Dimethyl fumarate and curcumin attenuate hepatic ischemia/reperfusion injury via Nrf2/HO-1 activation and anti-inflammatory properties

Ibrahim, Shaimaa G.; El-Emam, Soad Z.; Mohamed, Eman A.; Ellah, M. F. Abd

doi:10.1016/j.intimp.2019.106131

Cited by 50 publications

(42 citation statements)

References 38 publications

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“…Curcumin can mediate antiinflammatory, anti-oxidative, and anti-fibrosis effects and thus has therapeutic potential in IRI [30,31]. Mounting studies have confirmed that curcumin has protective effects against renal, hepatic and cardiac IRIs in rat due to its pharmacological activities [32][33][34][35][36]. In the present study, we found IRI could cause an increase in renal apoptosis and severe damage to renal tubules.…”

Section: Discussionsupporting

confidence: 66%

Curcumin attenuates renal ischemia reperfusion injury via JNK pathway with the involvement of p300/CBP-mediated histone acetylation

Yang

Chen

et al. 2021

Korean J Physiol Pharmacol

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Apoptosis is proved responsible for renal damage during ischemia/reperfusion. The regulation for renal apoptosis induced by ischemia/reperfusion injury (IRI) has still been unclearly characterized to date. In the present study, we investigated the regulation of histone acetylation on IRI-induced renal apoptosis and the molecular mechanisms in rats with the application of curcumin possessing a variety of biological activities involving inhibition of apoptosis. Sprague-Dawley rats were randomized into four experimental groups (SHAM, IRI, curcumin, SP600125). Results showed that curcumin significantly decreased renal apoptosis and caspase-3/-9 expression and enhanced renal function in IRI rats. Treatment with curcumin in IRI rats also led to the decrease in expression of p300/cyclic AMP response element-binding protein (CBP) and activity of histone acetyltransferases (HATs). Reduced histone H3 lysine 9 (H3K9) acetylation was found near the promoter region of caspase-3/-9 after curcumin treatment. In a similar way, SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), also attenuated renal apoptosis and enhanced renal function in IRI rats. In addition, SP600125 suppressed the binding level of p300/CBP and H3K9 acetylation near the promoter region of caspase-3/-9, and curcumin could inhibit JNK phosphorylation like SP600125. These results indicate that curcumin could attenuate renal IRI via JNK/p300/CBP-mediated anti-apoptosis signaling.

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Section: Discussionsupporting

confidence: 66%

Curcumin attenuates renal ischemia reperfusion injury via JNK pathway with the involvement of p300/CBP-mediated histone acetylation

Yang

Chen

et al. 2021

Korean J Physiol Pharmacol

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“…Nrf2 upregulation is thought to be a therapeutic target for APAP‐triggered liver injury 68 . Curcumin encourages Nrf2/HO‐1 signaling due to suppression of lipid peroxidation in hepatic tissues 88 . Activation of Nrf2 may be implicated in the activation of phase II detoxifying antioxidant enzymes and blocking NF‐κB activation signaling 66 .…”

Section: Discussionmentioning

confidence: 99%

Biochemical study on the protective effect of curcumin on acetaminophen and gamma‐irradiation induced hepatic toxicity in rats

Eassawy

Salem

Ismail

2020

Environmental Toxicology

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Acetaminophen (APAP) is one of the few recommended analgesic and antipyretic drugs in some critical cases such as viral disease COVID‐19. However, the unrestricted use of APAP develops liver disorders. Hepatotoxicity and liver injury can also be induced by ionizing radiation (IR) during radiotherapy. The data of the current study represents that treatment of rats with either APAP‐overdose, or gamma‐irradiation (R) induces hepatotoxicity, results in significant increases of the hepatic‐enzymes activities (ALT, AST, ALP, GGT, LDH, and MDH), as well as enhancement of triglycerides, total cholesterol levels, combined with declines in albumin and total protein contents. An enhancement of the lipid peroxides (malondialdehyde; MDA), and nitric oxide levels along with a decline of reduced glutathione contents and suppression of superoxide dismutase, catalase, and glutathione peroxidase activities are also observed within the liver tissues of intoxicated animals. TNF‐α, IL‐1β, IL‐6, iNOS, Cytochrome P450 2E1 (CYP2E1), miR‐802 gene expression, NF‐κB, and calcium levels are up‐regulated, while Nuclear factor erythroid‐related factor‐2 (Nrf2), Hemoxygenase‐1 (HO‐1) protein and gene expressions, as well as, glutamate‐cysteine ligase catalytic subunit (GCLC), NAD(P)H‐Quinone oxidoreductase (NQO1), and miR‐122 gene expressions are down‐regulated in the livers of intoxicated animals. All these parameters show significant improvement in R/APAP intoxicated animals. Curcumin pretreatment develops an amelioration of these effects in APAP‐overdose, R‐exposure, or R/APAP treatments. In conclusion, oral administration of curcumin shows hepatoprotective effects against APAP‐overdose induced hepatic damage in normal and gamma‐irradiated rats through prospective regulation of the therapeutic targets CYP2E1, Nrf2, and NF‐κB, via organizing the miR‐122 and miR‐802 gene expression.

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“…IL-17a knockout mice and wild mice fed a high-fat diet to form the fatty liver and undergo IRI treatment. The results show that IL-17a knockout mice can significantly slow down liver damage caused by IRI, and this specific mechanism is related to the inhibition of the IL-17a/NF- κ B signaling pathway [ 88 ]. IPC can reduce the production of proinflammatory cytokines induced by CD4+, especially IL-2.…”

Section: Protective Mechanisms Of Irimentioning

confidence: 99%

The Role of Mitochondria in Liver Ischemia‐Reperfusion Injury: From Aspects of Mitochondrial Oxidative Stress, Mitochondrial Fission, Mitochondrial Membrane Permeable Transport Pore Formation, Mitophagy, and Mitochondria‐Related Protective Measures

Zhang

Yan

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Ischemia-reperfusion injury (IRI) has indeed been shown as a main complication of hepatectomy, liver transplantation, trauma, and hypovolemic shock. A large number of studies have confirmed that microvascular and parenchymal damage is mainly caused by reactive oxygen species (ROS), which is considered to be a major risk factor for IRI. Under normal conditions, ROS as a kind of by-product of cellular metabolism can be controlled at normal levels. However, when IRI occurs, mitochondrial oxidative phosphorylation is inhibited. In addition, oxidative respiratory chain damage leads to massive consumption of adenosine triphosphate (ATP) and large amounts of ROS. Additionally, mitochondrial dysfunction is involved in various organs and tissues in IRI. On the one hand, excessive free radicals induce mitochondrial damage, for instance, mitochondrial structure, number, function, and energy metabolism. On the other hand, the disorder of mitochondrial fusion and fission results in further reduction of the number of mitochondria so that it is not enough to clear excessive ROS, and mitochondrial structure changes to form mitochondrial membrane permeable transport pores (mPTPs), which leads to cell necrosis and apoptosis, organ failure, and metabolic dysfunction, increasing morbidity and mortality. According to the formation mechanism of IRI, various substances have been discovered or synthesized for specific targets and cell signaling pathways to inhibit or slow the damage of liver IRI to the body. Here, based on the development of this field, this review describes the role of mitochondria in liver IRI, from aspects of mitochondrial oxidative stress, mitochondrial fusion and fission, mPTP formation, and corresponding protective measures. Therefore, it may provide references for future clinical treatment and research.

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Dimethyl fumarate and curcumin attenuate hepatic ischemia/reperfusion injury via Nrf2/HO-1 activation and anti-inflammatory properties

Cited by 50 publications

References 38 publications

Curcumin attenuates renal ischemia reperfusion injury via JNK pathway with the involvement of p300/CBP-mediated histone acetylation

Curcumin attenuates renal ischemia reperfusion injury via JNK pathway with the involvement of p300/CBP-mediated histone acetylation

Biochemical study on the protective effect of curcumin on acetaminophen and gamma‐irradiation induced hepatic toxicity in rats

The Role of Mitochondria in Liver Ischemia‐Reperfusion Injury: From Aspects of Mitochondrial Oxidative Stress, Mitochondrial Fission, Mitochondrial Membrane Permeable Transport Pore Formation, Mitophagy, and Mitochondria‐Related Protective Measures

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