title: [Activation of TNF-α and signaling pathway in the hypothalamus of the rats subjected to chronic unpredictable mild stressors after middle cerebral artery occlusion].
abstract: This study was aimed to investigate the changes of the hypothalamic-pituitary-adrenal axis (HPAA) activity and the cytokines system in the hypothalamus of the depressive rats which were exposed to chronic unpredictable mild stressors (CUMS) after middle cerebral artery occlusion (MCAO). By means of qRT-PCR, ELISA and Western blot, mRNA and/or protein expressions of corticotropin releasing factor (CRF), tumor necrosis factors-α (TNF-α), suppressor of cytokines signaling 3 (SOCS3), phosphorylation of signal transducers and activators of transcription 3 (pSTAT3) were measured in the hypothalamus of rats. The results showed that, compared with control group, CUMS+MCAO group exhibited increased mRNA levels of CRF, TNF-α, SOCS3, as well as up-regulated CRF, TNF-α, SOCS3 and pSTAT3 protein expressions. Furthermore, there were correlations between CRF and TNF-α, TNF-α and SOCS3, SOCS3 and pSTAT3, respectively. These observations indicated the CRF system was activated in the post stroke depression (PSD) status. The TNF-α and its signaling pathway, STAT3/SOCS3, were up-regulated in mRNA and protein levels. In conclusion, this study presents the evidence which supports the hypothesis of signaling cross-talk between the CRF system and TNF-α signaling pathway after ischemic stroke and CUMS.
authors.affiliation: Department of Neurology in Nanlou Clinical Division, PLA General Hospital, Beijing 100853, China. jessicass33@gmail.com.
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Wang
authors.forename: Hai-Ying
authors.initials: HY
authors.lastname: Chen
authors.forename: Hong
authors.initials: H
authors.lastname: Sun
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.forename: Jin-Qun
authors.initials: JQ
authors.lastname: Guan
mesh_terms: D000818:Animals; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology*; D020244:Infarction, Middle Cerebral Artery; D010766:Phosphorylation; D010913:Pituitary-Adrenal System / Q000502:physiology; D051381:Rats; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D050796:STAT3 Transcription Factor; C491410:Socs3 protein, rat; C494088:Stat3 protein, rat; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D014409:Tumor Necrosis Factor-alpha