ArticleAmerican journal of translational research2019
Protective effects of Ulinastatin on oxidative stress and inflammation of rat-derived cardiomyocytes H9c2.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The effect of Ulinastatin on postoperative course in cardiopulmonary bypass patients in Asia: a meta-analysis of randomized controlled trials.Journal of cardiothoracic surgery · 2022Pooled it
- Salubrious effects of ulinastatin and quercetin alone or in combination in endothelial dysfunction and vascular dementia.Pharmacological reports : PR · 2022Article
- Ulinastatin combined with glutamine improves liver function and inflammatory response in patients with severe acute pancreatitis.American journal of translational research · 2022Article
- Efficacy of Ulinastatin and Sulforaphane Alone or in Combination in Rat Model of Streptozotocin Diabetes Induced Vascular Dementia.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2021Article
- Ulinastatin attenuates protamine-induced cardiotoxicity in rats by inhibiting tumor necrosis factor alpha.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Research progress of ulinastatin in the treatment of liver diseases.International journal of clinical and experimental pathology · 2020Review
- Opa1 Reduces Hypoxia-Induced Cardiomyocyte Death by Improving Mitochondrial Quality Control.Frontiers in cell and developmental biology · 2020Article
- Ulinastatin attenuates monocyte-endothelial adhesion via inhibiting ROS transfer between the neighboring vascular endothelial cells mediated by Cx43.American journal of translational research · 2020Article
- Ulinastatin Promotes Regeneration of Peripheral Nerves After Sciatic Nerve Injury by Targeting let-7 microRNAs and Enhancing NGF Expression.Drug design, development and therapy · 2020Article
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
Ischemic heart disease (IHD) is a common clinical disease and has a younger tendency in recent years. This study focused on the role of Ulinastatin (UTI) in the anti-oxidative stress and anti-inflammatory response of cardiomyocytes. H9c2 cells were divided into control group, ischemia-anoxic group (ischemic hypoxia group) and ischemia-anoxia + UTI group (UTI group). Cell morphology was observed by light microscopy, Cell staining, Western blotting, quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were conducted to research the effect of UTI on the nuclear factor-κB (NF-κB) signaling pathway. H9c2 cells in the ischemic hypoxia group showed hypertrophy and irregular shape, while the cell morphology of the UTI group was close to the fusiform shape. The cell hypertrophy was lighter, and the number of irregular morphological cells decreased in UTI group than ischemic hypoxia group. The content of interleukin-1β (IL-1β) in the ischemic hypoxic group was significantly higher than that in the control group. In the UTI group, IL-1β was significantly lowly expressed than the ischemia hypoxia group. In addition, the expressions of SOD1, SOD2, GPX1, GPX3, Bcl-2 and Sirt1 in UTI group were higher than ischemic hypoxia group (P<0.05). The expressions of p65, Iκk-α kinase, Caspase3 and Bax in UTI group were lower than ischemic hypoxia group (P<0.05). UTI protects H9c2 cells from ischemia and hypoxia injuries by inhibiting the NF-κB pathway, thereby reducing inflammation, resisting oxidative stress, inhibiting apoptosis, and delaying cell senescence.
Indexed as
Identifiers
31814912PMC6895533W2998052311What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.