ArticleImmunity, inflammation and disease2022
Parecoxib sodium alleviates ischemia reperfusion-induced pulmonary injury via inhibiting ERK/NF-κB and further activating the HIF-1α pathway.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Expression and Regulation of Hypoxia-Inducible Factor Signalling in Acute Lung Inflammation.Cells · 2024Review
- Ischemia/reperfusion-activated ferroptosis in the early stage triggers excessive inflammation to aggregate lung injury in rats.Frontiers in medicine · 2023Article
- Parecoxib sodium alleviates ischemia reperfusion-induced pulmonary injury via inhibiting ERK/NF-κB and further activating the HIF-1α pathway.Immunity, inflammation and disease · 2022Article
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2 authors at 1 institution in 1 country.
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Abstract
introductionThe lungs are extremely vulnerable to ischemia/reperfusion (I/R), which is characterized by intense inflammation, oxidative stress, alveolar damage, and vascular permeability. Parecoxib sodium (Pare) has been shown to exert protective effects against multiple I/R-induced tissue injuries. However, its role in I/R-induced lung injury remains unknown. This study aimed to reveal the roles and mechanisms of Pare in pulmonary I/R injury.
methodsSixty-six rats were randomly divided into three groups: The sham-operated group, the pulmonary I/R group, and the Pare-pretreated I/R group. Pare at 10 mg/kg or saline (vehicle control) were intraperitoneally administered to rats once per day for 5 consecutive days before ischemia. Serum and tissue samples were harvested following 2 h of reperfusion. The oxygenation index (OI) and alveolar-arterial oxygen partial pressure difference (PA-aO
resultsPare significantly increased the OI, decreased the PA-aO
conclusionsPare pretreatment attenuated lung I/R injury by inhibiting oxidative stress and the inflammatory response possibly via inhibiting the activation of the ERK/NF-κB pathway and further activating the HIF-1α pathway.
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