rolipram  (MedChemExpress)

Journal: bioRxiv

Article Title: Dietary Non-protein Amino Acid AZE as an Environmental Trigger Activating Latent Genetic Susceptibility in C9orf72 -ALS Pathogenesis

doi: 10.64898/2026.01.12.697838

Figure Lengend Snippet: a-c , Western blot analysis showing the effect of MG132 treatment (24 hours) on poly-GA levels in HeLa cells transfected with GA(50)-V5-expressing plasmids. Quantitative analysis was conducted by normalizing both soluble and insoluble protein fractions to β-actin as a loading control ( b,c ). n ≥ 3 independent experiments. Note that inhibition of UPS activity by MG132 treatment significantly increased the poly-GA levels. d-f , Western blot analysis showing the effect of rolipram treatment (24 hours) on poly-GA levels in HeLa cells transfected with GA(50)-V5-expressing plasmids. Quantitative analysis was conducted by normalizing both soluble and insoluble protein fractions to β-actin as a loading control ( e,f ). n ≥ 3 independent experiments. Rolipram treatment, which enhances UPS activity, significantly decreased the poly-GA levels. g-i , Western blot analysis showing that the AZE-induced upregulation of poly-GA levels was diminished by rolipram treatment in HeLa cells transfected with GA(50)-V5-expressing plasmids (AZE, 1000μM; rolipram, 30μM). Quantitative analysis was conducted by normalizing both soluble and insoluble protein fractions to Tubulin as a loading control ( h,i ). n ≥ 3 independent experiments. j , Cell viability of iPSC-derived motor neurons from C9-ALS patients following 24-hour treatment with AZE (1000μM) or rolipram (30μM). Note that rolipram treatment attenuated the selective vulnerability of C9-ALS neurons to AZE-induced neurotoxicity. n ≥ 3 biological replicates. Data in b,c,e,f,h,i,j are represented as mean ± SEM. Student’s t test, *p < 0.05; **p < 0.01; ***p < 0.001; n.s., not significant. See also .

Article Snippet: MG132(1.25-20μM, MedChemExpress, HY-13259), rolipram (3.75-30μM; MedChemExpress, HY-16900), Thapsigargin (TG, 1μM; MedChemExpress, HY-13433) or KIRA8(0.1μM; MedChemExpress, HY-114368).

Techniques: Western Blot, Transfection, Expressing, Control, Inhibition, Activity Assay, Derivative Assay

Journal: bioRxiv

Article Title: Dietary Non-protein Amino Acid AZE as an Environmental Trigger Activating Latent Genetic Susceptibility in C9orf72 -ALS Pathogenesis

doi: 10.64898/2026.01.12.697838

Figure Lengend Snippet: a , b , Western blot analysis showing the effect of MG132 (10μM, 24 hours) or rolipram (30μM, 24 hours) treatment on DPR levels in HeLa cells transfected with DPR-expressing plasmids: GP(50)-GFP, GR(50)-GFP, PA(50)-GFP, PR(50)-GFP. Note that modulating UPS activity had no detectable effect on these DPR levels. c , d , Western blot analysis showing the effect of MG132 or rolipram treatment (24 hours) on the expression levels of ALS-associated mutant proteins in HeLa cells. Note that modulating UPS activity had no detectable effect on SOD1 G93A , FUS R521C , and TDP43 M337V levels. e , Representative images of HeLa cells transfected with plasmids encoding GA(50)-V5, SOD1 G93A -V5, TDP43 M337V -V5, and FUS R521C -V5. V5 staining is depicted in green, and DAPI staining is shown in blue. Note that poly-GA(50) shows pronounced protein inclusions, a phenotype not shared by other ALS-associated mutant proteins under similar conditions. Scale bar, 50μm. Inset: higher magnification of the white boxed area. Scale bar, 10μm. f-h , Western blot analysis showing the AZE-induced upregulation of endogenous poly-GA levels was diminished by rolipram treatment in motor neuron cultures derived from C9-ALS patient iPSCs (AZE, 1000μM; rolipram, 30μM; 24-hour treatment). Quantitative analysis was conducted by normalizing both soluble and insoluble protein fractions to β-actin as a loading control. Note that AZE treatment induced a significant increase in soluble poly-GA levels, whereas the insoluble forms exhibited minimal changes. This observation is consistent with . Data in g,h, are represented as mean ± SEM. n ≥ 3 independent experiments. Student’s t test, *p < 0.05.

Article Snippet: MG132(1.25-20μM, MedChemExpress, HY-13259), rolipram (3.75-30μM; MedChemExpress, HY-16900), Thapsigargin (TG, 1μM; MedChemExpress, HY-13433) or KIRA8(0.1μM; MedChemExpress, HY-114368).

Techniques: Western Blot, Transfection, Expressing, Activity Assay, Mutagenesis, Staining, Derivative Assay, Control

Journal: Frontiers in Pharmacology

Article Title: Bitter taste receptor agonists induce vasorelaxation in porcine coronary arteries

doi: 10.3389/fphar.2025.1578913

Figure Lengend Snippet: Inhibition of various agents on vasorelaxation induced by flufenamic acid in segments of the porcine coronary artery precontracted with 100 nM U46619. (A) The presence of tetrodotoxin (TTX) did not significantly alter the vasorelaxant action of flufenamic acid. (B) The addition of rolipram and vardenafil also did not significantly modify the vasorelaxation induced by flufenamic acid. (C) Neither KT5720 nor KT5823 significantly affected the vasorelaxant response to flufenamic acid, whereas NG-nitro-L-arginine (L-NNA) significantly inhibited the flufenamic acid-induced vasorelaxation. (D) Iberiotoxin (IbTX) and tetraethylammonium (TEA) had no significant impact on the relaxation response to flufenamic acid, but apamin and glibenclamide significantly decreased the relaxation effect. Error bars represent the standard error of the mean (SEM). The single asterisk (*) denotes a statistically significant deviation from the relaxation effect at 30 μM flufenamic acid, with p < 0.05.

Article Snippet: Additional agents included rolipram, vardenafil, and tetraethylammonium (TEA) from Santa Cruz Biotechnology (Santa Cruz, CA, United States), iberiotoxin (IbTX) from Alomone Labs (Jerusalem, Israel), glibenclamide from Research Biochemicals International (Natick, MA, United States), and tetrodotoxin (TTX) from Tocris Bioscience (Bristol, United Kingdom).

Techniques: Inhibition

Journal: Communications Biology

Article Title: AI-guided laser purification of human iPSC-derived cardiomyocytes for next-generation cardiac cell manufacturing

doi: 10.1038/s42003-025-08162-0

Figure Lengend Snippet: a Cryopreserved TTN-GFP atrial hiPSC-CMs phase contrast and GFP images, 20×. b Zoomed image of sarcomere structures in hiPSC-CMs. c Representative time-space plots indicate functional monolayer electrophysiological activations across the width of each well of the 96-well plate (9 mm diameter). Rolipram increased hiPSC-CM monolayer beat rate. d Representative calcium transient traces indicating the effect of rolipram to increase calcium transient amplitude. e Rolipram increased 2D monolayer beat rate (VEH = 80.0 ± 11.8; 1.0 µM Rolipram = 113.3 ± 33.0; 10.0 µM Rolipram = 129.2 ± 9.4 bpm, n = 8 per group). One way ANOVA, multiple comparisons, * P = 0.01; *** P = 0.0004. f Rolipram increased calcium transient amplitude (VEH = 0.53 ± 0.17; 1.0 µM Rolipram = 0.72 ± 0.40; 10.0 µM Rolipram=1.22 ± 0.50 ∆F/F 0 , n = 8 per group). One way ANOVA, multiple comparisons, ** P = 0.004. g Rolipram increased calcium impulse conduction velocity (VEH = 23.5 ± 4.1; 1.0 µM Rolipram = 30.3 ± 17.6; 10.0 µM Rolipram = 47.9 ± 20.4 cm/s, n = 8 per group). One way ANOVA, Brown-Forsythe and Welch tests, multiple comparisons, * P = 0.02.

Article Snippet: Rolipram (1, 10 μM, Enzo BML-PD175) was also applied to 2D hiPSC-CM monolayers to further probe the function of the β-adrenergic signaling pathway (Fig. ).

Techniques: Functional Assay