Targeting Nrf-2 is a promising intervention approach for the prevention of ethanol-induced liver disease

Zhao, Ning; Guo, Fangfang; Xie, Keqin; Zeng, Tao

doi:10.1007/s00018-018-2852-6

Cited by 60 publications

(36 citation statements)

References 187 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nuclear factor erythroid 2-related factor 2 (Nrf-2) has been shown to up-regulate the expression of the various antioxidants while role of ROS in inflammation in NF-kB mediated inflammation has been studied in cisplatin-induced organ injury [50]. Nuclear factor erythroid 2-related factor 2 (Nrf-2) is a basic leucine zipper transcription factor present in inactive form and associated with cytoskeleton-associated protein, Keap1, in cytoplasm [76]. The activation of this transcription factor is regarded as a crucial molecular target of several chemopreventive agents [77,78].…”

Section: Discussionmentioning

confidence: 99%

“…The function of Nrf-2 is to prevent oxidative stress via antioxidant response element (ARE)-mediated inductions of numerous phase-2 detoxifying enzymes, specifically HO-1 [78,79]. Generally, the activation of the transcription factor Nrf-2 is induced by cellular oxidative stress and acts as a marker of pro-oxidant stressors and electrophiles [76,80]. Many research groups have shown strong interaction between Nrf-2 and NF-κB [81,82].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Rehman

Rather

2019

Plants

View full text Add to dashboard Cite

Cisplatin [cis-diamminedichloroplatinum II] is an extensively prescribed drug in cancer chemotherapy; it is also useful for the treatment of diverse types of malignancies. Conversely, cisplatin is associated with a range of side effects such as nephrotoxicity, hepatotoxicity, gastrointestinal toxicity, and so on. Myricetin (3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-4chromenone) is a very common natural flavonoid found in fruits, tea, and plants. It has been found to have high-value pharmacological properties and strong health benefits. To examine the role of myricetin in colon toxicity induced by cisplatin, we conducted a concurrent prophylactic study in experimental animals that were treated orally with myricetin for 14 days at two doses—25 and 50 mg/kg of body weight. On the 14th day, a single intraperitoneal injection of cisplatin (7.5 mg/kg body weight) was administered in all groups except control. The effects of myricetin in cisplatin-induced toxicity in the colon were assessed in terms of antioxidant status, phase-II detoxification enzymes, the level of inflammatory markers, and goblet cell disintegration. Myricetin was found to restore the level of all the antioxidant enzymes analyzed in the study. In addition, the compound ameliorated cisplatin-induced lipid peroxidation, increase in xanthine oxidase activity, and phase-II detoxifying enzyme activity. Myricetin also attenuated deteriorative effects induced by cisplatin by regulating the level of molecular markers of inflammation (NF-κB, Nrf-2, IL-6, and TNF-α), restoring Nrf-2 levels, and controlling goblet cell disintegration. The current study reinforces the conclusion that myricetin exerts protection in colon toxicity via up-regulation of inflammatory markers, improving anti-oxidant status, and protecting tissue damage.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Rehman

Rather

2019

Plants

View full text Add to dashboard Cite

show abstract

“…In fact, Nrf-2 is essential for the antioxidant responsive element (ARE)-mediated induction of endogenous antioxidant enzymes such as heme oxygenase 1 (HO-1), NAD(P)H dehydrogenase [quinone] 1 (NQO-1), and GCL. 41 Interestingly, it has been proposed that targeting the heme-heme oxygenase system may prevent severe complications following COVID-19 infection. 42 In parallel, NAC inhibits the oxidative stress-mediated activation of nuclear factor kappa-lightchain-enhancer of activated B cells (NFκB) and biochemical pathways upregulating pro-inflammatory genes.…”

Section: Inflammatory Mechanisms Of Nacmentioning

confidence: 99%

Rationale for the use of N ‐acetylcysteine in both prevention and adjuvant therapy of COVID‐19

Balansky²,

2020

View full text Add to dashboard Cite

COVID‐19 may cause pneumonia, acute respiratory distress syndrome, cardiovascular alterations, and multiple organ failure, which have been ascribed to a cytokine storm, a systemic inflammatory response, and an attack by the immune system. Moreover, an oxidative stress imbalance has been demonstrated to occur in COVID‐19 patients. N‐ Acetyl‐L‐cysteine (NAC) is a precursor of reduced glutathione (GSH). Due to its tolerability, this pleiotropic drug has been proposed not only as a mucolytic agent, but also as a preventive/therapeutic agent in a variety of disorders involving GSH depletion and oxidative stress. At very high doses, NAC is also used as an antidote against paracetamol intoxication. Thiols block the angiotensin‐converting enzyme 2 thereby hampering penetration of SARS‐CoV‐2 into cells. Based on a broad range of antioxidant and anti‐inflammatory mechanisms, which are herein reviewed, the oral administration of NAC is likely to attenuate the risk of developing COVID‐19, as it was previously demonstrated for influenza and influenza‐like illnesses. Moreover, high‐dose intravenous NAC may be expected to play an adjuvant role in the treatment of severe COVID‐19 cases and in the control of its lethal complications, also including pulmonary and cardiovascular adverse events.

show abstract

“…In chronic alcohol abuse, alcohol increases the expression of CYP2E1 in liver, causing dysregulations in lipid peroxidation through ROS free radicals. Therefore, it leads to the dynamic imbalance of antioxidant systems which target the important antioxidant regulatory gene nuclear factor erythroid 2-related factor 2 (Nrf-2) in ALD [38]. It also damages other antioxidant genes which have important roles in ROS scavenging, such as superoxide dismutase (SOD), glutathione (GSH), catalase, peroxidase-1, metallothionein, and heme oxygenase (HO-1) [39,40].…”

Section: Pathogenesis Of Aldmentioning

confidence: 99%

Pathogenesis, Early Diagnosis, and Therapeutic Management of Alcoholic Liver Disease

Kong

Chandimali

Han

et al. 2019

IJMS

141

110

View full text Add to dashboard Cite

Alcoholic liver disease (ALD) refers to the damages to the liver and its functions due to alcohol overconsumption. It consists of fatty liver/steatosis, alcoholic hepatitis, steatohepatitis, chronic hepatitis with liver fibrosis or cirrhosis, and hepatocellular carcinoma. However, the mechanisms behind the pathogenesis of alcoholic liver disease are extremely complicated due to the involvement of immune cells, adipose tissues, and genetic diversity. Clinically, the diagnosis of ALD is not yet well developed. Therefore, the number of patients in advanced stages has increased due to the failure of proper early detection and treatment. At present, abstinence and nutritional therapy remain the conventional therapeutic interventions for ALD. Moreover, the therapies which target the TNF receptor superfamily, hormones, antioxidant signals, and MicroRNAs are used as treatments for ALD. In particular, mesenchymal stem cells (MSCs) are gaining attention as a potential therapeutic target of ALD. Therefore, in this review, we have summarized the current understandings of the pathogenesis and diagnosis of ALD. Moreover, we also discuss the various existing treatment strategies while focusing on promising therapeutic approaches for ALD.

show abstract

Targeting Nrf-2 is a promising intervention approach for the prevention of ethanol-induced liver disease

Cited by 60 publications

References 187 publications

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Rationale for the use of N ‐acetylcysteine in both prevention and adjuvant therapy of COVID‐19

Pathogenesis, Early Diagnosis, and Therapeutic Management of Alcoholic Liver Disease

Contact Info

Product

Resources

About