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Research Paper Volume 13, Issue 7 pp 9542-9565
Gastrodin ameliorates learning and memory impairment in rats with vascular dementia by promoting autophagy flux via inhibition of the Ca2+/CaMKII signal pathway
Relevance score: 12.141448Ting-Ting Chen, Xue Zhou, Yi-Ni Xu, Yue Li, Xiao-Ying Wu, Quan Xiang, Ling-Yun Fu, Xiao-Xia Hu, Ling Tao, Xiang-Chun Shen
Keywords: gastrodin, vascular dementia, autophagic flux, Ca2+, CaMKII
Published in Aging on March 10, 2021
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Research Paper Volume 12, Issue 11 pp 10912-10930
Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer’s disease patients, animal models and cell models
Relevance score: 12.141448Zhimin Long, Jingfei Chen, Yueyang Zhao, Wen Zhou, Qiuhui Yao, Yingxiong Wang, Guiqiong He
Keywords: Alzheimer’s disease, autophagic flux, β-amyloid peptide, transgenic mice, lysosome
Published in Aging on June 13, 2020
The expression of LC3, Lamp1 and CTSB in the brain of postmortem patients. (A) Immunofluorescence staining showed the expression of LC3 in the brain tissue of controls and AD patients (a, d: the expression of LC3; b, e: cell nuclei counterstained with DAPI; c, f: the merged images of Lamp1 and DAPI; c1 and f1 are partial magnifications of c and f. a-f: scale bar = 25 μm). (B) Quantitative analysis showing that the ratio of LC3-positive cells in the brain tissue. (C) Quantitative analysis showing the average LC3 puncta in brain tissue cells of AD patients and controls. (D) Immunofluorescence staining showing that the expression of Lamp1 in the brain tissue of controls (a-c1) and AD patients (d-f1). Scale bar = 25 μm. (E) Statistical analysis showing the average gray level of Lamp1. (F) Immunofluorescence staining showing that the expression of CTSB in the brain tissue of controls (a-c1) and AD patients (d-f1). Scale bar = 25 μm. (G) Statistical analysis showing the average gray level of CTSB. (H) Double immunofluorescence staining showing co-expression of autophagy- and lysosome-associated markers in the brain tissue of controls (a-d) and AD patients (c-f1). Scale bar = 10 μm. (I) Immunohistochemistry staining showing SPs in the postmortem cortexes of control patients (a) and AD patients (b), scale bar: 100 μm, the arrow indicates SP. The data are plotted as the mean ± SEM of three independent experiments and were analyzed by t test (**P < 0.01, ***P < 0.001 vs. control, n = 8).
The accumulation of APs in the brain tissue of APP/PS1 DTg AD mice. (A) TEM showing little autophagy in wild-type (Wt) mice in the same litter (a-c); APs were also not easily observed in the brains of 3-month-old DTg mice (d); APs could be observed in the brains of 6-month-old DTg mice (e); a large number of APs and ALs had accumulated in the damaged axonal of brain in 10-month-old DTg mice (f). AL: autolysosome, AP: autophagosome, GA: Golgi apparatus, LYS: lysosome, MIT: mitochondria, Scale bar = 500 nm. (B) anti-Aβ 4G8 immunofluorescence staining showing no SPs in the cortex of the wild-type mice (a-c), while many SPs formed by the excessive accumulation of Aβ outside the cells in the cortex of DTg mice, (d-f, The arrow represents SP). Scale bar = 100 μm. (C) Double immunofluorescence staining showing that compared with that in Wt mice (a-d1), the expression of LC3 in 10-month-old APP/PS1 DTg mice increased significantly (e), the expression of CTSB decreased significantly (f), cell nuclei were counterstained with DAPI (g), and the co-expression of autophagosomal and lysosomal markers reduced (h). Scale bar = 20 μm, d1, h1 is a partial magnification of d and h.
Autophagic flux in the brains of APP/PS1 DTg AD mice of ages. (A) Western blot showing LC3, BECN-1, p62 and Lamp1 expression in the brains of wild-type (Wt) and APP/PS1 DTg mice. (B–E) Relative gray density analysis of LC3-II/LC3-I, BECN-1, p62, and Lamp1 expression levels. The data are presented as the mean ± SEM and were analyzed by t test. (Compared with Wt mice, * P < 0.05, ** P < 0.01, *** < 0.001; “ns” denotes that there was no significant difference, n=3).
The co-existence of APs, ALs and SPs in the brains of APP/PS1/LC3 autophagic flux AD model mice. (A) In the brains of 3-month-old 3×Tg mice, the AP and AL proportion increased, but no SPs were found. In the brains of 6- and 10-month-old 3×Tg mice, SPs coexisted with APs and ALs. Scale bar = 20 μm. (B and C) The quantification of SPs in 3×Tg mice and littoral LC3 mice. (*P < 0.05, **P < 0.01, ***P < 0.001, n=3). (D) Autophagic flux in the different brain regions of 10-month-old 3×Tg mice. There were more APs but less ALs in the cortex and hippocampus, while there were less APs but more ALs in the white matter. Scale bar: a, 500 μm, b-e, 10 μm.
The expression of AP and AL in the brains of APP/PS1/LC3 autophagic flux AD model mice. (A–C) The APs and ALs in the hippocampus and cortex of 3, 6, 10 -month-old LC3 and 3×Tg mice. Scale bar: a-d, 50 μm, a1-d1, 10 μm, a and c: hippocampus, b and d: cortex, a1-d1 are partial magnifications of a-d. (D–K) The number of mRFP and GFP spots in 30 cells from 5 high-power fields was counted. The yellow dots of mRFP and GFP colocalization represent APs, and the free red dots represent ALs. (Compared with LC3 mice, *P<0.05, **P<0.01, ***P<0.001; “ns” denotes that there was no significant difference, n = 3).
Comparison of SH-SY5Y cells (Control), SH-SY5Y cells transfected with empty vector (APPWT), APPswe-overexpressing SH-SY5Y cells (APPswe) and SH-SY5Y cells treated with 30 μM Aβ25-35 (SH-SY5Y +Aβ 25-35). (A) Real-time PCR assay showing the expression of APP, BACE1 and PS1 mRNA in the four group cells. (B and C) Western blot showing the expression of APP, BACE1 and PS1 in APPWT and APPswe cells, SH-SY5Y cells and SH-SY5Y +Aβ 25-35 cells. (D and E) Relative protein gray density analysis. (F) Tubulin staining showing the morphology of the four group cells. Scale bar = 20 μm. (G) Statistical analysis of the longest processes. (H) Acridine orange staining showing membrane stability of the four group cells. a –c: Scale bar = 50 μm, a1 – c1: Scale bar = 20 μm. (I) Statistical analysis of the apoptosis rate. (* P < 0.05, ** P < 0.01, *** P < 0.001; “ns” denotes that there was no significant difference, n=3).
The effects of exogenous Aβ 25-35 treatment and endogenous overexpression of APPswe on autophagic flux. (A) Fluorescence microscopy images of control SH-SY5Y, APPWT, APPswe and SH-SY5Y +Aβ 25-35 (30 μM) cells infected with mRFP-GFP-LC3 adenovirus for 24 h and then treated with 100 nM rapamycin for 10 min (scale bar, 10 μm). (B) mRFP and GFP puncta were quantified to determine the number of APs and ALs per cell. For each group, 30 cells from 5 visual fields were randomly selected for counting (*P < 0.05, **P < 0.01, ***P < 0.001). (C) Western blot showing the expression of ATG5, ATG12, ATG16L, BECN1, ATG14, LC3, p62 and Lamp1 in APPWT and APPswe cells. (D and E) Relative protein gray density analysis. (F) Western blot analysis showing the expression of ATG5, ATG12, ATG16L, BECN1, ATG14, LC3, p62 and Lamp1 in SH-SY5Y and SH-SY5Y +Aβ 25-35 (30 μM) cells. (G and H) Protein band relative gray density analysis. (I) Different concentrations of Aβ 25-35 (0, 20, 40, and 60 μM) were used to treat SH-SY5Y cells for 24 h and the expression of LC3, p62, BECN1, ATG14 and Lamp1 were assessed by Western blot. (J and K) Relative protein gray density analysis. (* P < 0.05, ** P < 0.01, *** P < 0.001; “ns” denotes that there was no significant difference, n = 3).