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prka pka inhibitor h89  (MedChemExpress)


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    Structured Review

    MedChemExpress prka pka inhibitor h89
    Prka Pka Inhibitor H89, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 107 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/prka pka inhibitor h89/product/MedChemExpress
    Average 95 stars, based on 107 article reviews
    prka pka inhibitor h89 - by Bioz Stars, 2026-05
    95/100 stars

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    MedChemExpress pka agonists forskolin
    <t>PKA</t> agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + <t>Forskolin.</t>
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    <t>PKA</t> agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + <t>Forskolin.</t>
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    <t>PKA</t> agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + <t>Forskolin.</t>
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    Selleck Chemicals pka inhibitor h 89 2hcl
    <t>PKA</t> agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + <t>Forskolin.</t>
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    Image Search Results


    PKA agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + Forskolin.

    Journal: Materials Today Bio

    Article Title: PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis

    doi: 10.1016/j.mtbio.2026.103021

    Figure Lengend Snippet: PKA agonist improved silica nanoparticle-induced myocardial injury and dysfunction in rats. Histopathology examination for cardiac HE staining (A) and score analysis (B), n = 5 per group. Scale bar, 100 μm. Serum CK-MB (C) and cTnT (D) determination to indicate myocardial injury, n = 9-10 for each group. Also, analysis of rat heart function and structural parameters via echocardiography was performed. Mitral valve Doppler echocardiography (E) and cardiac structural assessment metrics (F). M-model (G) and cardiac systolic (H) and diastolic function (I)-related measurements. n = 7 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + Forskolin.

    Article Snippet: PKA agonists Forskolin and 8-Br-cAMP, H-89 (a PKA inhibitor), and Elesclomol (a copper ion carrier) were obtained from MedChemExpress, USA, while Mdivi-1 (a mitochondrial fission inhibitor for selectively inhibiting DRP1, dynamin related protein 1) was got from Sigma-Aldrich, USA.

    Techniques: Histopathology, Staining, Control

    PKA agonist greatly inhibited silica nanoparticle-induced systemic and cardiac oxidative stress in rats. (A) ROS measurement in myocardial tissues. (B) MDA levels in both the myocardial tissue (a) and serum (b) were measured. (C) The cardiac (a) and serum (b) levels of GSH and GSSG were detected, and the ratio of GSH/GSSG was calculated. n = 8-10 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + Forskolin.

    Journal: Materials Today Bio

    Article Title: PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis

    doi: 10.1016/j.mtbio.2026.103021

    Figure Lengend Snippet: PKA agonist greatly inhibited silica nanoparticle-induced systemic and cardiac oxidative stress in rats. (A) ROS measurement in myocardial tissues. (B) MDA levels in both the myocardial tissue (a) and serum (b) were measured. (C) The cardiac (a) and serum (b) levels of GSH and GSSG were detected, and the ratio of GSH/GSSG was calculated. n = 8-10 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs + Forskolin.

    Article Snippet: PKA agonists Forskolin and 8-Br-cAMP, H-89 (a PKA inhibitor), and Elesclomol (a copper ion carrier) were obtained from MedChemExpress, USA, while Mdivi-1 (a mitochondrial fission inhibitor for selectively inhibiting DRP1, dynamin related protein 1) was got from Sigma-Aldrich, USA.

    Techniques: Control

    PKA agonist alleviated silica nanoparticle-induced cardiac mitochondrial injury and dysfunction. (A) TEM was used to observe mitochondrial morphology. Flameng score analysis of at least 100 mitochondria per group was performed to indicate mitochondrial injury. Scale bar, 1.0 μm. (B) The contents of Mitochondrial Complex I (a), Mitochondrial Complex III (b), Mitochondrial Complex V (c), and ATP (d) in myocardial tissues were measured. n = 9-10 per group. (C) Mitochondrial stress assay was performed to evaluate mitochondrial function in vitro cultured AC16 cardiomyocytes. Schematic representation of the Seahorse XFe cell mitochondrial stress test (a), OCR curves for each group (b), and the relevant indicators (basal respiration, proton leak, ATP production, maximal respiration, spare respiratory capacity, and non-mitochondrial oxygen consumption) of mitochondrial respiration measurement (c). n = 3 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Journal: Materials Today Bio

    Article Title: PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis

    doi: 10.1016/j.mtbio.2026.103021

    Figure Lengend Snippet: PKA agonist alleviated silica nanoparticle-induced cardiac mitochondrial injury and dysfunction. (A) TEM was used to observe mitochondrial morphology. Flameng score analysis of at least 100 mitochondria per group was performed to indicate mitochondrial injury. Scale bar, 1.0 μm. (B) The contents of Mitochondrial Complex I (a), Mitochondrial Complex III (b), Mitochondrial Complex V (c), and ATP (d) in myocardial tissues were measured. n = 9-10 per group. (C) Mitochondrial stress assay was performed to evaluate mitochondrial function in vitro cultured AC16 cardiomyocytes. Schematic representation of the Seahorse XFe cell mitochondrial stress test (a), OCR curves for each group (b), and the relevant indicators (basal respiration, proton leak, ATP production, maximal respiration, spare respiratory capacity, and non-mitochondrial oxygen consumption) of mitochondrial respiration measurement (c). n = 3 per group. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Article Snippet: PKA agonists Forskolin and 8-Br-cAMP, H-89 (a PKA inhibitor), and Elesclomol (a copper ion carrier) were obtained from MedChemExpress, USA, while Mdivi-1 (a mitochondrial fission inhibitor for selectively inhibiting DRP1, dynamin related protein 1) was got from Sigma-Aldrich, USA.

    Techniques: In Vitro, Cell Culture, Control

    PKA mitigated copper overload triggered by SiNPs. (A) In the SiNPs-instilled rats, enhanced copper contents in both serum (a) and myocardial tissues (b) were detected, but PKA agonist Forskolin reversed it. n = 9-10 per group. (B) The dose-dependent elevation of intracellular Cu 2+ content by SiNPs treatment in the in vitro cultured AC16 cardiomyocytes (a), which could be greatly reduced by PKA stimulator 8-Br-cAMP but increased by PKA inhibitor H89 (b). (C) The expressions of copper metabolism-related protein (FDX1, SLC31A1, and ATP7B) in AC16 cells were measured (C-a, protein bands; C-b, bands analysis). Also, the expression of ATP7B was measured in rat myocardial tissue (D). n = 3. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Journal: Materials Today Bio

    Article Title: PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis

    doi: 10.1016/j.mtbio.2026.103021

    Figure Lengend Snippet: PKA mitigated copper overload triggered by SiNPs. (A) In the SiNPs-instilled rats, enhanced copper contents in both serum (a) and myocardial tissues (b) were detected, but PKA agonist Forskolin reversed it. n = 9-10 per group. (B) The dose-dependent elevation of intracellular Cu 2+ content by SiNPs treatment in the in vitro cultured AC16 cardiomyocytes (a), which could be greatly reduced by PKA stimulator 8-Br-cAMP but increased by PKA inhibitor H89 (b). (C) The expressions of copper metabolism-related protein (FDX1, SLC31A1, and ATP7B) in AC16 cells were measured (C-a, protein bands; C-b, bands analysis). Also, the expression of ATP7B was measured in rat myocardial tissue (D). n = 3. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Article Snippet: PKA agonists Forskolin and 8-Br-cAMP, H-89 (a PKA inhibitor), and Elesclomol (a copper ion carrier) were obtained from MedChemExpress, USA, while Mdivi-1 (a mitochondrial fission inhibitor for selectively inhibiting DRP1, dynamin related protein 1) was got from Sigma-Aldrich, USA.

    Techniques: In Vitro, Cell Culture, Expressing, Control

    PKA/DRP1/ATP7B-mediated copper overload induced by SiNPs, contributing to apoptosis of cardiomyocytes. (A) Representative protein images (a) and quantification analysis (b) of p -PKA, PKA, p -DRP1 (S637) , and DRP1 in myocardial tissue were performed. The effects of Mdivi-1 pre-treatment on Cu 2+ (B) content, and the expression of p -DRP1 (S637) and ATP7B in AC16 cells were detected (C-a, protein bands; C-b, bands analysis). The effects of Elesclomol pre-treatment on Cu 2+ content (D) and cell apoptosis (E) were assessed in AC16 cells. The representative flow cytometry images were shown (E-a), and apoptotic rates were quantified (E-b). n = 3. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Journal: Materials Today Bio

    Article Title: PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis

    doi: 10.1016/j.mtbio.2026.103021

    Figure Lengend Snippet: PKA/DRP1/ATP7B-mediated copper overload induced by SiNPs, contributing to apoptosis of cardiomyocytes. (A) Representative protein images (a) and quantification analysis (b) of p -PKA, PKA, p -DRP1 (S637) , and DRP1 in myocardial tissue were performed. The effects of Mdivi-1 pre-treatment on Cu 2+ (B) content, and the expression of p -DRP1 (S637) and ATP7B in AC16 cells were detected (C-a, protein bands; C-b, bands analysis). The effects of Elesclomol pre-treatment on Cu 2+ content (D) and cell apoptosis (E) were assessed in AC16 cells. The representative flow cytometry images were shown (E-a), and apoptotic rates were quantified (E-b). n = 3. ∗ p < 0.05 vs control, # p < 0.05 vs SiNPs or SiNPs + Forskolin.

    Article Snippet: PKA agonists Forskolin and 8-Br-cAMP, H-89 (a PKA inhibitor), and Elesclomol (a copper ion carrier) were obtained from MedChemExpress, USA, while Mdivi-1 (a mitochondrial fission inhibitor for selectively inhibiting DRP1, dynamin related protein 1) was got from Sigma-Aldrich, USA.

    Techniques: Expressing, Flow Cytometry, Control