u0126  (Alomone Labs)

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Molecular components of the FPR2/ALX pathway participate in astrocyte-neuron resolution responses to afford maneb-induced toxicity

doi: 10.1007/s00018-025-05841-3

Figure Lengend Snippet: The receptor FPR2/ALX is involved in the neuron-glia responses elicited by MB challenge. (A) Fpr2 mRNA expression measured by RT-qPCR in neurons and astrocytes co-incubated with MB and the N-Sec and A-Sec, respectively. (B) Neuronal viability when co-incubating with FPR2/ALX antagonist (Quin-C7) and agonist (MMK-1) and the A-Sec under MB toxicity. (C) Fpr2 mRNA expression measured by RT-qPCR in neurons exposed to Quin-C7 and MMK-1 and challenged with the A-Sec. (D) Representative immunostaining of the expression of p65 (red) in neurons incubated with MMK-1 or Quin-C7 and quantification of fluorescence intensity of p65 (nuclear/cytosol ratio). DAPI was used as nuclear staining (blue) (E) Representative immunoblots and quantification of ERK1/2 phosphorylation in neurons with MMK-1 and Quin-C7. (F) Astrocytes proliferation assay and quantification of BrdU + astrocytes (green) challenged with Quin-C7 and MMK-1 together with the N-Sec under MB toxicity. (G) Representative immunoblots and quantification of ERK1/2 phosphorylation in astrocytes co-incubated with MB and N-Sec. (H) Astrocytes proliferation assay in the presence of ERK1/2 inhibitor (ERKi-U0126). The data shown are the mean ± SD (at least three independent experiments). Two-way ANOVA with Tukey’s post-hoc tests were used. * p < 0.05, ** p < 0.01, *** p < 0.001. Created with https://smart.servier.com/

Article Snippet: Cells at 80–90% confluence were treated with 20 μM MB (#45554, Sigma-Aldrich, USA) or vehicle (dimethyl sulfoxide 0.1%) for 24 h and/or pre-incubated with pharmacological inhibitors, agonist or antagonist of different components of the inflammation/resolution pathways: 20 μM luteolin (LUT, sc-203119, Santa Cruz Biotechnology, USA) for ALOX-15, 10 μM celecoxib (Cx, sc-217869, Santa Cruz Biotechnology, USA) and 100 μM acetylsalicylic acid (ASA #50-78-2, Sigma-Aldrich, USA) for cyclooxygenase-2 (COX-2), 10 μM PPOH (sc-205442, Santa Cruz Biotechnology, USA) for CYP450, 10 μM U0126 (sc-222395, Santa Cruz Biotechnology, USA) for ERK1/2, 10 μM YM-26734 (sc-204410, Santa Cruz Biotechnology, USA) for sPLA2, 0.1 μM MMK-1 (ALO-GPM-120, Alomone Labs, Ltd., Israel) as FPR2/ALX agonist and 10 μM Quin-C7 (ALO-Q-155, Alomone Labs, Ltd., Israel) as FPR2/ALX antagonist (viability assay testing Quin-C7 and MMK-1 concentrations are shown in Supplementary Fig. 5), lipoxin A4 0.2 nM and resolvin D1 0.2 nM (#490414 and #400384, respectively, Cayman Chemicals, USA), concentration was selected by performing a concentration screening.

Techniques: Expressing, Quantitative RT-PCR, Incubation, Immunostaining, Fluorescence, Staining, Western Blot, Phospho-proteomics, Proliferation Assay

Journal: International Journal of Nanomedicine

Article Title: Optimized Nanostructured Lipid Carriers for Metformin: Enhanced Anti-Inflammatory Activity and Protection Against Type 2 Diabetes-Induced Organ Damage

doi: 10.2147/IJN.S506631

Figure Lengend Snippet: Effect of MTF and MTF-NLC on diabetic alteration of serum ( A ) creatinine and blood urea nitrogen (BUN) ( B ) liver function markers ( C ) alanine amino transferase (ALT) and ( D ) aspartate aminotransferase (AST). Data were expressed as mean±SD. P < 0.05 was considered significant, compared to control (*), diabetic (#), significance between MTF-NLC and MTF ($), n=3.

Article Snippet: Serum samples were assessed for quantitative determination of activity of both alanine aminotransferase (ALT) ((BEIS11-I, SPINREACT) detection range from 0 U/L to 400 U/L) and aspartate aminotransferase (AST) ((MDBEIS46-I, SPINREACT) detection limit of 0 U/L to linearity limit of 467 U/L.) as indicators of liver function.

Techniques: Control