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diltiazem hydrochloride  (MedChemExpress)


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    Structured Review

    MedChemExpress diltiazem hydrochloride
    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 <t>diltiazem</t> <t>hydrochloride.</t> Data expressed as mean ± standard deviation (n = 3), analyzed using Student’s t-test; *p < 0.05, **p < 0.01, ****P<0.0001.
    Diltiazem Hydrochloride, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/diltiazem/Diltiazem+hydrochloride/pmc12926480-38-8-29
    Average 94 stars, based on 7 article reviews
    diltiazem hydrochloride - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Disruption of cellular calcium homeostasis by duck Tembusu virus facilitates viral replication via AMPK pathway activation"

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

    Journal: Frontiers in Cellular and Infection Microbiology

    doi: 10.3389/fcimb.2026.1743907

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

    Techniques Used: Infection, Control, Standard Deviation

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

    Techniques Used: Activation Assay, Western Blot, Infection, Control

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    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice.
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    Staining:

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    Article Snippet: The related drugs used included niclosamide (IN1580; Solarbio, CHN), diltiazem (HY-14656; MedChemExpress, USA), and phosphatidylethanolamine (190286; Solarbio, CHN).

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca 2+ , mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice.
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca2+, mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

    Negative Control:

    Article Title: Calcium channel blockers increase the risk of aortic aneurysm and dissection.
    Article Snippet: Amlodipine (HY-B0317), Nifedipine (HY-B0284), Diltiazem (HY-14656), Verapamil (HY-14275), Losartan (HY-17512), human angiotensin II (HY13948) was purchased from Med Chem Express (Monmouth Junction, NJ, USA).

    Article Title: Calcium channel blockers increase the risk of aortic aneurysm and dissection
    Article Snippet: Amlodipine (HY-B0317), Nifedipine (HY-B0284), Diltiazem (HY-14656), Verapamil (HY-14275), Losartan (HY-17512), human angiotensin II (HY13948) was purchased from Med Chem Express (Monmouth Junction, NJ, USA).

    Article Title: S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and Ca 2+ dysregulation.
    Article Snippet: The related drugs used included niclosamide (IN1580; Solarbio, CHN), diltiazem (HY-14656; MedChemExpress, USA), and phosphatidylethanolamine (190286; Solarbio, CHN).

    Article Title: S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and Ca 2+ dysregulation
    Article Snippet: The related drugs used included niclosamide (IN1580; Solarbio, CHN), diltiazem (HY-14656; MedChemExpress, USA), and phosphatidylethanolamine (190286; Solarbio, CHN).

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca 2+ , mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice.
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca2+, mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

    Dissection:

    Article Title: Calcium channel blockers increase the risk of aortic aneurysm and dissection.
    Article Snippet: Amlodipine (HY-B0317), Nifedipine (HY-B0284), Diltiazem (HY-14656), Verapamil (HY-14275), Losartan (HY-17512), human angiotensin II (HY13948) was purchased from Med Chem Express (Monmouth Junction, NJ, USA).

    Article Title: Calcium channel blockers increase the risk of aortic aneurysm and dissection
    Article Snippet: Amlodipine (HY-B0317), Nifedipine (HY-B0284), Diltiazem (HY-14656), Verapamil (HY-14275), Losartan (HY-17512), human angiotensin II (HY13948) was purchased from Med Chem Express (Monmouth Junction, NJ, USA).

    Article Title: S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and Ca 2+ dysregulation.
    Article Snippet: The related drugs used included niclosamide (IN1580; Solarbio, CHN), diltiazem (HY-14656; MedChemExpress, USA), and phosphatidylethanolamine (190286; Solarbio, CHN).

    Article Title: S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and Ca 2+ dysregulation
    Article Snippet: The related drugs used included niclosamide (IN1580; Solarbio, CHN), diltiazem (HY-14656; MedChemExpress, USA), and phosphatidylethanolamine (190286; Solarbio, CHN).

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca 2+ , mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

    Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice.
    Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca2+, mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.



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    Image Search Results


    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.

    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

    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.

    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

    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.

    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

    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.

    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

    Effect of diltiazem hydrochloride on PIEZO1 channel sensitivity. A) Applied deformation after AFM loading. B) Magnitude of the intracellular Ca 2+ response to mechanical compression. C) Percentage of cells that responded to AFM compression. D) Magnitude of the intracellular Ca 2+ response to Yoda1 addition. E) Percentage of cells that responded Yoda1 addition. Data presented as mean ​± ​95 ​% confidence interval. Kruskal-Wallis testing was significant ( p ​= ​0.0343) but Dunn’s test revealed no significant differences between any groups. One way ANOVA with Tukey’s post-hoc test or Kruskal-Wallis testing with Dunn’s post-hoc test was used for group comparisons A-B and D-E. Different letters indicate statistical significance ( p ​< ​0.05). If the same letter is assigned to multiple groups, those groups are not significantly different from each other. Conversely, if two groups are denoted with completely different letters, the two groups are significantly different. N ​= ​14–80.

    Journal: Osteoarthritis and Cartilage Open

    Article Title: PIEZO mechanosensitivity in chondrocytes is differentially modulated by L-type and T-type voltage-sensitive ion channels

    doi: 10.1016/j.ocarto.2025.100710

    Figure Lengend Snippet: Effect of diltiazem hydrochloride on PIEZO1 channel sensitivity. A) Applied deformation after AFM loading. B) Magnitude of the intracellular Ca 2+ response to mechanical compression. C) Percentage of cells that responded to AFM compression. D) Magnitude of the intracellular Ca 2+ response to Yoda1 addition. E) Percentage of cells that responded Yoda1 addition. Data presented as mean ​± ​95 ​% confidence interval. Kruskal-Wallis testing was significant ( p ​= ​0.0343) but Dunn’s test revealed no significant differences between any groups. One way ANOVA with Tukey’s post-hoc test or Kruskal-Wallis testing with Dunn’s post-hoc test was used for group comparisons A-B and D-E. Different letters indicate statistical significance ( p ​< ​0.05). If the same letter is assigned to multiple groups, those groups are not significantly different from each other. Conversely, if two groups are denoted with completely different letters, the two groups are significantly different. N ​= ​14–80.

    Article Snippet: In order to analyze the effects of various VGCC inhibitors on PIEZO1 channel activity, primary chondrocytes were treated with CaV1.x blockers: verapamil (10, 50, and 100 μM, 10–20 min, Tocris, Bristol, United Kingdom), nifedipine (10, 50, and 100 μM, 10–20 min, Tocris, Bristol, United Kingdom), diltiazem hydrochloride (50, 100, and 200 μM, 10–20 min, Tocris, Bristol, United Kingdom), or CaV3.x blocker NNC-55 (0.1, 1, and 5 μM, 10–20 min, Tocris, Bristol, United Kingdom).

    Techniques:

    Effects of inhibitors and Yoda1 on chondrocyte death in cartilage explants subjected to injurious loading. A) Verapamil B) Diltiazem Hydrochloride C) Yoda1 D) GsMTx-4 E) Nifedipine F) NNC-55. Data presented as mean ​± ​95 ​% confidence interval. Student t-tests were used for group comparisons in A-F, ∗ p ​< ​0.05, ∗∗ p ​< ​0.005, ∗∗∗ p ​< ​0.001, ∗∗∗∗ p ​< ​0.0001, n ​= ​10–43.

    Journal: Osteoarthritis and Cartilage Open

    Article Title: PIEZO mechanosensitivity in chondrocytes is differentially modulated by L-type and T-type voltage-sensitive ion channels

    doi: 10.1016/j.ocarto.2025.100710

    Figure Lengend Snippet: Effects of inhibitors and Yoda1 on chondrocyte death in cartilage explants subjected to injurious loading. A) Verapamil B) Diltiazem Hydrochloride C) Yoda1 D) GsMTx-4 E) Nifedipine F) NNC-55. Data presented as mean ​± ​95 ​% confidence interval. Student t-tests were used for group comparisons in A-F, ∗ p ​< ​0.05, ∗∗ p ​< ​0.005, ∗∗∗ p ​< ​0.001, ∗∗∗∗ p ​< ​0.0001, n ​= ​10–43.

    Article Snippet: In order to analyze the effects of various VGCC inhibitors on PIEZO1 channel activity, primary chondrocytes were treated with CaV1.x blockers: verapamil (10, 50, and 100 μM, 10–20 min, Tocris, Bristol, United Kingdom), nifedipine (10, 50, and 100 μM, 10–20 min, Tocris, Bristol, United Kingdom), diltiazem hydrochloride (50, 100, and 200 μM, 10–20 min, Tocris, Bristol, United Kingdom), or CaV3.x blocker NNC-55 (0.1, 1, and 5 μM, 10–20 min, Tocris, Bristol, United Kingdom).

    Techniques: