16α,17α-Epoxypregnenolone-20-oxime prevent LPS-induced NO production and iNOS expression in BV-2 microglial cells by inhibiting JNK phosphorylation.

The free radical nitric oxide (NO), a main member of neuroinflammatory cytokine and a gaseous molecule produced by activated microglia, has many physiological functions, including neuroinflammation. In the present study, we evaluated the effects of serial 16-dehydropregnenolone-3-acetate derivatives on lipopolysaccharide (LPS)-induced NO production and inducible nitric oxide synthase (iNOS) expression in BV-2 microglial cells. Among the six derivatives tested, the increases in NO production and iNOS expression observed in BV-2 microglial cells after LPS stimulation were significantly inhibited by treatment with 16α, 17α-epoxypregnenolone-20-oxime. Moreover, the inhibitory effect of 16α,17α-epoxypregnenolone-20-oxime on NO production was similar to that of S-methylisothiourea sulfate (SMT), an iNOS inhibitor. Further studies showed that 16α,17α-epoxypregnenolone-20-oxime inhibited c-Jun N-terminal kinase (JNK) phosphorylation but not inhibitor kappa B (IκB)-α degradation. Our data in LPS-stimulated microglia cells suggest that 16α,17α-epoxypregnenolone-20-oxime might be a candidate therapeutic for treatment of NO induced neuroinflammation and could be a novel iNOS inhibitor.

[Molecular mechanism of ORFV intervention strategies based on the UPS of host cell: a review].

In order to compete the antiviral effects of the host cell in the process of infection, ORFV(known as Orf virus) relies on a series of functional genes developed through long-term population evolution, such as interferon resistance genes, Bcl-2 protein genes and cell cycle inhibitor gene and so on, with these weapons this virus is able to effectively counteract immune clearance and immune regulation from a host cell. Concurrently, ORFV also focuses on exploiting signal transduction pathways of the ubiquitin-proteasome system(UPS), circumvents the intracellular signal transduction and CD8+ T activation, for shielding virus particles towards maturation and releasing outside. This review introduced inner link between the UPS of host cell and intervention mechanism by virus, and analyzed the key roles of certains components in UPS, these all together showed the evolution tendency of ORFV that was involved in the designing of inhibition to immune response and for intracellular immune escape upon the selection pressure in host cell infected.

[Molecular characteristics and immune evasion strategies of ORFV: a review].

Contagious ecthyma (also known as orf) is an acute skin zoonosis caused by orf virus (ORFV), which affects sheep, goats and humans. As one of the typical species of the Parapoxvirus genus of the Poxviridae family, orf virus has distinctive and unique characteristics of these species. A range of immuno-modulatory/pathogenesis -related genes acquired by virus that function is to limit (at least transiently) the effectiveness of host immunity during its evolution. This review is aimed to describe the latest progress on the molecular characteristics of ORFV, and upon which we analyzed molecular mechanism of the immune escape designed and a set of strategies developed for ORFV to effective against immune clearance of the host. Known as an essential component in evolutionary system, host is regulated by ORFV for using in population evolution. By the ORFV evolutional immune regulation components and its effect approach, we can understand the viral biological characteristics of ORFV, and it is helpful for us to further study the counter-measures of this disease.

1,1'-Azobis-1,2,3-triazole: a high-nitrogen compound with stable N8 structure and photochromism.

Treatment of 1-amino-1,2,3-triazole with sodium dichloroisocyanurate led to isolation of 1,1'-azobis-1,2,3-triazole, which was well characterized. Its structure was determined by X-ray crystallographic analysis, and its thermal stability and photochromic properties were investigated.

Apoptotic study in Graves disease treated with thyroid arterial embolization.

OBJECTIVE: To investigate apoptosis in the thyroid of Graves disease (GD) induced by thyroid arterial embolization. MATERIALS AND METHODS: Forty one patients with clinically and laboratorily ascertained GD were treated with thyroid arterial embolization and followed up for 3-54 months following embolization. Prior to embolization and at 1, 3, 6, 12 and 36 months following embolization, thyroid autoimmunue antibodies were tested respectively, including thyroid stimulating antibody (TSAb), thyroglobulin antibody (TGAb) and thyroid microsomal antibody (TMAb). Thyroid biopsy was performed under the guidance of computed tomography for immunohistochemistry examination using semi-quantity analysis. RESULTS: The positive staining of Fas and FasL was mostly in the cytoplasma and cell membrane, the positive expression of Bax was mainly in the cytoplasma, and no positive expression of P53 was detected in the thyroid cells before embolization. After arterial embolziation, the positive cell number and staining degree of these genes were both greater than before embolization. CONCLUSION: The treatment method of thyroid arterial embolization can effectively enhance the positive expression of pro-apoptotic genes of Fas, FasL, Bax, Bcl-2 and P53 in GD thyroid, thus promoting apoptosis of GD thyroid and helping restore the thyroid size and function to normal conditions.