RESUMO
This study explored the potential therapeutic efficacy of GSYJ in attenuating asthma symptom severity and aimed to determine the immunomodulatory mechanism of GSYJ. A mouse model of chronic asthma induced by repeated Dermatophagoides pteronyssinus (Der p) challenge was established. In addition, 30 minutes before Der p challenge, the mice were orally administered GSYJ (1 g/kg). The mice were sacrificed to evaluate inflammatory cell infiltration, collagen deposition in the lung, total IgE in serum, and expression profiles of various cytokines in bronchoalveolar lavage fluid (BALF) and various genes in lung tissue. Furthermore, 30 minutes after the addition of GSYJ to RAW264.7 cell cultures, 100 ng/ml LPS was added to evaluate the effect of the drug on the LPS-induced expression of genes, proteins, and transcription factors. GSYJ may regulate transcription factors (cJUN/IRF3/NF-κB) to decrease the expression of IL-1ß, IL-6, RANTES, and iNOS in macrophages and affect the IL-12, IFN-γ, IL-5, and IL-6 levels in the BALF of mice to relieve asthma symptoms, such as inflammatory cell infiltration, hyperresponsiveness, and increased serum total IgE levels. Therefore, GSYJ has the potential to be developed into a drug treatment for chronic asthma.
RESUMO
This study was designed to monitor the stability of salmon calcitonin during storage conditions, under the electric fields generated during iontophoresis and electroporation, in contact with transdermal glass diffusion cells, and during transport through skin. The formulation in a citrate buffer (pH 4.0) was stable in storage for short-term studies but degraded significantly on extended storage. Albumin was able to minimize adsorption in contact with glass surfaces, and aprotinin was able to minimize proteolytic degradation in contact with skin. The formulation was stable under electric field, but there was a loss due to adsorption if salt bridges were used.
