Skip to main content
Fig. 2 | Cell & Bioscience

Fig. 2

From: β-amyloid protein induces mitophagy-dependent ferroptosis through the CD36/PINK/PARKIN pathway leading to blood–brain barrier destruction in Alzheimer’s disease

Fig. 2

Aβ1-40 is transported to pericytes via CD36 and upregulates the expression of CD36 protein. A Aβ1-40 was incubated with pericytes for 1 h, and the pericytes overlapped with red fluorescent Aβ1-40 under an optical microscope. B Cellular immunofluorescence showed red fluorescent Aβ1-40 in the pericytes and CD36 (green light). Colocalization was observed. Blue indicates DAPI, scale 20 µm. C Western blotting was used to detect CD36 and LRP1 protein expression after 6 h of treatment of pericytes with Aβ1-40 (100 nM and 1 µM). D, E Semiquantitative analysis of CD36 and LRP1 protein levels. The data are presented as the means ± SD (n = 3 per group). F, G qRT–PCR was used to detect the changes in the transcriptional levels of CD36 and LRP1 in Aβ1-40 (100 nM and 1 µM)-treated pericytes for 6 h. H Western blots were used to detect CD36 expression at the protein level after RNA interference. I Semiquantitative analysis of CD36 protein levels. The data are presented as the means ± SD (n = 3 per group). J qRT–PCR detected the expression changes induced by si-CD36 at the transcriptional level (#p < 0.05, ##p < 0.01, ###p < 0.001 compared with the CTR group, ΔΔp < 0.01 compared with the 100 nM Aβ1-40 group, n = 3). si-NC indicates the control group

Back to article page