title: [Lipopolysaccharide induces astrocyte activation and downregulates the expression of Kir4.1 channel].
abstract: OBJECTIVE
  To explore the influence of lipopolysaccharide (LPS) on the activation of astrocytes and the expression of the inwardly rectifying K(+) channel Kir4.1.
  
  
  METHODS
  Astrocytes were separated from the cerebral cortex of newborn SD rats and cultured in the presence of LPS or LPS combined with interleukin-1 receptor antagonist (IL-1ra). The cell vitality was detected by MTT assay; the expression of glial fibrillary acidic protein (GFAP) was analyzed by immunocytochemistry; the production of IL-1β was tested by ELISA; the expression of Kir4.1 and IL-1β mRNAs were determined by quantitative real-time PCR.
  
  
  RESULTS
  LPS promoted the activation of astrocytes in a time- and dose-dependent manner. LPS significantly increased the production of IL-1β and the expression of IL-1β mRNA, while decreased the expression of Kir4.1 mRNA in cultured astrocytes. Compared with the LPS group, IL-1ra could effectively reversed the above two results.
  
  
  CONCLUSIONS
  The cultured astrocytes could be activated by LPS; LPS-induced downregulation of Kir4.1 mRNA in cultured astrocytes might be related with the inflammatory cytokine IL-1β.
authors.affiliation: Anhui Clinical and Preclinical Key Laboratory of Respiratory Disease, First Affiliated Hospital, Department of Histology and Embryology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Meiqun
authors.initials: M
authors.lastname: Sun
authors.affiliation: Department of Histology and Embryology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Haiqin
authors.initials: H
authors.lastname: Yan
authors.affiliation: Department of Histology and Embryology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Weiyan
authors.initials: W
authors.lastname: Zou
authors.affiliation: Department of Histology and Embryology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Histology and Embryology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Huihui
authors.initials: H
authors.lastname: Li
authors.affiliation: Anhui Clinical and Preclinical Key Laboratory of Respiratory Disease, First Affiliated Hospital, Bengbu 233030, China. *Corresponding author, E-mail: wangxiaojing8888@163.com.
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Wang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D053590:Interleukin 1 Receptor Antagonist Protein / Q000494:pharmacology; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics*; D011247:Pregnancy; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D000098854:Kcnj10 Channel
chemical_list: D005904:Glial Fibrillary Acidic Protein; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D000098854:Kcnj10 Channel; D008070:Lipopolysaccharides; D024661:Potassium Channels, Inwardly Rectifying