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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Proteintech anti phospho akt ser473 rabbit monoclonal antibody
Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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Molecular docking and dynamics simulations of <t>AKT1,</t> eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes
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MedChemExpress p akt1
Ra influences the <t>AKT1</t> / GSK3β signaling pathway under high-glucose conditions. a and b. Western blot analysis assessed AKT1 and p- AKT1 protein levels in HG-treated rMC-1 cells. a and c. Western blot analysis assessed GSK3β and p- GSK3β protein levels in HG-treated rMC-1 cells. d-f. Effects of Ra on GPX4 and xCT expression in HG-treated rMC-1 cells assessed by Western blotting ( n = 3, *P < 0.05, ns: no significance, compared to HG group). Ra: Ranitidine, HG: High-glucose, rMC-1: Mouse retinal Müller cells, GPX4: Glutathione peroxidase 4, xCT: Cystine/glutamate transporter
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Molecular docking and dynamics simulations of AKT1, eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes

Journal: Chinese Medicine

Article Title: Optimized New Shengmai Powder suppresses ferroptosis in ischemic cardiomyocytes via cGMP-PKG signalling

doi: 10.1186/s13020-026-01364-6

Figure Lengend Snippet: Molecular docking and dynamics simulations of AKT1, eNOS, and ONSMP active components. A Topological network analysis of AKT1, eNOS, and ONSMP active components. B Molecular docking of AKT1 with ONSMP active components. C Molecular dynamics simulations of AKT1–ONSMP active component complexes. D Molecular docking of eNOS with ONSMP active components. E Molecular dynamics simulations of eNOS–ONSMP active component complexes

Article Snippet: For IF co-localization, two primary antibodies from different host species were mixed and incubated together: AKT1 (bsm-52010R, BIOSS, Beijing, China) with eNOS (bsm-33176 M, BIOSS, Beijing, China), and STAT3 (bsm-33301 M, BIOSS, Beijing, China) with PKG1 (A01708-3, Boster, Wuhan, Hubei, China).

Techniques:

ONSMP activates the cGMP–PKG signaling pathway to inhibit cardiomyocyte ferroptosis. ONSMP activates AKT1, thereby regulating the cGMP–PKG signaling pathway and promoting GPX4 expression. GPX4 then uses GSH as an electron donor to maintain its antioxidant activity, effectively eliminating lipid peroxides and suppressing ferroptosis in cardiomyocytes

Journal: Chinese Medicine

Article Title: Optimized New Shengmai Powder suppresses ferroptosis in ischemic cardiomyocytes via cGMP-PKG signalling

doi: 10.1186/s13020-026-01364-6

Figure Lengend Snippet: ONSMP activates the cGMP–PKG signaling pathway to inhibit cardiomyocyte ferroptosis. ONSMP activates AKT1, thereby regulating the cGMP–PKG signaling pathway and promoting GPX4 expression. GPX4 then uses GSH as an electron donor to maintain its antioxidant activity, effectively eliminating lipid peroxides and suppressing ferroptosis in cardiomyocytes

Article Snippet: For IF co-localization, two primary antibodies from different host species were mixed and incubated together: AKT1 (bsm-52010R, BIOSS, Beijing, China) with eNOS (bsm-33176 M, BIOSS, Beijing, China), and STAT3 (bsm-33301 M, BIOSS, Beijing, China) with PKG1 (A01708-3, Boster, Wuhan, Hubei, China).

Techniques: Expressing, Antioxidant Activity Assay

Ra influences the AKT1 / GSK3β signaling pathway under high-glucose conditions. a and b. Western blot analysis assessed AKT1 and p- AKT1 protein levels in HG-treated rMC-1 cells. a and c. Western blot analysis assessed GSK3β and p- GSK3β protein levels in HG-treated rMC-1 cells. d-f. Effects of Ra on GPX4 and xCT expression in HG-treated rMC-1 cells assessed by Western blotting ( n = 3, *P < 0.05, ns: no significance, compared to HG group). Ra: Ranitidine, HG: High-glucose, rMC-1: Mouse retinal Müller cells, GPX4: Glutathione peroxidase 4, xCT: Cystine/glutamate transporter

Journal: Indian Journal of Ophthalmology

Article Title: Ranitidine protects Müller cells against ferroptosis in diabetic retinopathy by regulating the AKT1 / GSK3β pathway

doi: 10.4103/IJO.IJO_1522_25

Figure Lengend Snippet: Ra influences the AKT1 / GSK3β signaling pathway under high-glucose conditions. a and b. Western blot analysis assessed AKT1 and p- AKT1 protein levels in HG-treated rMC-1 cells. a and c. Western blot analysis assessed GSK3β and p- GSK3β protein levels in HG-treated rMC-1 cells. d-f. Effects of Ra on GPX4 and xCT expression in HG-treated rMC-1 cells assessed by Western blotting ( n = 3, *P < 0.05, ns: no significance, compared to HG group). Ra: Ranitidine, HG: High-glucose, rMC-1: Mouse retinal Müller cells, GPX4: Glutathione peroxidase 4, xCT: Cystine/glutamate transporter

Article Snippet: After being closed with 5% bovine serum albumin blocking solution for 2 h at room temperature, the membranes were incubated with primary antibodies against GPX4 (Med Chem Express, USA) (1:1000), xCT (Med Chem Express, USA) (1:1000), GSK3β (Med Chem Express, USA) (1:1000), p- GSK3β (Med Chem Express, USA) (1:1000), AKT1 (Zenbio, USA) (1:1000), or p- AKT1 (Med Chem Express, USA) (1:1000) proteins at 4°C overnight.

Techniques: Western Blot, Expressing

Ra inhibits HG-induced ferroptosis in rMC-1 cells, depending on GSK3β . a-c. The effects of Ra on the expression levels of AKT1 , P- AKT1 , GSK3β , and p- GSK3β in HG-cultured rMC-1 cells were assessed by Western blotting. d-f. The effects of Ra on the expression levels of GPX4 and xCT in HG-cultured rMC-1 cells were assessed by Western blotting ( n = 3, **P < 0.01, ***P < 0.001, ns: no significance, compared to HG group; # P < 0.05, ### P < 0.001, ns: no significance, compared to HG + Ra group). Ra: Ranitidine, HG: High-glucose, rMC-1: Mouse retinal Müller cells, GPX4: Glutathione peroxidase 4, xCT: Cystine/glutamate transporter

Journal: Indian Journal of Ophthalmology

Article Title: Ranitidine protects Müller cells against ferroptosis in diabetic retinopathy by regulating the AKT1 / GSK3β pathway

doi: 10.4103/IJO.IJO_1522_25

Figure Lengend Snippet: Ra inhibits HG-induced ferroptosis in rMC-1 cells, depending on GSK3β . a-c. The effects of Ra on the expression levels of AKT1 , P- AKT1 , GSK3β , and p- GSK3β in HG-cultured rMC-1 cells were assessed by Western blotting. d-f. The effects of Ra on the expression levels of GPX4 and xCT in HG-cultured rMC-1 cells were assessed by Western blotting ( n = 3, **P < 0.01, ***P < 0.001, ns: no significance, compared to HG group; # P < 0.05, ### P < 0.001, ns: no significance, compared to HG + Ra group). Ra: Ranitidine, HG: High-glucose, rMC-1: Mouse retinal Müller cells, GPX4: Glutathione peroxidase 4, xCT: Cystine/glutamate transporter

Article Snippet: After being closed with 5% bovine serum albumin blocking solution for 2 h at room temperature, the membranes were incubated with primary antibodies against GPX4 (Med Chem Express, USA) (1:1000), xCT (Med Chem Express, USA) (1:1000), GSK3β (Med Chem Express, USA) (1:1000), p- GSK3β (Med Chem Express, USA) (1:1000), AKT1 (Zenbio, USA) (1:1000), or p- AKT1 (Med Chem Express, USA) (1:1000) proteins at 4°C overnight.

Techniques: Expressing, Cell Culture, Western Blot