ArticleActa pharmacologica Sinica2013
Rho-kinase inhibitor Y-27632 attenuates pulmonary hypertension in hyperoxia-exposed newborn rats.
Article in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 16 citations in OpenAlex.
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- Anti-inflammatory Effects of Statins in Lung Vascular Pathology: From Basic Science to Clinical Trials.Advances in experimental medicine and biology · 2021Article
- Advances in biomechanical and biochemical engineering methods to stimulate meniscus tissue.American journal of translational research · 2021Review
- Biochemical Stimulus-Based Strategies for Meniscus Tissue Engineering and Regeneration.BioMed research international · 2018Review
- Human mesenchymal stem cells ameliorate experimental pulmonary hypertension induced by maternal inflammation and neonatal hyperoxia in rats.Oncotarget · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo test the hypothesis that neonatal hyperoxia induced pulmonary hypertension accompanied by increased Rho-kinase expression in rat lungs and that Rho-kinase inhibitor could attenuate right ventricular hypertrophy and pulmonary arterial remodeling.
methodsNewborn rats were exposed to >95% O2 in the first week after birth, then to 60% O2 in the following 2 weeks. Control pups were exposed to room air over the same periods. The pups were injected with either Rho-kinase inhibitor Y-27632 (10 mg·kg(-1)·d(-1), ip) or vehicle from postnatal d 14 to 20. Lung and heart tissues were collected on postnatal d 7 and 21. Rho-kinase activity in lungs was measured using Western blotting and immunohistochemistry. The right ventricular hypertrophy and arterial medial wall thickness (MWT) were assessed morphologically.
resultsRho-kinase activity in lungs was comparable between the hyperoxic and control pups on postnatal d 7, but it had a more than 2-fold increase in the hyperoxic pups on postnatal d 21. Moreover, the hyperoxic exposure induced structural features of pulmonary hypertension, as shown by the right ventricular hypertrophy and significantly increased arterial MWT. Administration with Y-27632 effectively blocked the hyperoxia-induced increase of Rho-kinase activity in lungs, and attenuated the right ventricular hypertrophy.
conclusionRho-kinase inhibitor may be a novel therapy for attenuating the hyperoxia-induced structural changes in pulmonary hypertension.
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