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Diabetes can cause serious health complications, which can affect every organ of the body, including the skin. The molecular etiology has not yet been clarified for all diabetic skin conditions. Thus, this study aimed to investigate the changes of diabetes in skin compared to non-diabetic skin in rats. Fifteen days after establishing the diabetic status, skin samples from the dorsum-cervical region were harvested for subsequent analysis of alterations caused by diabetes. Our results demonstrate that diabetes stimulated higher inflammation and oxidative stress in skin, but antioxidant defense levels were lower compared to the non-diabetic group (p < 0.05). This could have been related to a decreased number of blood vessels and low expression of VEGF, eNOS and TGF-β1. Finally, insulin signaling proteins IRS, Akt, Shc and ERK showed a low expression in the diabetic group. Thus, our study shows that the pathology of diabetes induced immunohistopathological and biochemical skin changes compared to non-diabetic skin in rats., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Nitric oxide (NO) levels increase considerably after 24h of exposure of skin to ultraviolet B (UVB) radiation, which leads to nitrosative skin injury. In addition, increased NO levels after exposure to UVB radiation are associated with inhibition of cell proliferation. Compared to the UV-control group, UV-genistein at 10 mg/kg (UV-GEN10) group showed tissue protection, decreased lipid peroxide and nitrotyrosine formation, and low CAT activity. Furthermore, NO levels and iNOS labeling remained high. In this group, the reduction in lipid peroxides and nitrotyrosine was accompanied by upregulation of cell proliferation factors (Ki67 and PCNA), which indicated that prevention of nitrosative skin injury promoted cell proliferation and DNA repair. Genistein also prevented nitrosative events, inhibited ONOO(-) formation, which leads to tissue protection and cell proliferation. The UV-GEN15 group did not result in a greater protective effect compared to that with UV-GEN10 group. In the UV-GEN15 group, histological examination of the epidermis showed morphological alterations without efficient protection against lipid peroxide formation, as well as inhibition of Ki67 and PCNA, and VEGF labeling, which suggested inhibition of cell proliferation. These results help to elucidate the mechanisms underlying the photoprotective effect of genistein and reveal the importance of UVB radiation-induced nitrosative damage., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Rosmarinic acid (RosmA) demonstrates antioxidant and anti-inflammatory properties. We investigated the effect of RosmA on liver ischemia/reperfusion injury. Rats were submitted to 60 min of ischemia plus saline or RosmA treatment (150 mg/kg BW intraperitoneally) followed by 6 h of reperfusion. Hepatocellular injury was evaluated according to aminotransferase activity and histological damage. Hepatic neutrophil accumulation was also evaluated. Oxidative/nitrosative stress was estimated by measuring the reduced glutathione, lipid hydroperoxide and nitrotyrosine levels. Endothelial and inducible nitric oxide synthase (eNOS/iNOS) and nitric oxide (NO) were assessed with immunoblotting and chemiluminescence assays. Hepatic tumor necrosis factor-alpha (TNF-α) and interleukin-1beta mRNA were assessed using real-time PCR, and nuclear factor-kappaB (NF-κB) activation was estimated by immunostaining. RosmA treatment reduced hepatocellular damage, neutrophil infiltration and all oxidative/nitrosative stress parameters. RosmA decreased the liver content of eNOS/iNOS and NO, attenuated NF-κB activation, and down-regulated TNF-α and interleukin-1beta gene expression. These data indicate that RosmA exerts anti-inflammatory and antioxidant effects in the ischemic liver, thereby protecting hepatocytes against ischemia/reperfusion injury. The mechanisms underlying these effects may be related to the inhibitory potential of RosmA on the NF-κB signaling pathway and the reduction of iNOS and eNOS expressions and NO levels, in addition to its natural antioxidant capability.

Riboflavin has been shown to exhibit anti-inflammatory and antioxidant properties in the settings of experimental sepsis and ischaemia/reperfusion (I/R) injury. We investigated the effect of riboflavin on normothermic liver I/R injury. Mice were submitted to 60 min of ischaemia plus saline or riboflavin treatment (30 μmoles/kg BW) followed by 6 h of reperfusion. Hepatocellular injury was evaluated by aminotransferase levels, reduced glutathione (GSH) content and the histological damage score. Hepatic neutrophil accumulation was assessed using the naphthol method and by measuring myeloperoxidase activity. Hepatic oxidative/nitrosative stress was estimated by immunohistochemistry. Liver endothelial and inducible nitric oxide synthase (eNOS/iNOS) and nitric oxide (NO) amounts were assessed by immunoblotting and a chemiluminescence assay. Riboflavin significantly reduced serum and histological parameters of hepatocellular damage, neutrophil infiltration and oxidative/nitrosative stress. Furthermore, riboflavin infusion partially recovered hepatic GSH reserves and decreased the liver contents of eNOS/iNOS and NO. These data indicate that riboflavin exerts antioxidant and anti-inflammatory effects in the ischaemic liver, protecting hepatocytes against I/R injury. The mechanism of these effects appears to be related to the intrinsic antioxidant potential of riboflavin/dihydroriboflavin and to reduced hepatic expression of eNOS/iNOS and reduced NO levels, culminating in attenuation of oxidative/nitrosative stress and the acute inflammatory response., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Arrabidaea chica leaf extract has been used by people as an anti-inflammatory and astringent agent as well as a remedy for intestinal colic, diarrhea, leucorrhea, anemia, and leukemia. A. chica is known to be a good producer of phenolics. Therefore, in the present study, we investigated its antioxidant activity. The phenolic composition of A. chica leaves was studied by liquid chromatography coupled to diode array detection (LC-DAD) and liquid chromatography coupled to electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS), and isoscutellarein, 6-hydroxyluteolin, hispidulin, scutellarein, luteolin, and apigenin were identified. The extract from leaves of A. chica was tested for antioxidant activity using the 2,2-diphenyl-1-picrylhydrazyl (DPPH) method, β-carotene bleaching test, and total reactive antioxidant potential (TRAP) method. The crude extract quenched DPPH free radicals in a dose-dependent manner, and the IC50 of the extract was 13.51 µg/mL. The β-carotene bleaching test showed that the addition of the A. chica extract in different concentrations (200 and 500 µg/mL) prevented the bleaching of β-carotene at different degrees (51.2% ±3.38% and 94% ±4.61%, respectively). The TRAP test showed dose-dependent correlation between the increasing concentrations of A. chica extract (0.1, 0.5, and 1.0 µg/mL) and the TRAP values obtained by trolox (hydro-soluble vitamin E) 0.4738±0.0466, 1.981±0.1603, and 6.877±1.445 µM, respectively. The 2 main flavonoids, scutellarein and apigenin, were separated, and their antioxidant activity was found to be the same as that of the plant extract. These 2 flavonoids were quantified in the plant extract by using a validated HPLC-UV method. The results of these tests showed that the extract of A. chica had a significant antioxidant activity, which could be attributed to the presence of the mixture of flavonoids in the plant extract, with the main contribution of scutellarein and apigenin.

Nitric oxide (NO) is produced by various mammalian cells and plays a variety of regulatory roles in normal physiology and in pathological processes. This article provides evidence regarding the participation of NO in UVB-induced skin lesions and in the modulation of skin cell proliferation following UVB skin irradiation. Hairless mice were subjected to UVB irradiation for 3 hours and the skin evaluated immediately, 6 and 24 hours postirradiation. The skin lipid peroxidation, and NO levels evaluated by chemiluminescence and inducible nitric oxide synthase (iNOS) and nitrotyrosine immunolabelling increased significantly 24 hours after irradiation and decreased under the treatment with aminoguanidine (AG). On the other hand, cell proliferation markers, PCNA and VEGF showed a strong labelling index when AG was used. The data indicate that NO mediates, at least in part, the lipid peroxidation and protein nitration and also promotes the down regulation of factors involved in cell proliferation. This work shows that the NO plays an important role in the oxidative stress damage and on modulation of cell proliferation pathways in UVB irradiated skin.

This study provides evidence that skin oxidative stress injury caused by UVB irradiation is mediated predominantly by reactive oxygen species immediately after irradiation and by reactive nitrogen species at later time points. Animals were pre-treated with free radical scavengers (deferrioxamine, histidine), α-tocopherol, or inhibitors of nitric oxide synthase (NOS) (L-NAME or aminoguanidine) or left untreated and subjected to UVB irradiation. α-Tocopherol inhibited the increase in lipid peroxidation, as evaluated by chemiluminescence at 0 h and 24 h after UVB irradiation. Immediately after UVB irradiation, lipid peroxidation increased moderately and was abolished by free radical scavengers but not by NOS inhibitors. Likewise, the reduction of antioxidant capacity was not reversed by NOS inhibitors. Nitric oxide augmentation was not observed at this time point. Twenty-four hours after irradiation, increased lipid peroxidation levels and nitric oxide elevation were observed and were prevented by NOS inhibitors. Low concentrations of GSH and reduced catalase activity were also observed. Altogether, these data indicate that reactive oxygen species (singlet oxygen and hydroxyl radicals) are the principal mediators of immediate damage and that reactive nitrogen species (*NO and possibly ONOO(-)) seem to be involved later in skin oxidative injury induced by UVB radiation. The reduced catalase activity and low level of GSH suggest that *NO and H(2)O(2) may react to generate ONOO(-), a very strong lipid peroxidant species., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The impact of chronological aging and photoaging on the skin is particularly concerning, especially when oxidative stress is involved. This article provides evidence of quantitative and qualitative differences in the oxidative stress generated by chronological aging and photoaging of the skin in HRS/J hairless mice. Analysis of the results revealed an increase in lipid peroxides as the skin gets older and in photoaged skin (10.086 ± 0.70 η MDA/mg and 14.303 ± 1.81 η MDA/mg protein, respectively), although protein oxidation was only verified in chronological aged skin (15.449 ± 0.99 η protein/mg protein). The difference between both skin types is the decay in the capacity of lipid membrane turnover revealed by the dislocation of older skin to the left in the chemiluminescence curve. Imbalance between antioxidant and oxidation processes was verified by the decrease in total antioxidant capacity of chronological and photoaged skins. Although superoxide dismutase remained unchanged, catalase increased in the 18 and 48-week-old skin groups and decreased in irradiated mice, demonstrating that neither enzyme is a good parameter to determine oxidative stress. The differences observed between chronological and photoaging skin represent a potential new approach to understanding the phenomenon of skin aging and a new target for therapeutic intervention., (Copyright © 2011 Elsevier B.V. All rights reserved.)

1. Outer-membrane protein patterns of Escherichia coli recovered from the peritoneal cavities of infected guinea pigs and grown in medium M9 containing 2,2'-dipyridyl were studied by polyacrylamide gel electrophoresis (SDS-PAGE) to determine whether in vivo conditions of growth affected the expression of these bacterial surface proteins. 2. Eleven strains of septicemic E. coli studied in vitro under conditions of iron restriction expressed iron-regulated outer-membrane proteins, mainly the protein of approximately 74 kDa, whereas avirulent strains grown under similar conditions did not present the 74-kDa protein. 3. These results show the distribution of iron-regulated outer-membrane proteins among avian E. coli and suggest that the protein of approximately 74 kDa may be important for the virulence of these strains.