ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Ripasudil Attenuates Lipopolysaccharide (LPS)-Mediated Apoptosis and Inflammation in Pulmonary Microvascular Endothelial Cells via ROCK2/eNOS Signaling.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Ripasudil, a Rho kinase inhibitor, attenuates testosterone-induced benign prostatic hyperplasia in rats: targeting inflammation, oxidative stress, and Rho kinase pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Targeting MAD2B as a strategy for ischemic stroke therapy.Journal of advanced research · 2025Article
- The Specific ROCK2 Inhibitor KD025 Alleviates Glycolysis through Modulating STAT3-, CSTA- and S1PR3-Linked Signaling in Human Trabecular Meshwork Cells.Biomedicines · 2024Article
- Ripasudil as a Potential Therapeutic Agent in Treating Secondary Glaucoma in HTLV-1-Uveitis: An In Vitro Analysis.International journal of molecular sciences · 2024Article
- CircHECTD1 promoted MIRI-associated inflammation via inhibiting miR-138-5p and upregulating ROCK2.The Kaohsiung journal of medical sciences · 2023Article
- iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1.Experimental and therapeutic medicine · 2023Article
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
- Inhibiting P2Y12 receptor relieves LPS-induced inflammation and endothelial dysfunction.Immunity, inflammation and disease · 2022Article
- ROCK2 knockdown alleviates LPS-induced inflammatory injury and apoptosis of renal tubular epithelial cells via the NF-κB/NLRP3 signaling pathway.Experimental and therapeutic medicine · 2022Article
- ROCK inhibitor fasudil reduces the expression of inflammatory factors in LPS-induced rat pulmonary microvascular endothelial cells via ROS/NF-κB pathway.BMC pharmacology & toxicology · 2022Article
- Article
- Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells InjuryFrontiers in pharmacology · 2022Article
- ROCK inhibitors modulate the physical properties and adipogenesis of 3D spheroids of human orbital fibroblasts in different manners.FASEB bioAdvances · 2021Article
- ROCK inhibitors enhance the production of large lipid-enriched 3D organoids of 3T3-L1 cells.Scientific reports · 2021Article
- Prostaglandin E1 Improves Cerebral Microcirculation Through Activation of Endothelial NOS and GRPCH1.Journal of molecular neuroscience : MN · 2020Article
- Effects of ROCK Inhibitors on Apoptosis of Corneal Endothelial Cells in CMV-Positive Posner-Schlossman Syndrome Patients.Investigative ophthalmology & visual science · 2020Article
- Time Course in Ocular Blood Flow and Pulse Waveform in a Case of Ocular Ischemic Syndrome with Intraocular Pressure Fluctuation.Vision (Basel, Switzerland) · 2020Article
- Ripasudil alleviated the inflammation of RPE cells by targeting the miR-136-5p/ROCK/NLRP3 pathway.BMC ophthalmology · 2020Article
- The Mechanism of Aureusidin in Suppressing Inflammatory Response in Acute Liver Injury by Regulating MD2.Frontiers in pharmacology · 2020Article
- Protection of ripasudil, a Rho kinase inhibitor, in lipopolysaccharides-induced acute pneumonia in mice.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Microvascular endothelial inflammation and apoptosis are responsible for septic acute lung injury (ALI). Ripasudil is a novel Rho/Rho kinase (ROCK) inhibitor which shows therapeutic effects on several vascular diseases. The aim of this study was to investigate the protective effects and correlated molecular mechanisms of ripasudil on lipopolysaccharide- induced inflammation and apoptosis of pulmonary microvascular endothelial cells (PMVECs). MATERIAL AND METHODS Cultured PMVECs were exposed to lipopolysaccharide (LPS). Ripasudil at various concentrations was used to treat the cells. Several cells were also co-administrated with the endothelial nitric oxide synthase (eNOS) inhibitor Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME). Cell viability was assessed by MTT assay. Terminal dUTP transferase nick-end labeling (TUNEL) assay was used to detect the apoptosis. The colorimetric method was used to measure the activity of eNOS and ROCK2. Protein phosphorylation and expression were assessed by Western blotting. RESULTS Ripasudil attenuated the LPS-induced inflammation and apoptosis in PMVECs, which was reversed by L-NAME. Ripasudil suppressed ROCK2 activity and further increased the eNOS activity. Ripasudil treatment increased the phosphorylation of eNOS, increased the expression level of Bcl2, and decreased the expression level of active caspase3 in LPS-treated PMVECs. Moreover, the ripasudil treatment also inhibited the nuclear translocation of NF-κB and further suppressed the levels of interleukin (IL) 6 and tumor necrosis factor (TNF) α. The co-treatment with L-NAME, however, impaired the anti-apoptotic and anti-inflammatory effects of ripasudil on PMVECs without affecting ROCK2. CONCLUSIONS The novel ROCK2 inhibitor ripasudil suppressed LPS-induced apoptosis and inflammation in PMVECs by regulating the ROCK2/eNOS signaling pathway.
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