Chinese Journal of Clinical Anatomy >
The protective effect of chlorogenic acid on Aβ25-35-induced damage to cerebral cortical neurons via macrophage activation
Received date: 2014-01-03
Online published: 2014-06-04
Objective To investigate the effect of chlorogenic acid on cerebral cortical neurons injury induced by amyloid β protein via macrophage activation in vitro. Methods Cerebral cortical neurons were obtained from the cerebellar cortex of Sprague-Dawley (SD) rats and cultured. At the day 8 of culture, peritoneal macrophage of mice were added to the cerebral cortical neurons cultures and continued to be cultured for additional 2 days. Thereafter, Aβ25-35 (10 μmol/L) 10 μl were added into the co-culture of cerebral cortical neurons and macrophages. The experiment was divided into blank isolated culture group, co-culture group, isolated culture Aβ25-35 group, co-culture Aβ25-35 group and co-culture CHA-treated group for 6, 12, 24, 48, 96h, respectively. The survival of neurons and macrophages was detected by an inverted phase contrast microscope. Expressions of p38MAPK, MAPKAPK-2, HSP27 protein were tested by Western blot. Results Application of chlorogenic acid significantly improved the morphology and survival of cerebral cortical neurons damaged by Aβ25-35-induced macrophage activation. In macrophages, the Aβ25-35-induced p38MAPK pathway activation was inhibited by CHA at different time points. Accordingly, both the decreased expressions of phosphorylated MAPKAPK-2 and phosphorylated HSP-27 in macrophages caused by Aβ25-35 exposure were suppressed by CHA. Conclusion Chlorogenic acid is effective in reducing Aβ25-35-induced damage to cerebral cortical neurons co-cultured with macrophages. Its protective effect may be in part achieved by action against the upregulation of p38MAPK expression in macrophages.
Key words： Chlorogenic acid; Aβ25-35; Cerebral cortical neurons; Macrophage; p38MAPK; MAPKAPK-2; HSP27
ZHOU Jing , DIAO Hong , QIN Shu-Jian , TAO Su-Yan , ZHENG De-Yu . The protective effect of chlorogenic acid on Aβ25-35-induced damage to cerebral cortical neurons via macrophage activation[J]. Chinese Journal of Clinical Anatomy, 2014 , 32(3) : 316 -320 . DOI: 10.13418/j.issn.1001-165x.2014
[1] Fan T, Jiang WL, Zhu J, et al. Arctigenin protects focal cerebral ischemia-reperfusio rats through inhibiting neuroinflammation
[J]. Biol Pharm Bull, 2012, 35(11): 2004-2009.
[2] Barnham KJ, Ciccotosto GD, Tickler AK, et al. Neurotoxic, redox competent Alzheimer's b-amyloid is released from lipid membrane by methionine oxidation
[J]. J Biol Chem, 2003, 278(44): 42959-42965.
[3] Hernandez-Ontiveros DG, Tajiri N, Acosta S, et al. Microglia activation as a biomarker for traumatic brain injury
[J]. Front Neurol, 2013, 4:30-32.
[4] Berk M, Dean O, Drexhage H, et al. Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness
[J].BMC Med, 2013, 11(1): 74-76.
[5] Jin Y, Fan Y, Yan EZ, et al. Effects of sodium ferulate on amyloid-beta-induce MKK3/MKK6-p38MAPK-HSP27 signal pathway and apoptosis in rat hippocampus
[J].Acta Pharmacol Sin, 2006, 27(10): 1309-1316.
[6] 隋海娟，金英，潘月星，等. 吡格列酮对脂多糖诱导的星形胶质细胞炎性细胞因子释放的影响［J］.中国药理学通报，2010, 26(9):1226-1230.
[7] Kim HS, Cho JY, Kim DH, et al. Inhibitory effects of long-term administration of ferulic acid on microglial activation induced by intracerebroventricular injection of b-amyloid peptide (1-42) in mice
[J].Biol Pharm Bull, 2004, 27(1):120-121.
[8] El Bekay R, Alba G, Reyes ME, et al. Rac2 GTPase activation by angiotensin II is modulated by Ca2+/calcineurin and mitogen-activated protein kinases in human neutrophils
[J].J Mol Endocrinol, 2007, 39(5):351-363.
[9] Pang HY, Liu G, Liu GT. Compound FLZ inhibits lipopolysaccharide-induced inflammatory effects via down-regulation of the TAK-IKK and TAK-JNK/p38MAPK pathways in RAW264.7 macrophages
[J].Acta Pharmacol Sin, 2009, 30(2):209-218.
[10]Churcher I. Tau therapeutic strategies for the treatment of Alzheimer，s disease
[J].Curr Top Med Chem, 2006, 6(6):579-595.
[11]Dalrymple SA. p38 mitogen activated protein kinase as a therapeutic target for Alzheimer，s disease
[J].J Mol Neurosci, 2002, 19(3):295-299.
[12]Franciosi S, Ryu JK, Choi HB, et al. Broad-spectrum effects of 4-aminopyridine to modulate amyloid betal-42-induced cell signaling and functional responses in human microglia
[J].J Neurosci, 2006, 26(45):11652-11664.
[13]Wang YJ, Zhou HD, Zhou XF. Modified im-munotherapies against Alzheimer’s disease: toward safer and effective amyloidn clearance
[J]. J Alzheimers Dis, 2010, 21:1065-1075.
[14]Buchanan MM, Hutchinson M, Watkins LR, et al. Toll-like receptor 4 in CNS pathologies
[J].J Neurochem, 2010, 114(1):13-27.
[15]McDonald DR, Bamberger ME, Combs CK, et al. Beta-Amyloid fibrils activate parallel mitogerr-activated protein kinase pathways in microglia and THP1 monocytes
[J]. J Neurosci, 1998, 18(12):4451-4460.
[16]Cribbs DH, Berchtold NC, Perreau V, et al. Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration:a microarray study
[J].J Neuroinflammation, 2012, 9:179-181.
[17] Terry RL, Getts DR, Deffrasnes C, et al. Inflammatory monocytes and the pathogenesis of viral encephalitis
[J]. J Neuroinflammation, 2012, 9(1)：270-273.
[18]Hensley K, Floyd RA, Zheng NY, et al. p38 kinase is activated in the Alzheimer’s disease brain
[J].J Neurochem,1999, 72(5): 2053-2058.
[19]Chen XW, Di YM, Zhang J, et al. Interaction of herbal compounds with biological targets: a case study with berberine
[J].Scientific World Journal, 2012, 2012:708292-708294.
[20] 刘卓，金英，隋海娟，等. 知母皂苷对Aβ25-35引起小脑颗粒细胞损伤的保护作用及其机制探讨
[J].中成药，2012, 34(1)：20-23.
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