Study on the molec
Jun Wu1, 2, Zhe Min2, Yongjie Xiong2, Qiuyue Yan2, Yuming Xu1,*, Suming Zhang2,*
1 Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China;
2 Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;
*Co corresponding authors:Yuming Xu. Email: email@example.com; Suming Zhang. Email:firstname.lastname@example.org.
Abstract: Background. The study is to explore the molecular mechanisms of the inflammation induced by β-amyloid (Aβ) in the tissue of cortex and hippocampus of mice. Methods. The tissue of cortex and hippocampus of mice, were exposed to Aβ1-42 with or without Pyrrolidinedithiocarbamate ammonium (PDTC), then Enzyme linked immunosorbent assay (ELISA) for interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα); Quantitative real time polymerase chain reaction (RT-PCR) for IL-1β and TNFα mRNA, western blot analyses of IκBα and NF-κB p65. Results. PDTC inhibited the protein expression of IL-1β, TNFα, IL-1β and TNFα mRNA, inhibited the decreasion of IκBα in the cytoplasm, and also inhibited elevation of NF-κB p65 in the nucleus in Aβ-stimulated tissue of cortex and hippocampus of mice. Conclusion. Our findings suggest that the IL-1β, TNFα protein and mRNA were induced by Aβ via the NF-κB signal pathway in the tissue of cortex and hippocampus of mice.
[Jun Wu, Zhe Min, Yongjie Xiong, Qiuyue Yan, Yuming Xu, Suming Zhang. Study on the molecular mechanisms of the inflammation induced by β-amyloid in vivo. Life Sci J 2012;9(1):750-755] (ISSN:1097-8135). http://www.lifesciencesite.com. 108
Keywords: Aβ; PDTC; IL-1β; TNFα; NF-κB Full Text 108