ArticleOncology letters2018
Ulinastatin protects the lungs of COPD rats through the HMGB1/TLR4 signaling pathway.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies.International journal of chronic obstructive pulmonary disease · 2025Review
- Plumbagin inhibits fungal growth, HMGB1/LOX-1 pathway and inflammatory factors inFrontiers in microbiology · 2024Article
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- Pharmacological effects of Bufei Jianpi granule on chronic obstructive pulmonary disease and its metabolism in rats.Frontiers in pharmacology · 2022Article
- Review
- Ulinastatin attenuates monocyte-endothelial adhesion via inhibiting ROS transfer between the neighboring vascular endothelial cells mediated by Cx43.American journal of translational research · 2020Article
- Xiaoqinglong Decoction Protects the Lungs of AECOPD Mice through the AMPK/mTOR Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2020Review
- Inhibition of LOX-1 alleviates the proinflammatory effects of high-mobility group box 1 inInternational journal of ophthalmology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the protective mechanism of ulinastatin against lung injury. Rat models with chronic obstructive pulmonary disease (COPD) were used to provide guidance for the medical treatment of this disease. The rats were divided into three groups: A control group, a model group and an experimental group (each, n=10). With the exception of the control group, all of the rats were prepared as models of COPD, using the composite molding method of smoking and intratracheal instillation of lipopolysaccharide. The rats in the model group all received a conventional treatment, while the rats in the experimental group received ulinastatin. A small animal lung function detector was used to examine lung function. The forced expiratory volume/sec (FEV) was negatively correlated with the protein expression levels of Toll-like receptor 4 (TLR4) and high mobility group box protein 1 (HMGB1). Real-time fluorescence quantitative polymerase chain reaction and western blot analyses were used to detect TLR4, MyD88 (myeloid differentiation factor 88), TRAF-6 (TNF receptor-associated factor 6), LOX-1 (lectin-type oxidized LDL receptor 1) and HMGB1 mRNA, along with their protein expression levels. The lung function of rats in the model group was significantly decreased compared with in the control group (P<0.05). In the experimental group the lung function was significantly greater, when compared with in the model group; however, it remained lower than in the control group. The mRNA and protein expression levels of TLR4, MyD88, TRAF-6, LOX-1 and HMGB1 were significantly higher in the model group than in the control and experimental groups; however, levels in the experimental group were significantly higher when compared with in the control group (P<0.05). The TLR4 and HMGB1 expression levels were positively correlated in all groups, which indicated involvement of the HMGB1/TLR4 signaling pathway. The FEV was negatively correlated with the protein expression levels of TLR4 and HMGB1. Thus, the protective effect of ulinastatin in the lungs of rats with COPD is associated with changes in the HMGB1/TLR4 signaling pathway.
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