Figure 7 | Scientific Reports

Figure 7

From: Uric Acid Produces an Inflammatory Response through Activation of NF-κB in the Hypothalamus: Implications for the Pathogenesis of Metabolic Disorders

Figure 7

MRI-based quantitative assessment of hypothalamic gliosis in hyperuricemia rodents and humans.

(A,B) Regions of interest (circles) and representative images of the normal rats (A) and hyperuricemia rats (B). a. High-resolution, 2-dimensional rapid acquisition; b. T2 map generated from a multiecho sequence; c. DTI for tensor trace measurement; d. DTI for fractional anisotropy. (C–E) Results of multiparametric quantitative assessment in hyperuricemia rats and chow-fed controls, including T2 relaxation time (C) (ms = millisecond), tensor trace (D) and fractional anisotropy (E) (n = 6 rats per group). (F,G) Representative coronal T2 FES FLAIR images through the hypothalamus in a normal serum UA subject (F) and a hyperuricemia subject (G). Insets show the placement of ROIs (white circles) in the mediobasal hypothalamus (MBH) and amygdala (AMY). (H) The average signal ratio on both sides that signal intensity within ROIs placed in the MBH versus ROIs in adjacent amygdala tissue was used for quantitative assessment in normal serum UA subjects (n = 16 subjects) and hyperuricemia subjects (n = 15 subjects). (I) Correlation of serum UA concentration with MBH hyperintensity, as measured by average MBH/amygdala signal ratio on both sides (n = 31 subjects; r = 0.41). All displayed values are the mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 versus control.

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