Highly Ordered Pd Nanowire Array by Template Fabrication for Propanol Electrooxidation

Highly ordered Pd nanowire arrays (NWAs) prepared by electrodeposition method using the fresh prepared anodic aluminum oxide (AAO) as the template have been characterized by X-ray diffraction pattern (XRD), X-ray photoelectron spectroscopy (XPS), transmission electron microscope (TEM), scanning electron microscopy (SEM), and electrochemical measurements. SEM results revealed that the brush-shaped Pd NWAs are dispersed uniformly. The diameter and length of the obtained Pd NWAs are about 50 nm and 850 nm, respectively. Furthermore, the electrocatalytic activity of Pd NWAs electrode for propanol oxidation in alkaline media has also been studied. It is found that the obtained nanostructurs exhibit excellent electrocatalytic activity toward the oxidation of propanol, demonstrating the potential application in portable direct alcohol fuel cells (DAFCs)

Mice Deficient in Cyp4a14 Have An Increased Number of Goblet Cells and Attenuated Dextran Sulfate Sodium-Induced Colitis

Background/Aims: Cyp4a14 is a member of cytochrome P450 (Cyp450) enzyme superfamily that possesses NADPH monooxygenase activity, which catalyzes omega-hydroxylation of medium-chain fatty acids and arachidonic acid. Study suggests that down-regulation of Cyp4a14 has an anti-inflammatory response in intestine. The present study was to test the function of Cyp4a14 in dextran sulfate sodium (DSS)-induced colitis. Methods: Female Cyp4a14-knockout (KO) and wild-type (WT) mice were treated with DSS for 6 days to induce colitis. The colon of mice was histologically observed by hematoxylin and eosin (H&E) and periodic acid Schiff (PAS) staining. The serum malondialdehyde (MDA), an endogenous indicator of oxidative stress, was chemically measured. Proinflammatory and NADPH oxidase genes were examined by quantitative polymerase chain reaction (qPCR). Results: Cyp4a14-KO mice had a significantly higher number of goblet cells in the colon and were more resistant to DSS-induced colitis compared with the WT mice. The DSS-treated KO mice had lower levels of MDA. Consistent with the milder inflammatory pathological changes, DSS-treated KO mice had lower levels of IL-1β, IL-6 and TNF-α mRNA in the liver and the colon. Moreover, the colon of DSS-treated Cyp4a14-KO and WT mice had higher mRNA levels of two members of NADPH oxidases, Nox2 and Nox4, suggesting that both Nox2 and Nox4 are inflammatory markers. By contrast, DSS-treated WT and KO mice had drastically decreased epithelium-localized Nox1 and dual oxidase (Duox) 2 mRNA levels, coinciding with the erosion of the mucosa induced by DSS. Conclusion: These results suggests a hypothesis that the increased goblet cell in the colon of Cyp4a14-KO mice provides protection from mucosal injury and Cyp4a14-increased oxidative stress exacerbates DSS-induced colitis. Therefore, Cyp4a14 may represent a potential target for treating colitis

The modulation of endoplasmic reticulum stress by chemical chaperone upregulates immune negative cytokine IL-35 in apolipoprotein E-deficient mice.

Interleukin (IL)-35 is a newly identified immune negative molecule which is secreted by CD4(+)Foxp3(+) T regulatory cells (Tregs) and contributes to their suppressive capacity. Early data have shown that IL-35 inhibits development of several autoimmune diseases. However, the role of IL-35 in atherosclerosis, a lipid-driven chronic inflammatory disease in arterial wall, remains to be investigated. Here, we found that IL-35 was involved in atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice. ApoE(-/-) mice with established atherosclerotic lesion displayed a lower level of IL-35 compared to age-matched wild type C57BL/6 mice without plaque. However, IL-35 expression increased significantly in ApoE(-/-) mice with attenuated plaque. More importantly, we found that modulation of ER stress treated by chemical chaperone, 4-Phenyl butyric acid (PBA) in vivo, mainly upregulated immune negative regulating molecule IL-35, as well as IL-10 and Foxp3, accompanied by increased Tregs. However, no obvious impact on pro-inflammatory molecules such as TNF-α, IFN-γ, IL-17 and IL-23 was observed, which provides new insight into the benefit of ER stress recovery from attenuated plaque. Our results suggest that IL-35 might have a potential value for atherosclerotic therapy

The influence of PBA treatment on cytokines in arterial wall.

<p>The expression of cytokine mRNAs in the thoracic and abdominal aorta was quantified by real -time PCR analysis and normalized to β-actin. Fold-changes in expression in PBA treated mice relative to controls are shown. <b>A.</b> IL-35-related four subunits, EBI3, IL-12a, IL-12b and p28. <b>B.</b> IL-10 and TGF-β. <b>C. TNF-α,</b> IFN-γ, IL-17 and <b>IL-23</b>. (n = 6 per group). *p<0.05, **p<0.01, ***p<0.001.</p

IL-35 expression in ApoE^−/− mice with atherosclerotic plaque.

<p><b>A.</b> Serum was obtained from C57BL/6 and ApoE^−/− mice at 8 weeks of age fed with normal diet, without plaque (8 weeks) and at 16 weeks of age, after 8 weeks on a high-fat diet, C57BL/6 without plaque and ApoE^−/− mice with established plaque (16 weeks). The concentrations of IL-35 (pg/mL) in serum were detected by ELISA. <b>B.</b> Total RNA was isolated from thoracic and abdominal aorta of C57BL/6 and ApoE^−/− mice at 8 weeks of age fed with normal diet, without plaque (8 weeks) and at 16 weeks of age, for 8 weeks after high-fat diet, C57BL/6 without plaque and ApoE^−/− mice with established plaque (16 weeks). The expression of IL-35-related subunits was analyzed by real-time PCR. (n = 3 per group), *p<0.05,***p<0.001.</p

PBA treatment influenced the stability of plaque.

<p>Representative photomicrographs and the quantitative analysis of smooth muscle cell (SMC), CD3, macrophage (Mφ), and TUNEL in lesion of aortic root of ApoE^−/− mice. The aortic root sections were stained with rabbit polyclonal to α- smooth muscle actin, rat anti-mouse macrophage Moma-2 and rat anti mouse CD3. The content of macrophage, smooth muscle cell, CD3 T cell in lesion was analyzed respectively by immunohistochemistry. For detection of cell apoptosis, sections were incubated with anti-TUNEL antibody and the content of apoptotic cells was analyzed by immunofluorescence. (n = 10 per group), *p<0.05, **p<0.01, ***p<0.001.</p

PBA treatment impacted Treg cells.

<p><b>A.</b> Spleen cells were obtained from ApoE^−/− mice with or without PBA treatment and percentage of CD4+ T cells in spleen cells and percentage of CD4+Foxp3+ Tregs in total CD4+ T cells was analyzed by flow cytometry. <b>B.</b> The expression of Foxp3 mRNAs in the thoracic and abdominal aorta was quantified by real time-PCR analysis. Normalized to β-actin, fold-changes in expression in PBA treated mice relative to controls are shown. <b>C</b>. The expression of Foxp3 in plaque was analyzed by immunohistochemistry and immunofluorescence. The bright red dots in pictures are Foxp3⁺ cells (n = 6 per group). *P<0.05, ***p<0.001.</p