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. 2019 Jul 9;20(3):2135–2142. doi: 10.3892/mmr.2019.10483

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Copyright: © Yu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — AGEs promote neuroinflammation in the AD cell model by inducing MIF expression. The mRNA expression of (A) IL-1β, (B) IL-6, (C) TNF-α and (D) MIF were determined in the blank, AD cell model, AGEs-treated AD model and the ISO-1-pretreated groups via reverse transcription-quantitative PCR. AGEs promoted neuroinflammation in the AD cell model by inducing MIF expression. Data are presented as the mean ± SD; n=4. *P<0.05, **P<0.01, ***P<0.001 vs. Blank control; ^#P<0.05, ^##P<0.01. AGEs, advanced glycation end products; Aβ_1–40, amyloid β 1–40; AD, Alzheimer's disease; ISO-1, (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester; IL, interleukin; TNF-α, tumor necrosis factor-α.