISO) on the development of inflammation and apoptosis caused by zymosan (ZY) in mice. We found that ZY-challenged mice exhibited significant body weight loss, markedly high mortality, and significant lung injury characterized by the deterioration of histopathology, histologic scores, and wet-to-dry ratio after ISO treatment. ISO dramatically attenuated ZY-induced lung neutrophil recruitment and inflammation, as evidenced by the reduced levels of total cells, neutrophils, and proinflammatory cytokines (i.e., tumor necrosis factor-α, interleukin- (IL-) 1β, IL-6, and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid and of their mRNA expression in lung tissues. ISO also inhibited ZY-induced expression and activation of nuclear factor-kappaB p65 and inducible nitric oxide synthase in pulmonary tissue. ZY administration also resulted in the upregulation of heme oxygenase-1 expression and activity in the lung, which was further enhanced by ISO treatment. Moreover, ISO markedly prevented ZY-induced pulmonary cell apoptosis in mice, as reflected by the decrease in expression of procaspase-8, procaspase-3, cleaved caspase-8, and cleaved caspase-3, as well as in caspase-3 activity and Bcl-2-associated X/B-cell lymphoma 2 ratio. These results indicate that ISO is a potential therapeutic drug for treating ZY-induced lung injury, and further investigations are warranted.

We found gender differences in leptin levels and leptin-adiposity associations. In both genders, leptin levels were strongly associated with %BF and FMI, particularly in males. Shared genetic factors contributed largely to the phenotypic correlation between leptin and %BF. Our findings underscored the importance of further investigation of leptin as a biomarker of adiposity in adolescents.

Diabetic retinopathy (DR) is a chronic microvascular complication of diabetes that may lead to loss of vision. The pathogenesis of DR is complex and elevated expression levels of T helper (Th)17 cells and interleukin (IL)-17 have been suggested to be associated with the development and progression of DR. Sirtuin 1 (SIRT1) is a nicotinamide-adenine dinucleotide-dependent histone deacetylase that is downregulated in patients with DR. Previous studies have demonstrated that SIRT1 is capable of inhibiting the production of IL-17. In the present study, 19 patients with proliferative diabetic retinopathy (PDR) and 20 non-diabetic controls with idiopathic macular epiretinal membranes were recruited and the SIRT1 expression levels of excised specimens were analyzed using immunohistochemistry. IL-17 expression levels in the sera from patients with PDR and controls were determined by enzyme-linked immunosorbent assay (ELISA). Furthermore, SIRT1 mRNA and protein expression levels in peripheral blood mononuclear cells (PBMCs) from the two groups were analyzed following culture with or without a SIRT1 activator, resveratrol. IL-17 expression levels in the supernatants of PBMCs were determined using ELISA and the results demonstrated that IL-17 expression levels were increased in the sera of patients with PDR, as compared with the controls. Furthermore, increased expression levels of SIRT1 and IL-17 were detected in fibrovascular membranes and PBMCs harvested from patients with PDR, respectively. Notably, SIRT1 mRNA and protein expression levels were decreased in the PBMCs of patients with PDR and IL-17 production was inhibited following SIRT1 activation. The results of the present study indicated that imbalanced IL-17 and SIRT1 expression levels may contribute to the pathogenesis of DR, and SIRT1 may have a protective role in PDR by inhibiting the production of IL-17.