title: [The levels of neuropeptide S in the brain of asthmatic mice with anxiety and the relationship with the inflammatory mediators].
abstract: Objective:To investigate the levels of neuropeptide S in the brain of asthmatic mice with anxiety and the effects of inflammatory mediatores on changes of neuropeptide S inin vitroexperiments.Methods:According to the random number table method, 40 BALB/C mice were randomly divided into 4 groups: the control group, the asthma group, the anxiety group and the asthma and anxiety group. The relative expressions of neuropeptide S mRNA in the brain tissue of each group were detected by quantitative real-time polymerase chain reaction(QRT-PCR). Rat cortex neurons obtained by primary culture were divided into 4 groups: the PBS control group, the interleukin-1 beta group, the interleukin-6 group and the tumor necrosis factor-alpha group. After stimulation with inflammatory cytokines the mRNA expressions of neuropeptide S were measured by QRT-PCR and neuropeptide S levels in the cell culture supernatants were measured by emzyme linked immunosorbent assay(ELISA).Results:The relative expressions of neuropeptide S mRNA were decreased in the anxiety group(0.87±0.05) and the asthma and anxiety group(0.79±0.03)compared with the control group(1.00±0.05)and the asthma group(0.96±0.06), most notably in the asthma and anxiety group (allP<0.05). Compared to the PBS control group[(1.00±0.06), (50.6±1. 8)ng/L] and the interleukin-1 beta group[(0.94±0.08), (49.5±1.0)ng/L], the levels of neuropeptide S mRNA and neuropeptide S were decreased in the interleukin-6 group[(0.88±0.07), (45.4±1.2)ng/L] and the tumor necrosis factor-alpha group[(0.86±0.07), (46.0±1.0)ng/L](allP<0.05). There were no significant differences between the interleukin-1 beta group and the PBS control group(allP>0.05).Conclusions:Up-regulated interleukin-6 and tumor necrosis factor-alpha in asthma can inhibit the secretion of neuropeptide S in neuronal cells. The decline of brain neuropeptide S, which has anti-anxiety effect, may lead to the occurrence of anxiety, which may be a potential mechanism of comorbidity of asthma and anxiety.
authors: Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
authors: Z
authors: Z
authors: Cheng
authors: P F
authors: PF
authors: Li
authors: L L
authors: LL
authors: Dai
authors: L Q
authors: LQ
authors: Jia
authors: X
authors: X
authors: Wang
authors: Y
authors: Y
authors: Liu
authors: X G
authors: XG
authors: Jing
authors: H
authors: H
authors: Wang
authors: M
authors: M
authors: Liu
authors: L
authors: L
authors: An
mesh_terms: D000818:Animals; D001007:Anxiety; D001249:Asthma; D001921:Brain / Q000378:metabolism*; D016207:Cytokines; D004797:Enzyme-Linked Immunosorbent Assay; D018836:Inflammation Mediators; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009479:Neuropeptides / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D014409:Tumor Necrosis Factor-alpha
chemical_list: D016207:Cytokines; C508600:IL6 protein, human; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D009479:Neuropeptides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha