【摘 要】
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Objective: Surgical trauma stress has been reported to induce immunosuppression.The mechanisms involved are still unclear.The mitogen-activated protein kinases (MAPK) transmit extracellular stimuli in
【机 构】
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Department of Integrative Medicine and Neurobiology, Institute of Acupuncture Research WHO Collabora
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Objective: Surgical trauma stress has been reported to induce immunosuppression.The mechanisms involved are still unclear.The mitogen-activated protein kinases (MAPK) transmit extracellular stimuli into intracellular transcriptional and post-translational responses.Activation of the intracellular signal transduction pathways ERK1/2 in cortex may contributes to post-traumatic immunosuppression.In the present study we investigated the role of the activation of ERK5, a new member of MAPK family, in a surgical trauma stress induced immunosuppression model.Methods: The phosphorylation of ERK5 in cortex was measured by immunohistochemistry and western blot assay.The specific ERK5 inhibitor BIX02188 was administrated by intracerebroventricular (icv.) injection to traumatic rat, and the NK cell activity and lymphocyte proliferation was conducted to estimate the immune response in vitro.Results: (1) ERK5 was activated in rat cortex 24 h post surgical trauma stress; (2) Icy.of BIX02188 (4 nmol or 20 nmol), an inhibitor of ERK5 phosphorylation, antagonized the surgical trauma induced downregulation of NK cell activity and lymphocyte proliferation.Conclusion: These findings suggest that ERK5 play an important role in post-traumatic immunodepression.
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