Blood F2-isoprostanes are significantly associated with abnormalities of lipid status in rats with steatosis

Zhu, Manjie; Sun, Lijuan; Liu, Yueqin; Feng, Yanling; Tong, Hai-Tao; Hu, Yinghe; Zhao, Zheng

doi:10.3748/wjg.14.4677

Cited by 14 publications

(9 citation statements)

References 32 publications

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“…But even before these published reports, we had obtained similar results in an experimental hepatic steatosis study and in a clinical NASH study [33,139]. Increased F2-isoprostanes have been reported in NASH patients, suggesting an oxidative imbalance in the steatotic liver as well [188]. HSCs also can be activated by exposure to products of LPO.…”

Section: Oxidative Stress Markerssupporting

confidence: 74%

Markers in Nonalcoholic Steatohepatitis

Armutçu¹,

Akyol²,

Uçar³

et al. 2013

Advances in Clinical Chemistry

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Section: Oxidative Stress Markerssupporting

confidence: 74%

Markers in Nonalcoholic Steatohepatitis

Armutçu¹,

Akyol²,

Uçar³

et al. 2013

Advances in Clinical Chemistry

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“…15,40 Besides being markers for oxidative damage and inducers of inflammation, F 2 -isoprostanes can stimulate proliferation and collagen production in HSCs, and also induce the secretion of TGF- β from cultured cells. 14 The much lower level of F 2 -isoprostanes in MCD-fed Gclm null mice suggests that, compared with wt mice, these animals produce less ROS, and also have a better capacity to dispose of ROS through catalase activity.…”

Section: Discussionmentioning

confidence: 99%

“…The presence of oxidized lipids and proteins in the livers of patients with NASH and animals fed the MCD diet is another indication of an increased oxidative state under these conditions. 14,15 On the basis of these and other observations, it has been proposed that ROS-mediated lipid peroxidation could be an initiating event in NASH pathogenesis that might precede steatosis. 4 …”

mentioning

confidence: 96%

Attenuated progression of diet-induced steatohepatitis in glutathione-deficient mice

Haque

McMahan

Campbell

et al. 2010

Laboratory Investigation

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In nonalcoholic fatty liver disease (NAFLD), depletion of hepatic antioxidants may contribute to the progression of steatosis to nonalcoholic steatohepatitis (NASH) by increasing oxidative stress that produces lipid peroxidation, inflammation, and fibrosis. We investigated whether depletion of glutathione (GSH) increases NASH-associated hepatic pathology in mice fed a diet deficient in methionine and choline (MCD diet). Wild-type (wt) mice and genetically GSH-deficient mice lacking the modifier subunit of glutamate cysteine ligase (Gclm null mice), the rate-limiting enzyme for de novo synthesis of GSH, were fed the MCD diet, a methionine/choline-sufficient diet, or standard chow for 21 days. We assessed NASH-associated hepatic pathology, including steatosis, fibrosis, inflammation, and hepatocyte ballooning, and used the NAFLD Scoring System to evaluate the extent of changes. We measured triglyceride levels, determined the level of lipid peroxidation products, and measured by qPCR the expression of mRNAs for several proteins associated with lipid metabolism, oxidative stress, and fibrosis. MCD-fed GSH-deficient Gclm null mice were to a large extent protected from MCD diet-induced excessive fat accumulation, hepatocyte injury, inflammation, and fibrosis. Compared with wt animals, MCD-fed Gclm null mice had much lower levels of F2-isoprostanes, lower expression of acyl-CoA oxidase, carnitine palmitoyltransferase 1a, uncoupling protein-2, stearoyl-coenzyme A desaturase-1, transforming growth factor-β, and plas-minogen activator inhibitor-1 mRNAs, and higher activity of catalase, indicative of low oxidative stress, inhibition of triglyceride synthesis, and lower expression of profibrotic proteins. Global gene analysis of hepatic RNA showed that compared with wt mice, the livers of Gclm null mice have a high capacity to metabolize endogenous and exogenous compounds, have lower levels of lipogenic proteins, and increased antioxidant activity. Thus, metabolic adaptations resulting from severe GSH deficiency seem to protect against the development of steatohepatitis.

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“…Τα αποτελέσµατα είναι συνηγορητικά αυτών από µελέτη σε ποντίκια, στα οποία δηµιουργήθηκε στεάτωση (Zhu 2008). Στο πειραµατικό αυτό µοντέλο, η αυξηµένη παραγωγή ισοπροστανίων ανιχνεύεται πριν τη δηµιουργία ηπατοκυτταρικής νέκρωσης.…”

Section: Yesilova 2005)unclassified

Δείκτες Οξειδωτικού Στρες Λιπιδίων, DNA Και Πρωτεϊνών Σε Χρόνιες Παθήσεις Του Ήπατος

Kaffe¹,

Καφφέ²

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Blood F2-isoprostanes are significantly associated with abnormalities of lipid status in rats with steatosis

Cited by 14 publications

References 32 publications

Markers in Nonalcoholic Steatohepatitis

Markers in Nonalcoholic Steatohepatitis

Attenuated progression of diet-induced steatohepatitis in glutathione-deficient mice

Δείκτες Οξειδωτικού Στρες Λιπιδίων, DNA Και Πρωτεϊνών Σε Χρόνιες Παθήσεις Του Ήπατος

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