Nitric Oxide Donor Regulated mRNA Expressions of LTC4 Synthesis Enzymes in Hepatic Ischemia Reperfusion Injury Rats

Hong, FF; He, CS; Gl, Tu; Guo, Fang; Chen, XB; Sl, Yang

doi:10.1007/978-94-007-7618-0_435

Cited by 1 publication

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“…Our previous study has suggested that the NO donor sodium nitroprusside (SNP) downregulated the mRNA expression of LTC4S by inhibiting NF-κB activation in an IκBα-independent manner (12). Recently, we reported that a selective liver NO V-PYRRO/NO downregulates mRNA expression levels of leukotriene C4 synthase during hepatic ischemia reperfusion injury in rats via inhibition of the nuclear factor-κB activation pathway donor, O 2 -vinyl1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), downregulated the mRNA expression of LTC4S (18). However, whether the underlying influence on LTC4S mRNA expression levels is involved in NF-κB activation remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

V-PYRRO/NO downregulates mRNA expression levels of leukotriene C4 synthase during hepatic ischemia reperfusion injury in rats via inhibition of the nuclear factor-κB activation pathway

Hong

Wang²,

Liu

et al. 2015

Biomedical Reports

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The aim of the present study was to explore the mechanism underlying the effects of a selective liver nitric oxide (NO) donor, O-vinyl1-(pyrrolidin-1-yl)-diazen-1-ium-1,2-diolate (V-PYRRO/NO), on the gene expression of leukotriene C4 synthase (LTC4S) during hepatic ischemia/reperfusion (I/R). Adult male Sprague-Dawley rats were divided into 3 groups: Sham (control), I/R and V-PYRRO/NO + I/R groups. The liver was subjected to 1 h of partial hepatic ischemia followed by 5 h of reperfusion, saline or V-PYRRO/NO (1.06 µmol/kg/h) administered intravenously. The mRNA expression levels of LTC4S in rat liver tissue were examined by the reverse transcription-polymerase chain reaction method, the protein expression levels of nuclear factor-κB (NF-κB) p65, p50 and IκBα in liver cell lysates and nuclear extracts were detected by western blot analysis. Hepatic mRNA expression of LTC4S was lower in V-PYRRO/NO + I/R group compared to the I/R group. In addition, the protein expression levels of NF-κB p65 and p50 in the nucleus extract were lower in the V-PYRRO/NO + I/R group when compared with the I/R group. However, the IκBα protein in the 3 groups was not changed. Immunohistochemistry staining revealed that the I/R liver exhibited strong cytoplasmic and nuclear staining for NF-κB p65; however, the V-PYRRO/NO + I/R group liver presented slight cytoplasmic and nuclear staining. In conclusion, V-PYRRO/NO may downregulate LTC4S mRNA expression by inhibiting NF-κB activation independent of IκBα during hepatic I/R injury.

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Section: Introductionmentioning

confidence: 99%