Fig. 2

IHT reduces plaque accumulation, enhances Aβ degradation, and attenuates the expression of pro-inflammatory factors. During IHT, 8-month-old APP/PS1 mice underwent IHT for 28 days. A Mice brain sections were probed with anti-Aβ1–16 (6E10) and anti-Iba1 antibodies to detect Aβ plaques and microglia. The cortex and CA1 region of the hippocampus are circled and zoomed in. Scale bar = 2 mm or 300 μm. B, C Total of 12 evenly spaced brain slices were acquired from each mouse, and the number of plaques in the hippocampus and cortex was quantified by counting the 6E10 signals. n = 5. D Plaque area was obtained by measuring the average area of the 6E10 signals. n > 40. E Microglia number was estimated by counting all Iba1⁺ cells in the hemispheres. n = 3. F, G Aβ1–42 and Aβ1–40 concentrations in the brain tissues were determined via ELISA. n = 4 and 6. H Brain sections were co-stained with anti-LAMP1, anti-Iba1, and anti-Aβ1–16 (6E10) antibodies to observe the degraded Aβ in PAM. Scale bar = 10 μm. I LAMP1 in PAM were calculated by measuring the mean intensity of LAMP1 in Iba1⁺6E10⁺ cells. n > 90. J Colocalization ratio of Aβ with LAMP1 in Iba1⁺ cells were determined using Manders' colocalization coefficients. n > 50. K mRNA levels of Il1b, Tnfa, and Tgfb in the hippocampus were obtained via qRT-PCR. n = 4. *P < 0.05, **P < 0.01, and ***P < 0.001 using Student's t test. Ctx cortex, Hipp hippocampus, TG APP/PS1 transgenic mice