Serum Melatonin And Hippocampus MT1Expression In Asthmatic Rat Models

Purpose To investigate the expression of serum melatonin and hippocampus MelatoninReceptor1(MT1) in the asthmatic rats, and the functions of peripheral melatonin andhippocampus MT1in the development of asthma, and explore the mechanism aboutprobable neuroprotective and neuroimmunomodulatory effects of hippocampus MT1.Methods Sixty male adult SD rats were divided into two groups at random: asthmagroup (n=40) and control group (n=20). In control group, twenty rats were randomlydivided into two groups which sacrificed at day17, ten rats were used for Enzymelinked immunosorbent assay (ELISA), Reverse transcription PCR (RT-PCR) andWestern Blot, and the others were used for Immunohistochemistry (IHC). While inasthma group, forty rats were randomly divided into four groups. One of four weresacrificed at day17for IHC, and the other three groups were sacrificed at day5,10,17respectively for ELISA, RT-PCR and Western Blot. Asthma rat model was establishedby sensitization and challenge with ovalbumin (OVA). IHC, Western Blot, RT-PCRwere used to evaluate the expression of hippocampus MT1. ELISA was used to detectserum melatonin level.Results The asthmatic rat model was successfully duplicated, which had the symptomsof restlessness and impatience, breathlessness, abdominal respiratory rhythms andwheezing rale after challenge with OVA. While the symptoms were not observed incontrol group. The expression of hippocampus MT1at gene and protein levels weresignificantly elevated in asthmatic group (P<0.05) when compared to control group,whereas serum melatonin was obviously reduced (P<0.05). Compared with Day5andDay10in the asthmatic group, there was a significant increase of MT1in hippocampus in Day17(P <0.05), while there was no significant difference between Day5and Day10(P>0.05).Conlusion Melatonin and hippocampus MT1may be involved in the pathogenesis ofasthma. The up-regulation of hippocampus MT1with time-dependent pattern in geneand protein levels may be a compensatory response to decreased peripheral melatoninlevels for augmenting melatonin’s neuroprotective and neuroimmunomodulatory effectsagainst inflammatory reaction and stress in asthma.