Journal: The Journal of international medical research

Article Title: Telmisartan, an angiotensin II type 1 receptor blocker, inhibits advanced glycation end-product (AGE)-induced monocyte chemoattractant protein-1 expression in mesangial cells through downregulation of receptor for AGEs via peroxisome proliferator-activated receptor-gamma activation.

doi: 10.1177/147323000703500407

Figure Lengend Snippet: FIGURE 1: Effects of telmisartan on (A) advanced glycation-end products (AGEs) receptor (RAGE) gene expression and (B) superoxide generation in mesangial cells incubated for 4 h with: non-glycated bovine serum albumin (BSA); 100 µg/ml AGEs–BSA; 100 µg/ml AGEs–BSA plus 100 nM telmisartan; 100 µg/ml AGEs–BSA plus 100 nM telmisartan plus 500 nM GW9662; 100 µg/ml AGEs–BSA plus 100 nM candesartan. (A, upper panel) 30 ng poly(A)+ RNAs transcribed and amplified by polymerase chain reaction. (A, lower panel) Mean ± SE representation of RAGE gene induction normalized by intensity of β-actin mRNA-derived signals relative to BSA. (B, upper panel) Dihydroethidium staining of mesangial cells. (B, lower panel) Mean ± SE of superoxide generation evaluated by fluorescent intensity. *P < 0.01 vs AGEs–BSA; #P < 0.01 vs AGEs–BSA plus telmisartan.

Article Snippet: Candesartan was obtained from Toronto Research Chemicals Inc. (North York, Canada).

Techniques: Gene Expression, Incubation, Amplification, Polymerase Chain Reaction, Derivative Assay, Staining

Journal: Theranostics

Article Title: Therapeutic potential of a TrkB agonistic antibody for Alzheimer's disease

doi: 10.7150/thno.44165

Figure Lengend Snippet: The specificity of TrkB agonistic antibody AS86. (A) AS86 at different concentrations (0.1 nM, 1 nM and 10 nM) was added to the plates coated with different proteins (0.1 μg TrkA, TrkB, TrkC, or p75 respectively), and ELISA was used to examine the binding capacity of AS86. (B, C) Cultured hippocampal neurons (DIV10) were pretreated with the Trk inhibitors k252a (300 nM) or AZD-1332 (100 nM) for 60 min before incubation with mIgG (3 nM), BDNF (1 nM), or AS86 (3 nM) for 15 min (N = 2, n = 3). The Western blots of TrkB Y515 and Y816 sites activation (B) and the quantitative plots (C) are presented. Unless specifically indicated otherwise, statistical analyses in this and all other figures were carried out using one-way ANOVA followed by post hoc test. Symbols for P values (for both ANOVA and Student's t -test): *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: P < 0.0001. The quantification data in this and all other figures were presented as mean ± SEM.

Article Snippet: The reagents included BDNF protein (Sino Biological Inc, 50240-MNAS), Mouse IgG (YEASEN, 3611ES10), and β-Amyloid protein (25-35) (Synpeptide), K252a (Bio Vision, 2013-500), AZD-1332 (Alomeone labs, A-495).

Techniques: Enzyme-linked Immunosorbent Assay, Binding Assay, Cell Culture, Incubation, Western Blot, Activation Assay

Journal: Theranostics

Article Title: Therapeutic potential of a TrkB agonistic antibody for Alzheimer's disease

doi: 10.7150/thno.44165

Figure Lengend Snippet: Cell survival function of AS86. ( A ) Attenuation of serum-deprivation induced cell death by AS86. Different doses of BDNF or AS86 were applied to serum-deprived cultures of hTrkB-PC12 cells in the absence or presence of Trk inhibitors (300 nM K252a or 50 nM AZD-1332) for 16 hours, and the levels of apoptosis were determined by the ratio of the number of caspase 3 positive cells to total number of cells, using a caspase 3-substrate kit. Survival rates were measured by the decreased apoptotic levels normalized to that of vehicle treatment (n = 3). ( B ) Attenuation of Aβ induced cell death by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (5 µM). Cell viability was analyzed with ATP level quantification assay 48 hours later (N = 2 independent experiments, n = 6 samples). ( C, D ) Inhibition of Aβ induced apoptotic signals by AS86. Hippocampal neurons were pretreated with AS86 or BDNF for 30 minutes, followed by treatment with Aβ (25-35) (15 µM) for 24 hours. Total and cleaved caspase3 levels were measured using Western blotting (N = 3 independent experiments, n = 3 replicates). Representative Western blots (D) and quantitative plots (C) are presented.

Article Snippet: The reagents included BDNF protein (Sino Biological Inc, 50240-MNAS), Mouse IgG (YEASEN, 3611ES10), and β-Amyloid protein (25-35) (Synpeptide), K252a (Bio Vision, 2013-500), AZD-1332 (Alomeone labs, A-495).

Techniques: Inhibition, Western Blot