Expression of Inflammatory Cytokines in the Brain, Blood Serum and Periodontal Tissue in Alzheimer's Disease Rat Model Induced by a Combined Treatment Procedure

doi:10.3969/j.issn.1674-5817.2013.06.005

Abstract

Abstract: Objective To establish rat Alzheimer's Disease by a combined treatment with Amyloid protein1-42 (Aβ1-42) and D-galactose (D-gal) andinvestigate the levels of CRP,IL-1,IL-6,TNF-α in the brain, blood serum and periodontal tissue. Methods Twenty-four two-month old SD male rats were randomly divided into two groups: peritoneal injection with D-gal combined with lateral ventricle injection with Aβ1-42 to establish AD animal model, and injection of physiological saline served as the control group. The learning and memory function of the rats were evaluated by Morris water-maze test, the number and morphology of neuron in hippocampus and cortex were observed, and the expressions of CRP,IL-1,IL-6,TNF-〈 in the brain (hippocampus and cortex), serum and periodontal tissue were measured by ELISA. Results Comparing with the control group, the number of neurons stained in AD animal model reduced significantly (P<0.05), but no morphological change was observed. The expression of CRP, IL-1, IL-6, TNF-〈 in the brain (hippocampus and cortex), serum and periodontal tissue were increased in model group. Conclusion This model can better imitate inflammation in central nerve system; periodontal inflammation may involve in the progress of AD.

Key words: amyloid protein, D-galactose, Alzheimer's disease;, Inflammation factors, SD rat

YIN Xiu-hua, JIANG Zhen, LIU Tian-yun, PANG Ping, QIN Ting, XIA Chun-lin, SUN Mao-min. Expression of Inflammatory Cytokines in the Brain, Blood Serum and Periodontal Tissue in Alzheimer's Disease Rat Model Induced by a Combined Treatment Procedure[J]. Laboratory Animal and Comparative Medicine, 2013, 33(6): 439-443.

References

[1] Thies W, Bleiler L.Alzheimer’s disease facts and figures[J]. 2011, 7(2):208-244.
[2] Lin MT, Beal MF.Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases[J]. Nature, 2006, 443(7113): 787-795.
[3] Brown GC, Neher JJ.Inflammatory Neurodegeneration and Mechanisms of Microglial Killing of Neurons[J]. Mol Neurobiol, 2010, 41(2-3):242-347.
[4] Krstic D, Madhusudan A, Doehner J, et al. Systemic immune challenges trigger and drive Alzheimer-like neuropathology 5 in mice[J]. J-Neuroinflammation, 2012, 9(1):151-174.
[5] Han WF, Ji T, Wang LL, et al.Abnormalities in periodontal and salivary tissues in conditional presenilin 1 and presenilin 2 double knockout mice[J]. Mol Cell Biochem, 2011, 347(1-2):13-20.
[6] 汪润, 赵丽娟, 王全英, 等. β淀粉样蛋白1~42与D-半乳糖联合作用建立复合阿尔茨海默病样模型[J]. 解剖学报, 2011, 42(4):461-464.
[7] 包新民, 舒斯云. 大鼠脑立体定位图谱[M]. 北京: 人民卫生出版社, 1991:12-18.
[8] 戎志斌, 禤璇, 刘纯, 等. 新型阿尔茨海默病大鼠模型的建立及其行为学研究[J].中国中医药科技, 2013, 20(1):48-49.
[9] McGeer PL, Schulzer M, MeGetr EG. Arthtitis and antiinflammatory agents as possible protective factors for AIzheimers’ disease: a review of epidemiologic studies[J]. Neurology, 1996, 47(2):425-432.
[10] Rubio-Perez JM, Morillas-Ruiz JM.A review: inflammatory process in Alzheimer’s disease, role of cytokines[J]. Scientific World Journal, 2012, 2012:1-15.
[11] Zotova E, Nicoll j, Kalaria R, et al. Inflammation in Alzheimer’s disease: relevance to pathogenesis and therapy [J]. Alzheimer’s Research and Therapy,2010, 22;2(1):1.
[12] Halliday G, Robinson SR, Shepherd C, et al.Alzheimer’s disease and inflammation: a review of cellular and therapeutic mechanisms[J]. Clin Exp Pharmacol Physiol, 2000, 27(1-2):1-8.
[13] Combs CK.Inflammation and microglia actions in Alzheimer’s disease[J]. Neuroimmune Pharmacol, 2009, 4(4):380-388.
[14] Vom Berg J, Prokop S, Miller KR, et al.Inhibition of IL-12/IL-23 signaling reduces Alzheimer’s disease-like pathology and cognitive decline[J].Nature medicin, 2012, 18(12):1812-1819.
[15] Carnevale D, Mascio G, Ajmone-Cat MA, et al. Role of neuroinflammation in hypertension induced brain amyloid pathology[J]. Neurobiology of Aging, 2012, 33(1):205.e19-29.
[16] Lee DC, Rizer J, Selenica ML,et al.LPS- induced inflammation exacerbates phospho-tau pathology in rTg4510 mice[J]. J Neuroinflammation, 2010, 7(1):56-71.
[17] 戴立彬, 吴金娟, 刘涛. 炎症反应参与老年痴呆病的研究近况[J]. 中医学报, 2013, 28(3):425-426.
[18] Kamer AR, Craig RG, Dasanayake AP, et al.Inflammation and Alzheimer’s disease: possible role of periodontal diseases[J]. Alzheimers Dement, 2008, 4(4):242-250.