Heme oxygenase-1 mediates the protective role of quercetin against ethanol-induced rat hepatocytes oxidative damage

Liu, Shuang; Hou, Wei; Yao, Ping; Li, Na; Zhang, Biyun; Hao, Liping; Nüssler, Andreas K.; Liu, Liegang

doi:10.1016/j.tiv.2011.10.013

Cited by 62 publications

(43 citation statements)

References 46 publications

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“…The treatments with rutin and, to a lesser extent, quercetin were associated with increased Nrf2 and HO-1 expression in the liver, which coincided with the suppression of NF-κB activation. Most recently, Liu et al [43] showed that quercetin acts as an inducer of HO-1 in primary rat hepatocytes. Interestingly, the induction of HO-1 was found in quercetin-treated but not in rutin-treated rat glioma C6 cells [44] and in the hydrogen peroxide-induced apoptosis of RAW264.7 macrophages [45] .…”

Section: Discussionmentioning

confidence: 99%

Differential hepatoprotective mechanisms of rutin and quercetin in CCl4-intoxicated BALB/cN mice

et al. 2012

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Aim: To investigate the mechanisms underlying the protective effects of quercetin-rutinoside (rutin) and its aglycone quercetin against CCl 4 -induced liver damage in mice. Methods: BALB/cN mice were intraperitoneally administered rutin (10, 50, and 150 mg/kg) or quercetin (50 mg/kg) once daily for 5 consecutive days, followed by the intraperitoneal injection of CCl 4 in olive oil (2 mL/kg, 10% v/v). The animals were sacrificed 24 h later. Blood was collected for measuring the activities of ALT and AST, and the liver was excised for assessing Cu/Zn superoxide dismutase (SOD) activity, GSH and protein concentrations and also for immunoblotting. Portions of the livers were used for histology and immunohistochemistry. Results: Pretreatment with rutin and, to a lesser extent, with quercetin significantly reduced the activity of plasma transaminases and improved the histological signs of acute liver damage in CCl 4 -intoxicated mice. Quercetin prevented the decrease in Cu/Zn SOD activity in CCl 4 -intoxicated mice more potently than rutin. However, it was less effective in the suppression of nitrotyrosine formation. Quercetin and, to a lesser extent, rutin attenuated the inflammation in the liver by down-regulating the CCl 4 -induced activation of nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α) and cyclooxygenase (COX-2). The expression of inducible nitric oxide synthase (iNOS) was more potently suppressed by rutin than by quercetin. Treatment with both flavonoids significantly increased NF-E2-related factor 2 (Nrf2) and heme oxygenase (HO-1) expression in injured livers, although quercetin was less effective than rutin at an equivalent dose. Quercetin more potently suppressed the expression of transforming growth factor-β1 (TGF-β1) than rutin. Conclusion: Rutin exerts stronger protection against nitrosative stress and hepatocellular damage but has weaker antioxidant and antiinflammatory activities and antifibrotic potential than quercetin, which may be attributed to the presence of a rutinoside moiety in position 3 of the C ring.

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Section: Discussionmentioning

confidence: 99%

Differential hepatoprotective mechanisms of rutin and quercetin in CCl4-intoxicated BALB/cN mice

et al. 2012

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“…HO-1 gene expression can be up-regulated through its multiple stress response and cadmium response elements, as well as by numerous important transcription factors, including Jun B, activator proteins 1 and 2, and NF-kB [10] . Conversely, the transcription factors Bach1 and Jun D act as negative regulators of human HO-1 gene expression [2,11] . Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, Figure 1 The heme oxygenase enzyme reaction.…”

Section: Regulation Of Ho-1mentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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“…Antioxidant activity [4], [5], [6], [7], [8] [16], [17], [18], [19], [20], [21], [22] Anticancer activity [2], [23], [24], [25], [26] Cardiovascular protection [4], [27], [28], [29], [30] Antimicrobial activity [31], [32], [33] Anti-inflammatory activity [34], [35], [36], [37], [38], [39] Hepatoprotective activity [40], [41], [42] …”

Section: Pharmacological Property Referencesmentioning

confidence: 99%

“…Moreover, in vivo study in mice relating to the hepatoprotective mechanism of quercetin reported that it is the hemeoxygenase 1 that triggers the function of quercetin against induced hepatotoxicity; hepatoprotectivity was then observed by the decrease in plasma concentration of alanine aminotransferase [41]. Oxidative damage induced by ethanol in rat hepatocytes has been reported to be curable with the quercetin administration [42]. Hepatoprotectivity of quercetin suggests that its administration may be helpful to prevent liver damage, thus quercetin may be a suitable natural product as hepatoprotective agent.…”

Section: Hepatoprotective Activitymentioning

confidence: 99%

Pharmacological Applications of Quercetin and its Derivatives: A Short Review

Maalik¹,

Fa²,

Mumtaz³

et al. 2014

Trop. J. Pharm Res

125

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Quercetin (3,3ʹ,4ʹ,5,7-pentahydroxyl- flavone) is a flavonol, and it belongs to a class of plant secondary metabolites known as flavonoids. It is present in man's daily diet and is known for biological activities such as antioxidant, antiviral, anticancer, antimicrobial, anti-inflammatory and many more. Quercetin has been reported for its antioxidant and antiviral applications, hence, it is not only used as such but also its various derivatized forms have potentials for development into drugs for the treatment of diseases caused by oxidative stress and lethal viruses.

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Heme oxygenase-1 mediates the protective role of quercetin against ethanol-induced rat hepatocytes oxidative damage

Cited by 62 publications

References 46 publications

Differential hepatoprotective mechanisms of rutin and quercetin in CCl4-intoxicated BALB/cN mice

Differential hepatoprotective mechanisms of rutin and quercetin in CCl4-intoxicated BALB/cN mice

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Pharmacological Applications of Quercetin and its Derivatives: A Short Review

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