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1.
Exp Lung Res ; 43(8): 301-310, 2017 10.
Artigo em Inglês | MEDLINE | ID: mdl-29140131

RESUMO

BACKGROUND: The tumor necrosis factor superfamily member LIGHT (the official gene symbol approved by NCBI Gene Database), an inflammatory factor secreted by T cells after allergen exposure, recently discovered to play crucial roles in asthmatic airway remodeling. However, it is unclear whether LIGHT could be controlled by inhaled corticosteroids, a key component of asthma management. This study was to investigate the effects and potential mechanisms of inhaled budesonide on the expressions of LIGHT and its receptors (LTßR and HVEM) of lung tissues in ovalbumin-sensitized mice. MATERIALS AND METHODS: Thirty-three BALB/c mice were randomly divided into the control, asthma model, and budesonide treatment groups (11 in each group). Mice were sensitized and challenged by OVA to develop mouse model of chronic asthma, and treated with aerosolized budesonide before OVA challenge. Bronchoalveolar lavage fluid (BALF) and lungs were obtained after the final OVA challenge. Protein and mRNA Levels of LIGHT, LTßR, and HVEM in the lungs were investigated by immunohistochemistry, image analysis, and real-time PCR. Expressions of IL-6 and IFN-γ in BALF were measured by ELISA. RESULTS: Inhaled budesonide significantly reduced protein and mRNA levels of lung LIGHT, LTßR, and HVEM in asthmatic mice. Correspondingly, the number of eosinophils and neutrophils and IL-6 levels in BALF after budesonide treatment were found to be decreased, whereas the IFN-γ levels in BALF were increased. Moreover, the expressions of LIGHT and HVEM mRNA showed positive correlation with IL-6 levels in the treatment group. CONCLUSIONS: Inhaled budesonide can down-regulate the expressions of LIGHT, LTßR, and HVEM in the lungs of asthmatic mice, and LIGHT/LTßR/HVEM interactions may be a potentially key target for asthma treatment.


Assuntos
Corticosteroides/farmacologia , Asma/tratamento farmacológico , Fatores de Necrose Tumoral/metabolismo , Corticosteroides/administração & dosagem , Animais , Asma/metabolismo , Budesonida/administração & dosagem , Budesonida/farmacologia , Receptor beta de Linfotoxina/efeitos dos fármacos , Receptor beta de Linfotoxina/metabolismo , Camundongos , Membro 14 de Receptores do Fator de Necrose Tumoral/efeitos dos fármacos , Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo , Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/efeitos dos fármacos , Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
2.
Arch Virol ; 152(7): 1417-24, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17458622

RESUMO

In this paper, we describe that the oxoquinolinic acid derivative (compound A) inhibited HSV-1 adsorption on Vero cells. This effect was achieved with an EC(50) value of 10 +/- 2.0 microM and with low cytotoxicity, since the CC(50) value for compound A was >1000 microM. Moreover, we demonstrate for the first time that adsorption inhibition was due to the blockage of the interactions between HSV-1 and the cellular receptor herpes virus entry mediator (HVEM). These results show that compound A can prevent HSV-1 infection in Vero cells, encouraging further studies to determine at what level compound A inhibits HSV-1-HVEM interactions.


Assuntos
Herpesvirus Humano 1/efeitos dos fármacos , Quinolonas/farmacologia , Membro 14 de Receptores do Fator de Necrose Tumoral/efeitos dos fármacos , Aciclovir/farmacologia , Adsorção , Animais , Antivirais/química , Antivirais/farmacologia , Células CHO , Chlorocebus aethiops , Cricetinae , Cricetulus , Herpesvirus Humano 1/patogenicidade , Técnicas In Vitro , Quinolonas/química , Membro 14 de Receptores do Fator de Necrose Tumoral/fisiologia , Células Vero
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