ArticleExperimental and therapeutic medicine2018
Activated protein C inhibits lung injury induced by LPS via downregulating MAPK signaling.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- A novel peptide-compound conjugate alleviates endotoxin-induced inflammation via NF-κB/MAPK modulation.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Platelets at the intersection of inflammation and coagulation in the APC-mediated response to myocardial ischemia/reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Apelin‑36 protects against lipopolysaccharide‑induced acute lung injury by inhibiting the ASK1/MAPK signaling pathway.Molecular medicine reports · 2021Article
- Thrombomodulin Regulation of Mitogen-Activated Protein Kinases.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effect and the underlying mechanism of activated protein C (APC) in lipopolysaccharide (LPS) induced lung injury, as well as the potential mechanism. According to the treatment, 50 rats were randomly divided into 5 groups: Control, model (LPS), low-dose group [LPS + 0.1 mg/kg recombined human activated protein C (rhAPC)], median-dose group (LPS + 0.3 mg/kg rhAPC) and high-dose group (LPS + 0.5 mg/kg rhAPC). Then, inflammation in the lung was assessed using hematoxylin and eosin (H&E) staining. Following the collection of bronchoalveolar lavage fluid (BALF), the number of leukocytes and neutrophils in BALF was counted, and superoxide dismutase (SOD) activity was assessed, as well as the expression levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α using ELISA. Subsequently, the expression and phosphorylation of P-38, extracellular signal-regulated kinase (Erk)-1/2, and c-Jun N-terminal kinase (JNK) were estimated using western blotting. Based on H&E staining, rhAPC markedly suppressed inflammatory infiltration in the lung induced by LPS in a dose-dependent manner. In addition, rhAPC also significantly attenuated the accumulation of leptocytes and neutrophils, and the reduction of SOD in BALF induced by LPS in a dose-dependent manner. rhAPC also significantly attenuated the elevation of IL-1β, IL-6 and TNF-α in BALF induced by LPS in a dose-dependent manner. Further mechanistic analysis revealed that rhAPC treatment could evidently attenuate the phosphorylation levels of P-38, Erk1/2 and JNK in the lung induced by LPS in a dose-dependent manner. In conclusion, APC significantly alleviated the lung inflammation induced by LPS by downregulating the phosphorylation of P-38, ERK1/2 and JNK.
Indexed as
Identifiers
What 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.