Oxyresveratrol abrogates oxidative stress by activating ERK–Nrf2 pathway in the liver

Choi, Hee Yoon; Lee, Ju‐Hee; Jegal, Kyung Hwan; Cho, Il Je; Kim, Young Woo; Kim, Sang Chan

doi:10.1016/j.cbi.2015.06.024

Cited by 65 publications

(38 citation statements)

References 50 publications

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“…Pretreatment with DADS (50 and 100 mg/kg/day) significantly activated Nrf2 expression and antioxidant and phase II enzymes to reduce liver injury [52, 53]. Oxyresveratrol (OXY), an antioxidant present in mulberry fruits and twigs, ameliorated tert-butyl hydroperoxide- (t-BHP-) and CCl 4 -induced hepatotoxicity by reducing oxidative stress possibly via extracellular signal-regulated kinase- (ERK-) mediated Nrf2 activation in hepatocytes [59]. Other flavonoids such as carthamus red and naringenin also activate Nrf2 signaling to reduce CCl 4 injury in rats [50, 58].…”

Section: Role Of Nrf2 In Chemical-induced Liver Injurymentioning

confidence: 99%

Naturally Occurring Nrf2 Activators: Potential in Treatment of Liver Injury

Jadeja

Upadhyay

Devkar

et al. 2016

Oxidative Medicine and Cellular Longevity

107

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Oxidative stress plays a major role in acute and chronic liver injury. In hepatocytes, oxidative stress frequently triggers antioxidant response by activating nuclear erythroid 2-related factor 2 (Nrf2), a transcription factor, which upregulates various cytoprotective genes. Thus, Nrf2 is considered a potential therapeutic target to halt liver injury. Several studies indicate that activation of Nrf2 signaling pathway ameliorates liver injury. The hepatoprotective potential of naturally occurring compounds has been investigated in various models of liver injuries. In this review, we comprehensively appraise various phytochemicals that have been assessed for their potential to halt acute and chronic liver injury by enhancing the activation of Nrf2 and have the potential for use in humans.

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Section: Role Of Nrf2 In Chemical-induced Liver Injurymentioning

confidence: 99%

Naturally Occurring Nrf2 Activators: Potential in Treatment of Liver Injury

Jadeja

Upadhyay

Devkar

et al. 2016

Oxidative Medicine and Cellular Longevity

107

View full text Add to dashboard Cite

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“…However, 5 µM would have little impact compared to the totalplasma antioxidant capacity of ~0.5mmol [34].Furthermore, it is below the IC50 by the DPPH assay (table 1). At these lower concentrations, a more plausible mechanism of oxyresveratrol antioxidant action is through increased expression of endogenous antioxidant enzymes via their transcription factors, Nrf-2 [35], and FOXO3a [36]. Ultimately, these enzymes are trafficked to sources of particular ROSs where they are most effective.…”

Section: Post-treatment With Antioxidantsmentioning

confidence: 99%

Neuroprotective Effect of Artocarpus Lakoocha Extract and Oxyresveratrol Against Hydrogen Peroxide-Induced Toxicity in Sh-Sy5y Cells

Hasriadi

Wongon

Lapphanichayakool

et al. 2017

Int J Pharm Pharm Sci

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Objective: Artocarpuslakoocha Roxb. Is a traditional medical plant native to Southeast Asia and used as a dried aqueous extract so-called puaghaad. Its role (and its major ingredient, oxyresveratrol) as an antioxidant neuroprotectant were explored.Methods: Differentiated SH-SY5Y neuroblastoma cells in 96-well plates were challenged with 200 µM H2O2 for 4h and either Trolox (100 µM), oxyresveratrol (5-100 µM), or puaghaad (1.2-25 µg/ml) applied 2h before H2O2 or for 20 h after H2O2Results: Continuous presence of both H washout. Cell viability, mitochondrial function, intracellular ROS, and lipid peroxidation were assessed.2O 2 and antioxidant reduced mitochondrial function by ~50% but only by 30% with antioxidant. Sustained 24 h H2O2 showed no recoveries with antioxidants. Cell viability was modestly restored when antioxidants accompanied H2O2 for 4 h and both washed for another 20 h, but little recovery of mitochondrial function even though antioxidants removed ROS and prevent lipid peroxidation. Antioxidants added for 20 h after H2O2 Conclusion:These results show that mitochondrial protection was illusive, yet both tested compounds, puaghaad and oxyresveratrol, improved cell viability and especially ROS levels and lipid peroxidation. The potency oxyresveratrol on theredox-sensitive expression of antioxidant enzymes and its pharmacokinetics suggests that oral puaghaad could provide effective protection in transient neurodegenerative disease. marginally improve mitochondria and modestly restore cell viability, but lipid peroxidation was completely reversed.

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“…However, when excess iron exists, it may result in inflammatory conditions and cause higher release of AA, enhancing oxidative stress (Shin and Kim 2009). Therefore, a combination of AA and iron is used as an oxidative stress inducer in many studies because of its synergistic toxicity, in which iron might play a role as a catalyst of oxidation (Caro and Cederbaum 2001;Shin and Kim 2009;Dong et al 2014;Choi et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Emodin in Rheum undulatum inhibits oxidative stress in the liver via AMPK with Hippo/Yap signalling pathway

Lee

Baek

Park

et al. 2020

Pharmaceutical Biology

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Context: Emodin is a compound in Rheum undulatum Linne (Polygonaceae) that has been reported to exert anti-inflammatory, antibacterial, and antiallergic effects. Objective: Oxidative stress is a causative agent of liver inflammation that may lead to fibrosis and hepato-carcinoma. In this study, we investigated the antioxidant effects of emodin and its mechanism. Materials and methods: We used the hepatocyte stimulated by arachidonic acid (AA) þ iron cotreatment and the C57B/6 mice orally injected with acetaminophen (APAP, 500 mg/kg, 6 h), as assessed by immunoblot and next generation sequencing (NGS). Emodin was pre-treated in hepatocyte (3 $ 30 lM) for 1 h before AA þ iron, and in mice (10 and 30 m/kg, P.O.) for 3 days before APAP. Results: In vitro, emodin treatment inhibited the cell death induced by AA þ iron maximally at a dose of 10 lM (EC 50 > 3 lM). In addition, emodin attenuated the decrease of anti-apoptotic proteins, and restored mitochondria membrane potential as mediated by the liver kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) pathway. LKB1 mediated AMPK activation was verified using the LKB1 deficient cell line, HeLa. Emodin (10 lM; after 10 min) also induced the phosphorylation of Yes-associated protein 1 (YAP1), the main downstream target of the Hippo signalling pathway that mediated oxidative stress or the ROS-initiated signalling pathway. In vivo, the oral treatment of emodin (10 and 30 m/kg, 3 days) decreased APAP-induced hepatic damage, as indicated by decreases in antioxidant genes as well as tissue damage. Conclusion: Our results show that emodin inhibits oxidative liver injury via the AMPK/YAP mediated pathway.

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Oxyresveratrol abrogates oxidative stress by activating ERK–Nrf2 pathway in the liver

Cited by 65 publications

References 50 publications

Naturally Occurring Nrf2 Activators: Potential in Treatment of Liver Injury

Naturally Occurring Nrf2 Activators: Potential in Treatment of Liver Injury

Neuroprotective Effect of Artocarpus Lakoocha Extract and Oxyresveratrol Against Hydrogen Peroxide-Induced Toxicity in Sh-Sy5y Cells

Emodin in Rheum undulatum inhibits oxidative stress in the liver via AMPK with Hippo/Yap signalling pathway

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