ArticleInternational journal of clinical and experimental pathology2018
Transient cerebral ischemia/reperfusion-induced acute lung injury in rats associated with protein kinase C alpha expression.
Article in International journal of clinical and experimental pathology, 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
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Formononetin Protects Against Cerebral Ischemia-Reperfusion-Induced Lung Injury: Insights from Animal and Cell Models.Journal of inflammation research · 2026Article
- Expression of NGF, proNGF, p75Clinics (Sao Paulo, Brazil) · 2024Article
- Phosphorylation of Eukaryotic Initiation Factor 4G1 (eIF4G1) at Ser1147 Is Specific for eIF4G1 Bound to eIF4E in Delayed Neuronal Death after Ischemia.International journal of molecular sciences · 2022Article
- Inhibition of protein kinase C alpha attenuates lipopolysaccharide-triggered acute lung injury by alleviating the hyperinflammatory response and oxidative stress.Annals of translational medicine · 2022Article
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
objectiveThe pathogenesis and development timing of acute lung injury (ALI) following cerebral ischemia/reperfusion (I/R) are not fully understood. In this study, the development timing of ALI induced by transient global cerebral I/R as well as the underlying mechanisms of action were investigated.
methodsA cerebral I/R-induced ALI model in Wistar rats was established by electrocoagulation of bilateral vertebral arteries combined with ligation of the transient bilateral common carotid arteries. Rats were randomly divided into control and cerebral I/R groups. The latter was subdivided into 3 h, 24 h, 48 h and 72 h post reperfusion. Lung injury was assessed by histological examination. The mRNA and protein expression of protein kinase C alpha (PKCα) were determined using qRT-PCR and immunofluorescence analysis, respectively.
resultsLung histological injury could be detected as early as 3 h after global cerebral I/R, and was significant between groups at 48 h and 72 h. Compared with the control group, mRNA expression of PKCα in the lung was enhanced in rats in the cerebral I/R groups (P<0.001), and the highest expression was observed at 48 h (P<0.001). The intensity of PKCα reactivity gradually increased starting at 3 h, and peaked at 72 h after cerebral I/R (P<0.05).
conclusionsThe lung is very susceptible to transient global cerebral I/R injury
Indexed as
Identifiers
31949727PMC6962896W3026376215What 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.