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Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression.
Du, Juan; Zhang, Chunyan; Na, Xueqing; Li, Aizhi; Zhang, Qingfeng; Li, Kezhong; Ding, Yongbo.
Afiliação
  • Du J; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
  • Zhang C; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
  • Na X; Department of Anesthesiology, Hospital of Kunming Medical University, Kunming, China.
  • Li A; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
  • Zhang Q; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
  • Li K; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
  • Ding Y; Department of Anesthesiology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Braz J Med Biol Res ; 51(6): e7061, 2018.
Article em En | MEDLINE | ID: mdl-29694508
Andrographolide (ANDRO) has been studied for its immunomodulation, anti-inflammatory, and neuroprotection effects. Because brain hypoxia is the most common factor of secondary brain injury after traumatic brain injury, we studied the role and possible mechanism of ANDRO in this process using hypoxia-injured astrocytes. Mouse cortical astrocytes C8-D1A (astrocyte type I clone from C57/BL6 strains) were subjected to 3 and 21% of O2 for various times (0-12 h) to establish an astrocyte hypoxia injury model in vitro. After hypoxia and ANDRO administration, the changes in cell viability and apoptosis were assessed using CCK-8 and flow cytometry. Expression changes in apoptosis-related proteins, autophagy-related proteins, main factors of JNK pathway, ATG5, and S100B were determined by western blot. Hypoxia remarkably damaged C8-D1A cells evidenced by reduction of cell viability and induction of apoptosis. Hypoxia also induced autophagy and overproduction of S100B. ANDRO reduced cell apoptosis and promoted cell autophagy and S100B expression. After ANDRO administration, autophagy-related proteins, S-100B, JNK pathway proteins, and ATG5 were all upregulated, while autophagy-related proteins and s100b were downregulated when the jnk pathway was inhibited or ATG5 was knocked down. ANDRO conferred a survival advantage to hypoxia-injured astrocytes by reducing cell apoptosis and promoting autophagy and s100b expression. Furthermore, the promotion of autophagy and s100b expression by ANDRO was via activation of jnk pathway and regulation of ATG5.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Hipóxia Celular / Astrócitos / Diterpenos / Subunidade beta da Proteína Ligante de Cálcio S100 Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Braz J Med Biol Res Ano de publicação: 2018 Tipo de documento: Article País de afiliação: China País de publicação: Brasil
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Hipóxia Celular / Astrócitos / Diterpenos / Subunidade beta da Proteína Ligante de Cálcio S100 Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Braz J Med Biol Res Ano de publicação: 2018 Tipo de documento: Article País de afiliação: China País de publicação: Brasil