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Correlation analysis of osteopontin levels with inflammatory factors and severity of Alzheimer’s disease |
LIU Ting1,2 LI Dan1,2 LIU Jia1,2 MA Na1,2 MENG Xinling1,2 |
1.Xinjiang Uygur Autonomous Region Research Institute of Traditional Chinese Medicine, Xinjiang Uygur Autonomous Region, Urumqi 830000, China;
2.the First Department of Encephalopathy, Affiliated Chinese Medicine Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830000, China |
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Abstract Objective To analyze the correlation of osteopontin (OPN) levels with inflammatory factors and severity of Alzheimer’s disease. Methods A total of 30 patients with AD and mild cognitive impairment (MCI) who were diagnosed and treated in the First Department of Encephalopathy in Affiliated Chinese Medicine Hospital of Xinjiang Medical University from November 2016 to March 2019 were included in the study, served as AD group and MCI group respectively, while another 30 patients with non-inflammatory neuropathy (OND) were selected during the same period, served as the control group. The clinical baseline data and serum OPN, interleukin-1β (IL-1β), IL-6, IL-17A, transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α) level were compared, while the Pearson correlation model was used to analyze the correlation between the patient’s serum OPN levels and inflammation indicators and condition. Results The mini-mental state examination (MMSE) score of the AD group was higher than that of the MCI group and the control group, and the differences were statistically significant (P < 0.05). TNF-α and OPN in AD group were significantly higher than those in MCI group and control group, and the differences were statistically significant (P < 0.05). Multivariate linear regression showed that OPN and TNF-α levels were influence factor MMSE (t = 3.195, 3.545, P < 0.05). Correlation analysis showed that OPN level was positively correlated with TNF-α level (r = 0.749, P < 0.05). Conclusion The levels of OPN and TNF-α in AD patients are negatively correlated with the severity of the patient’s condition, and OPN may increase the expression level of TNF-α, thereby making the severity of the patient’s condition progress.
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[1] Lane CA,Hardy J,Schott JM. Alzheimer′s disease [J]. Eur J Neurol,2018,25(1):59-70.
[2] Kunkle BW,Grenier-Boley B,Sims R,et al. Genetic meta-analysis of diagnosed Alzheimer′s disease identifies new risk loci and implicates Aβ,tau,immunity and lipid processing [J]. Nat Genet,2019,51(3):414-430.
[3] 王晨旭,于泳浩,谢克亮,等.AMPA受体在阿尔兹海默症中的研究进展[J].天津医科大学学报,2020,26(3):292-295.
[4] Martin E,Delarasse C. Complex role of chemokine mediators in animal models of Alzheimer′s Disease [J]. Biomed J,2018,41(1):34-40.
[5] Torika N,Asraf K,Apte RN,et al. Candesartan ameliorates brain inflammation associated with Alzheimer′s disease [J]. CNS Neurosci Ther,2018,24(3):231-242.
[6] 郭忠伟,岳媛媛,邹哲华,等.急性脑梗死患者急性期血清骨桥蛋白和氧化应激指标水平与患者神经损伤和预后的相关性探讨[J].临床和实验医学杂志,2020,19(12):1307-1310.
[7] Tiwari S,Atluri V,Kaushik A,et al. Alzheimer′s disease:pathogenesis,diagnostics,and therapeutics [J]. Int J Nano-medicine,2019,14:5541-5554.
[8] Zhao H,Chen Q,Alam A,et al. The role of osteopontin in the progression of solid organ tumor [J]. Cell Death Dis,2018,9(3):356.
[9] 黄光成,胡欣,唐玉青,等.同型半胱氨酸与阿尔兹海默症相关研究进展[J].公共卫生与预防医学,2019,30(6):85-89.
[10] Gary C,Lam S,Hérard AS,et al. Encephalopathy induced by Alzheimer brain inoculation in a non-human primate [J]. Acta Neuropathol Commun,2019,7(1):126.
[11] Koenig LN,Day GS,Salter A,et al. Select Atrophied Regions in Alzheimer disease (SARA):An improved volumetric model for identifying Alzheimer disease dementia [J]. Neuroimage Clin,2020,26:102248.
[12] van Loenhoud AC,van der Flier WM,Wink AM,et al. Cognitive reserve and clinical progression in Alzheimer disease:A paradoxical relationship [J]. Neurology,2019, 93(4):e334-e346.
[13] Yamazaki Y,Zhao N,Caulfield TR,et al. Apolipoprotein E and Alzheimer disease:pathobiology and targeting strategies [J]. Nat Rev Neurol,2019,15(9):501-518.
[14] 闫静,叶琳.身体活动对阿尔兹海默病的预防及改善作用机制的研究进展[J].中国慢性病预防与控制,2020, 28(5):392-396.
[15] Grimaldi A,D′Alessandro G,Di Castro MA,et al. Kv1.3 activity perturbs the homeostatic properties of astrocytes in glioma [J]. Sci Rep,2018,8(1):7654.
[16] Diniz LP,Tortelli V,Matias I,et al. Astrocyte transforming growth factor beta 1 protects synapses against Aβ oligomers in Alzheimer′s disease model [J]. J Neurosci,2017,37(28):6797-6809.
[17] Zhen F,Brooks DJ,Aren O,et al. An early and late peak in microglial activation in Alzheimer′s disease trajectory [J]. Brain,2017,140(3):792-803.
[18] Bagyinszky E,Giau VV,Shim K,et al. Role of inflammatory molecules in the Alzheimer′s disease progression and diagnosis [J]. J Neurol Sci,2017,376:242-254.
[19] Cavanagh C,Tse YC,Nguyen HB,et al. Inhibiting tumor necrosis factor-α before amyloidosis prevents synaptic deficits in an Alzheimer′s disease model [J]. Neurobiol Aging,2016,47:41-49.
[20] 何璐,王瑛,徐玮,等.基于血浆免疫及炎症相关蛋白的阿尔茨海默病筛查标志物的研究[J].上海交通大学学报:医学版,2017,37(7):950-954.
[21] 杨萍萍,张微,迟立君.骨桥蛋白在免疫相关性疾病中作用的分子机制新进展[J].免疫学杂志,2017,33(3):263-267.
[22] 王晨习.骨桥蛋白与炎症的相关性研究综述[J].医药前沿,2016,6(16):7-8.
[23] 何瑞东,韩荣坤,张黎明,等.骨桥蛋白在神经退行性疾病中的作用[J].现代生物医学进展,2013,13(15):2993-2996.
[24] 赵士娇,韩雪,高燕军.骨桥蛋白及炎症反应与颈动脉粥样硬化斑块关系的研究进展[J].卒中与神经疾病,2018, 25(5):607-610.
[25] 许淼.骨膜蛋白、骨桥蛋白与支气管哮喘[J].国际儿科学杂志,2019,46(6):396-399. |
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