calcium channel blockers verapamil  (MedChemExpress)

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation

doi: 10.3389/fcimb.2026.1743907

Figure Lengend Snippet: DTMUV infection increases cytoplasmic Ca 2+ levels in DEFs. (A) Flow cytometry profiles showing cytoplasmic Ca2+ levels in DEFs with and without DTMUV infection and probed with Flou-4AM. (B) Cytoplasmic Ca2+ levels of DEFs with (red) and without (blue) DTMUV infection (MOI = 0.1) for 6, 8, 10, or 12 hours, expressed as mean fluorescence intensity (MFI). (C) Cytoplasmic Ca2+ levels of DEFs with and without DTMUV infection and concurrent treatment with DMSO (control) verapamil or diltiazem hydrochloride. Data expressed as mean ± standard deviation (n = 3), analyzed using Student’s t-test; *p < 0.05, **p < 0.01, ****P<0.0001.

Article Snippet: The calcium channel blockers verapamil (Cat# HY-14275) and diltiazem hydrochloride (Cat# HY-14656), the AMPK inhibitor Compound C (Cat# HY-13418A), and calcium chelating agent BAPTA-AM (Cat# HY-100545) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Infection, Flow Cytometry, Fluorescence, Control, Standard Deviation

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation

doi: 10.3389/fcimb.2026.1743907

Figure Lengend Snippet: VDCC blockers and a cytoplasmic Ca 2+ chelator reduce DTMUV particle production. (A, B) Analysis of plaque assays of DEFs infected with DTMUV and treated with verapamil (25 µM), diltiazem hydrochloride (50 µM), or DMSO (control; (A) ), and BAPTA-AM (25 µM) or DMSO (control; (B) ). Results expressed as the viral titer ratio (%) between each drug-treated group and the control group at 12, 24, and 36 hpi. Data expressed as mean ± standard deviation of triplicate samples, analyzed by two-way ANOVA with multiple comparisons. *p < 0.05, **p <0.01, ***p <0.001, ****p < 0.0001. Results shown are representative of three independent experiments.

Article Snippet: The calcium channel blockers verapamil (Cat# HY-14275) and diltiazem hydrochloride (Cat# HY-14656), the AMPK inhibitor Compound C (Cat# HY-13418A), and calcium chelating agent BAPTA-AM (Cat# HY-100545) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Infection, Control, Standard Deviation

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation

doi: 10.3389/fcimb.2026.1743907

Figure Lengend Snippet: VDCC blockers and a cytoplasmic Ca 2+ chelator inhibit the replication step of DTMUV infection. (A) Viral entry assay of DEFs pretreated with DMSO, diltiazem (50 µM), or BAPTA-AM (25 µM) for 1 hour prior to DTMUV infection (MOI = 1) at 4°C for 1 hour and fusion at 37°C. Viral RNA levels in the cytoplasm were quantified by RT-qPCR at 2 hours post-infection (hpi), expressed as relative DTMUV mRNA levels between the drug-treated groups and the control group. (B) Viral replication assay of DEFs infected with DTMUV (MOI = 1) prior to treatment with DMSO (control), diltiazem hydrochloride (50 µM), or EAPTA-AM (25 µM) at 2 hpi, and RT-qPCR analysis of viral RNA replication in infected cells at 6 hpi, expressed as relative DTMUV mRNA levels between the drug-treated and control groups. (C) Plaque assay of viral release in DEFs cultured infected with DTMUV (MOI = 1) prior to treatment with DMSO (control), diltiazem hydrochloride (50 µM), or EAPTA-AM (25 µM) at 10 hpi and plating at 12 hpi. Results expressed as the viral titer ratio (%) between the drug-treated groups and the control group. (D) Viral replication assay of DEFs infected with DTMUV (MOI = 1) prior to treatment with DMSO (control) or alternative forms of verapamil (25 µM), diltiazem hydrochloride (50 µM), or BAPTA-AM (25 µM) at 1 hpi. Infected cells were harvested for RT-qPCR analysis of DTMUV mRNA levels at 8, 10, and 12 hpi, expressed as relative DTMUV mRNA levels between the drug-treated and control groups. Data expressed as mean ± standard deviation of triplicate samples, analyzed by one-way or two-way ANOVA with multiple comparisons; *p < 0.05, **p <0.01, ***p <0.001, ****p <0.0001. Data shown are representative of three independent experiments. ns: no significant difference.

Article Snippet: The calcium channel blockers verapamil (Cat# HY-14275) and diltiazem hydrochloride (Cat# HY-14656), the AMPK inhibitor Compound C (Cat# HY-13418A), and calcium chelating agent BAPTA-AM (Cat# HY-100545) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Infection, Quantitative RT-PCR, Control, Viral Replication Assay, Plaque Assay, Cell Culture, Standard Deviation

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation

doi: 10.3389/fcimb.2026.1743907

Figure Lengend Snippet: DTMUV-mediated AMPK activation is markedly diminished by treatment with VDCC blockers or a cytoplasmic Ca 2+ chelator. (A) Western blotting of pAMPKα (Thr172) in DEFs infected with DTMUV (MOI = 1) and harvested at the indicated time points. (B) Immunoblotting analysis of pAMPKα (Thr172) levels in DEFs treated with DMSO (control), verapamil (25 µM; Vera), diltiazem hydrochloride (50 µM; Dilt), or BAPTA-AM (25 µM; BAP), with and without DTMUV infection (MOI = 1) for 12 hours.

Article Snippet: The calcium channel blockers verapamil (Cat# HY-14275) and diltiazem hydrochloride (Cat# HY-14656), the AMPK inhibitor Compound C (Cat# HY-13418A), and calcium chelating agent BAPTA-AM (Cat# HY-100545) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Activation Assay, Western Blot, Infection, Control

Journal: Journal of Clinical Medicine

Article Title: Experimental Methods to Simulate and Evaluate Postsurgical Peripheral Nerve Scarring

doi: 10.3390/jcm10081613

Figure Lengend Snippet: Drugs used as antiscarring agents.

Article Snippet: Xue et al., 2016 [ ] , Section + suture , Verapamil (calcium channel blockers) , Sprague–Dawley Rat Sciatic nerve , - Gross evaluation (qualitative evaluation) (4 and 12 weeks) - Nerve IHC (collagen I) (4 and 12 weeks) - Ultrastructural evaluation (TEM) (4 and 12 weeks) - Hydroxyproline and collagen assay (4 and 12 weeks) , The collagen content of nerve scar was apparently less than that of the control group; more cytoplasmic vesicles in the fibroblasts of the treated group were observed..

Techniques: Expressing, Functional Assay, Collagen Assay, Control, In Vitro, Staining, Membrane

Journal: Stem Cell Research & Therapy

Article Title: Extremely low frequency electromagnetic fields promote mesenchymal stem cell migration by increasing intracellular Ca 2+ and activating the FAK/Rho GTPases signaling pathways in vitro

doi: 10.1186/s13287-018-0883-4

Figure Lengend Snippet: The effect of the l -type calcium channel blocker verapamil on electromagnetic field (EMF)-mediated migration of MSCs. a Intracellular Ca 2+ content in MSCs after 50 Hz/1 mT EMF exposure with or without verapamil (10 μM) treatment examined using the Fura 2-AM fluorescence assay. b Migration ability of MSCs after 50 Hz/1 mT EMF exposure with or without verapamil (10 μM) treatment examined using the transwell migration assay. Migrated cells on the bottom surfaces of the transwell inserts were stained with crystal violet and observed under a microscope (100×). Quantitative results of cell migration. Data are presented as means ± SD. Statistically significant differences are indicated; n = 3; * p < 0.05, ** p < 0.01, vs control; # p < 0.05, ## p < 0.01, vs the EMF group

Article Snippet: For the EMF treatment, MSCs were serum starved for 6–8 h, and EMF exposure was applied for 24 h. To inhibit the l -type calcium channels or activities of FAK, cells were treated with 10 μg/ml of the l -type calcium channel blocker verapamil (Sigma-Aldrich, St. Louis, MO) or 5 μg/ml FAK inhibitor (PF-573228; Sigma-Aldrich, St. Louis, MO).

Techniques: Migration, Fluorescence, Transwell Migration Assay, Staining, Microscopy

Journal: Stem Cell Research & Therapy

Article Title: Extremely low frequency electromagnetic fields promote mesenchymal stem cell migration by increasing intracellular Ca 2+ and activating the FAK/Rho GTPases signaling pathways in vitro

doi: 10.1186/s13287-018-0883-4

Figure Lengend Snippet: Focal adhesion kinase (FAK) contributed to the formation of focal contacts in electromagnetic field (EMF)-mediated migration of MSCs. a – d Immunoblot analysis of the total cell lysates performed using antibodies against FAK, talin, and vinculin in MSCs after 50 Hz/1 mT EMF exposure with or without verapamil (10 μM) treatment. Data are presented as means ± SD. Statistically significant differences are indicated; n = 3; ** p < 0.01, vs control; ## p < 0.01, vs the EMF group)

Article Snippet: For the EMF treatment, MSCs were serum starved for 6–8 h, and EMF exposure was applied for 24 h. To inhibit the l -type calcium channels or activities of FAK, cells were treated with 10 μg/ml of the l -type calcium channel blocker verapamil (Sigma-Aldrich, St. Louis, MO) or 5 μg/ml FAK inhibitor (PF-573228; Sigma-Aldrich, St. Louis, MO).

Techniques: Migration, Western Blot