2014
DOI: 10.3892/mmr.2014.2094
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Post-conditioning with sevoflurane induces heme oxygenase-1 expression via the PI3K/Akt pathway in lipopolysaccharide-induced acute lung injury

Abstract: Abstract. The aim of the present study was to explore the regulatory mechanism of heme oxygenase-1 (HO-1) expression induced by sevoflurane (Sevo) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Sprague-Dawley rats were divided randomly into six groups: (A) Control, (B) 2.4% Sevo only, (C) LY294002 (PI3K inhibitor) only, (D) LPS + 2.4% Sevo, (E) LY294002 + LPS + 2.4% Sevo and (F) LPS only. The pathological changes in wet/dry weight ratio (W/D), the activities of superoxide dismutase, myeloperoxida… Show more

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Cited by 12 publications
(5 citation statements)
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“…PI3K/Akt has been shown to be a downstream component of receptor tyrosine kinases such as EGFR, which are activated by different stimuli [41,53] leading to HO-1 expression [29,54]. In PC12 cells, PI3K/Akt has been documented to mediate HO-1 expression induced by carnosol [55] and NGF [56].…”
Section: Discussionmentioning
confidence: 99%
“…PI3K/Akt has been shown to be a downstream component of receptor tyrosine kinases such as EGFR, which are activated by different stimuli [41,53] leading to HO-1 expression [29,54]. In PC12 cells, PI3K/Akt has been documented to mediate HO-1 expression induced by carnosol [55] and NGF [56].…”
Section: Discussionmentioning
confidence: 99%
“…Nonetheless, quite similar inhibitory effects of sevoflurane posttreatment on pro-inflammatory responses have been reported recently. In lipopolysaccharide challenged rats, for instance, sevoflurane posttreatment significantly reduced myeloperoxidase activity [ 41 ], tumor necrosis factor-α and IL-6 mRNA [ 42 ], or total cell counts and inflammatory mediators [ 43 ]. However, in all of these reports, rats received sevoflurane treatment as early as 2 h after the onset of LPS challenge for another 4 h; time dependent effects of sevoflurane treatment were not examined.…”
Section: Discussionmentioning
confidence: 99%
“…Pretreatment with LY294002, a PI3K inhibitor, prior to LPS, reduced HO-1 expression and partially reversed the protective sevoflurane effects. The authors concluded that sevoflurane alleviates ALI through the induction of HO-1 via the PI3K/Akt pathway [81]. The study underpins data from a previous study on sevoflurane postconditioning: Zheng et al showed that sevoflurane activates the PI3K/Akt pathway to protect isolated rat hearts against I/R-induced apoptosis [82].…”
Section: The Role Of Anesthetic Agents On Ho-1 Modulationmentioning
confidence: 87%
“…Besides conditions of oxidative stress (I/R-injury, VILI), possible protective effects of sevoflurane have also been investigated in inflammatory conditions. Zhao et al investigated the effect of sevoflurane postconditioning and the regulatory role of HO-1 in LPS-induced acute lung injury in male Sprague–Dawley rats [81]. Inhalation of sevoflurane (2.4 vol%), started 2 h after LPS (5 mg/kg intravenous (i.v.))…”
Section: The Role Of Anesthetic Agents On Ho-1 Modulationmentioning
confidence: 99%