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dc.contributor.authorHELAL, GOUDA K-
dc.date.accessioned2022-11-29T05:17:21Z-
dc.date.available2022-11-29T05:17:21Z-
dc.date.issued2010-04-02-
dc.identifier.citationHelal, G. K. (2010). Thymoquinone supplementation ameliorates acute endotoxemia-induced liver dysfunction in rats. Pakistan journal of pharmaceutical sciences, 23(2).en_US
dc.identifier.issn1011-601X-
dc.identifier.urihttp://142.54.178.187:9060/xmlui/handle/123456789/14180-
dc.description.abstractEndotoxemia caused by lipopolysaccharide (LPS) produced an inflammatory condition contributing to multiple organ failure. This study was carried out to investigate the effects of thymoquinone (TQ), the main constituent of Nigella sativa seeds, against LPS-induced hepatotoxicity. The obtained data revealed that LPS markedly depleted liver reduced glutathione (GSH) and significantly increased the level of malondialdehyde (MDA) and the activity of caspase-3 enzyme in the liver. Serum tumour necrosis factor-alpha (TNF-α) and bilirubin levels and the activities of alkaline phosphatase (ALP) and gamma-glutamyl transferase (γ-GT) enzymes were markedly increased in LPS-treated rats. TQ supplementation resulted in normalization of liver GSH and decreases in the levels of MDA and caspase-3 activity in the liver with reduction of serum TNF-α, serum total bilirubin and the actvities of ALP and γ-GTenzymes. Histopathological examination revealed that TQ administration improved LPS-induced pathological abnormalities in liver tissues. The present study conclude that TQ reduced acute endoxemia-induced liver dysfunction at least in part by its anti-inflammatory, antiapoptotic and antioxidant activities.en_US
dc.language.isoenen_US
dc.publisherKarachi: Faculty of Pharmacy & Pharmaceutical Sciences, Karachien_US
dc.subjectThymoquinoneen_US
dc.subjectendotoxemiaen_US
dc.subjectinflammationen_US
dc.subjectTNF-αen_US
dc.subject,oxidative stressen_US
dc.subjectliver dysfunctionen_US
dc.titleTHYMOQUINONE SUPPLEMENTATION AMELIORATES ACUTE ENDOTOXEMIA-INDUCED LIVER DYSFUNCTION IN RATSen_US
dc.typeArticleen_US
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