Role of Toll-like receptor 4 and Janus kinase and signal transducer and activator of transcription s

• 作 者: Haiyan Yin Jianrui Wei Rui Zhang Xiaoling Ye Youfeng Zhu
• 机 构: ICU Department,Guangzhou Red Cross Hospital Affiliated to Medical College of Jinan University,Guangz
• 出 处: 中国神经再生研究（英文版）
• 发表日期: 2011年32期
• 关键词: brain damage Janus kinase and signal transducer and activator of transcription s

The Janus kinase and signal transducer and activator of transcription (JAK/STAT) signal transduction pathway is involved in sepsis-induced functional damage to the heart, liver, kidney, and other organs.However, the cellular and molecular mechanisms underlying sepsis-induced brain damage remain elusive.In the present study, we found severe loss of neurons in the hippocampal CA1 region in rats with sepsis-induced brain damage following intraperitoneal injection of endotoxin, The expression of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 was significantly increased in brain tissues following lipopolysaccharide exposure.AG490 (JAK2 antagonist) and rapamycin (STAT3 antagonist) significantly reduced neuronal loss and suppressed the increased expression of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 in the hippocampal CA1 region in sepsis-induced brain damaged rats.Overall, these data suggest that blockade of the JAK/STAT signal transduction pathway is neuroprotective in sepsis-induced brain damage via the inhibition of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 expression.