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Aims: Our previous studies have shown that N-n-butyl haloperidol iodide (F2) can antagonize myocardial ischemia/reperfusion (I/R) injury by blocking intracellular Ca2+ overload and suppressing Egr-1 overexpression. The present study is to investigate the relation between the reduction of Ca2+ overload and the inhibition of Egr-1 overexpression. Methods: The Sprague-Dawley rat myocardial I/R model and cultured cardiomyocyte hypoxia-reoxygenation (H/R) model were established. Administration of Egr-1 antisense oligodeoxyribonucleotide (AS-ODN) only or combining with F2, Egr-1 protein expression was examined by Western-blot analyses. Hemodynamic parameters, creatine kinase (CK) and lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA), myeloperoxidase (MPO), cardiac troponin I (cTnI), and tumor necrosis factor-α (TNF-α) were measured to assess the degree of injury and inflammation of myocardial tissues and cells. Results: Treatment with Egr-1 AS-ODN significantly reduced Egr-1 protein expression and attenuated injury and inflammation of myocardium caused by I/R or H/R evidenced by the amelioration of hemodynamics, the decrease in leakage of CK, LDH, cTnI, the increase in MDA generation, the decrease in SOD activity, the reduction of MPO activity in myocardial tissues and release of TNF-α from cultured cardiomyocytes. Treatment with F2 combined with Egr-1 AS-ODN, the inhibition of Egr-1 protein expression and inflammation (MPO activity and TNF-α level) were not enhanced, but the protection from myocardial I/R (or H/R) injury was significantly increased in hemodynamics and cytomembrane permeability relative to the using of Egr-1 AS-ODN only. Conclusion: These data suggest that the inhibition of Egr-1 overexpression cannot involve all mechanisms of cardioprotection from I/R injury. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

To evaluate the potential adjuvant effect of chicken interferon-γ (IFN-γ) expressed by recombinant fowlpox virus (rFPV–IFN-γ), SPF chickens and commercial chickens with (MAb+) and without (MAb−) maternal antibodies were immunized with rFPV–IFN-γ plus either H5 subtype avian influenza vaccine based on recombinant fowlpox virus (rFPV–HA) or conventional inactivated vaccine. In the assay of humoral responses, rFPV–IFN-γ plus vaccines induced a slightly lower titre of haemagglutinin inhibition (HI) antibody response than either rFPV–HA or inactivated vaccine alone, in both MAb− and MAb+ chickens. As for protective efficacy, the combinations of rFPV–IFN-γ and both vaccines induced 95–100% protection against lethal challenge with highly pathogenic avian influenza virus in SPF chickens and MAb− chickens, which were equal to those induced by either vaccine alone. However, immunization of MAb+ chickens with 106 pfu rFPV–HA plus 105 pfu rFPV–IFN-γ showed higher protection efficacy (33.5%) than that (11.4–15.8%) induced by treatments with other dosage combinations. These findings show that IFN-γ expressed by recombinant fowlpox virus could not promote HI antibody response induced by H5 avian influenza vaccines in chickens. The results also suggest that rFPV–IFN-γ enhances the protection of chickens in a dose-dependent and immune status-dependent manner. [ABSTRACT FROM PUBLISHER]

Abstract As a newly identified factor in calcium-activated chloride channel, ANO1 participates in various physiological processes like proliferation and differentiation, and expresses in human cardiac fibroblasts. In this experiment, we investigated the function of ANO1 in cardiac fibrosis after myocardial infraction (MI) with methods of Western blotting, Quantitative real-time PCR (qRT-PCR), metabolic reduction of 3-(4,5-dimethylthiozol-2-yl)-2, 5-diphenyltetrazo-lium bromide (MTT), immunofluorescence and confocal imaging, and Masson’s trichrome staining. The results showed that the expression of ANO1 significantly increased in neonatal rats’ cardiac fibroblasts after hypoxia and in cardiac tissues after MI. After ANO1 over-expression, cardiac fibrosis was reduced in vitro and in vivo. Moreover, the expression of TGF-β and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-β/smad3 pathway in rats.