ArticleScientific reports2019
Oxytocin maintains lung histological and functional integrity to confer protection in heat stroke.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Overexpression of Parkin promotes the protective effect of mitochondrial autophagy on the lung of rats with exertional heatstroke.Journal of intensive medicine · 2025Article
- Protection of Parkin over-expression on lung in rats with exertional heat stroke by activating mitophagy.BMC pulmonary medicine · 2024Article
- Oxytocin: A Shield against Radiation-Induced Lung Injury in Rats.Tomography (Ann Arbor, Mich.) · 2024Article
- Activation of Pink1/Parkin-mediated mitochondrial autophagy alleviates exertional heat stroke-induced acute lung injury in rats.Clinical hemorheology and microcirculation · 2024Article
- Article
- ZBP1 and heatstroke.Frontiers in immunology · 2023Review
- Climate change and pregnancy complications: From hormones to the immune response.Frontiers in endocrinology · 2023Review
- Heatstroke-induced acute kidney injury and the innate immune system.Frontiers in medicine · 2023Review
- [Hydroxysafflor yellow A attenuates heat stroke-induced acute lung injury in mice by inhibiting necroptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Anti-Inflammatory and Anti-Oxidative Effects of Isorhamnetin for Protection Against Lung Injury in a Rat Model of Heatstroke in a Dry-Heat Environment.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Sucrose intake by rats affected by both intraperitoneal oxytocin administration and time of day.Psychopharmacology · 2022Article
- Oxytocin and Related Peptide Hormones: Candidate Anti-Inflammatory Therapy in Early Stages of Sepsis.Frontiers in immunology · 2022Review
- NF‑κB/IκBα signaling pathways are essential for resistance to heat stress‑induced ROS production in pulmonary microvascular endothelial cells.Molecular medicine reports · 2021Article
- Tetrandrine attenuates hyperoxia-induced lung injury in newborn rats via NF-κB p65 and ERK1/2 pathway inhibition.Annals of translational medicine · 2020Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxytocin (OT) has been reported to have a protective effect in lipopolysaccharide-induced experimental acute lung injury (ALI). However, its role in heat stroke-related ALI has never been investigated. Herein, we aimed to explore the therapeutic effects and potential mechanism of action of OT on heat-induced ALI. Rats were treated with OT 60 min before the start of heat stress (42 °C for 80 min). Twenty minutes after the termination of heat stress, the effects of OT on lung histopathological changes, edema, acute pleurisy and the bronchoalveolar fluid levels of inflammatory cytokines and indicators of ischemia, cellular damage, and oxidative damage were assessed. We also evaluated the influence of OT pretreatment on heat-induced hypotension, hyperthermia, ALI score, and death in a rat model of heat stroke. The results showed that OT significantly reduced heat-induced lung edema, neutrophil infiltration, hemorrhage score, myeloperoxidase activity, ischemia, and the levels of inflammatory and oxidative damage markers in bronchoalveolar lavage fluid. The survival assessment confirmed the pathophysiological and biochemical results. An OT receptor antagonist (L-368,899) was administered 10 min before the OT injection to further demonstrate the role of OT in heat-induced ALI. The results showed that OT could not protect against the aforementioned heat stroke responses in rats treated with L-368,899. Interestingly, OT treatment 80 min after the start of heat shock did not affect survival. In conclusion, our data indicate that OT pretreatment can reduce the ischemic, inflammatory and oxidative responses related to heat-induced ALI in rats.
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