<i>Rumex nervosus</i> could alleviate streptozotocin-induced diabetic nephropathy in rats by activating Nrf2 signaling

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Abstract

This study tested the protective effect of Rumex nervous (R. nervosus) methanol extract against streptozotocin (STZ)-mediated type 1 diabetes mellitus (T1DM)-induced nephropathy in rats and examined if this protection involves activating the nuclear factor erythroid 2 related factor-2 (Nrf2). Rats were divided into control, R. nervous (300 mg), STZ (T1DM), STZ + R. nervosus (100, 200, or 300 mg/kg), and STZ + R. nervosus (300 mg/kg) + brusatol (an Nrf2 inhibitor). With no effect on fasting glucose and insulin levels, R. nervosus methanol extract preserved kidney histological structure and alterations kidney function markers (e.g. albumin, creatinine, and urine volume) in the STZ-diabetic rats. R. nervosus also reduced levels of reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and interleukine-6 (IL-6), nuclear levels of the nuclear factor kappa beta (NF-κB), and mRNA of caspase-3 and Bax in the kidneys of these diabetic rats. Concomitantly, it stimulated renal mRNA levels of Bcl2 and Nrf2, cytoplasmic and nuclear levels of Nrf2, and levels of glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). All these effects were dose-dependent, with the maximum effect seen with the 300 mg/kg dose, all prevented by brusatol. Also, these effects occurred without any alteration in the transcription of the Kelch-like ECH-associated protein 1 (keap-1). Similar effects on levels of GSH, SOD, CAT, and NF-κB, as well as expression of Nrf2, were also observed in the kidney of control + R. nervous-treated rats. In conclusion, R. nervosus prevents diabetic nephropathy in rats by upregulating and activating Nrf2.

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Type 1 diabetes mellitus

Anastasia Katsarou, Soffia Gudbjörnsdottir, Araz Rawshani … (2017)

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Activation of Nrf2-antioxidant signaling attenuates NFkappaB-inflammatory response and elicits apoptosis.

Wenge Li, Tin Oo Khor, Changjiang Xu … (2008)

Oxidative stress has been implicated in the etiology of neurodegenerative disease, cancer and aging. Indeed, accumulation of reactive oxygen and nitrogen species generated by inflammatory cells that created oxidative stress is thought to be one of the major factor by which chronic inflammation contributes to neoplastic transformation as well as many other diseases. We have recently reported that mice lacking nuclear factor-erythroid 2-related factor 2 (Nrf2) are more susceptible to dextran sulfate sodium (DSS)-induced colitis and colorectal carcinogenesis. Nrf2 is a basic leucine zipper redox-sensitive transcriptional factor that plays a center role in ARE (antioxidant response element)-mediated induction of phase II detoxifying and antioxidant enzymes. We found that increased susceptibility of Nrf2 deficient mice to DSS-induced colitis and colorectal cancer was associated with decreased expression of antioxidant/phase II detoxifying enzymes in parallel with upregulation of pro-inflammatory cytokines/biomarkers. These findings suggest that Nrf2 may play an important role in defense against oxidative stress possibly by activation of cellular antioxidant machinery as well as suppression of pro-inflammatory signaling pathways. In addition, in vivo and in vitro data generated from our laboratory suggest that many dietary compounds can differentially regulate Nrf2-mediated antioxidant/anti-inflammatory signaling pathways as the first line defense or induce apoptosis once the cells have been damaged. In this review, we will summarize our thoughts on the potential cross-talks between Nrf2 and NFkappaB pathways. Although the mechanisms involved in the cross-talk between these signaling pathways are still illusive, targeting Nrf2-antioxidative stress signaling is an ideal strategy to prevent or treat oxidative stress-related diseases.

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Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications

Qingzheng Kang, Chunxue Yang (2020)

Oxidative stress, a cytopathic outcome of excessive generation of ROS and the repression of antioxidant defense system for ROS elimination, is involved in the pathogenesis of multiple diseases, including diabetes and its complications. Retinopathy, a microvascular complication of diabetes, is the primary cause of acquired blindness in diabetic patients. Oxidative stress has been verified as one critical contributor to the pathogenesis of diabetic retinopathy. Oxidative stress can both contribute to and result from the metabolic abnormalities induced by hyperglycemia, mainly including the increased flux of the polyol pathway and hexosamine pathway, the hyper-activation of protein kinase C (PKC) isoforms, and the accumulation of advanced glycation end products (AGEs). Moreover, the repression of the antioxidant defense system by hyperglycemia-mediated epigenetic modification also leads to the imbalance between the scavenging and production of ROS. Excessive accumulation of ROS induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, and structural and functional alterations in retina. Therefore, it is important to understand and elucidate the oxidative stress-related mechanisms underlying the progress of diabetic retinopathy. In addition, the abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy. Here, we also summarized the main antioxidant therapeutic strategies to control this disease.

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Author and article information

Journal

Journal ID (nlm-ta): Sci Prog

Journal ID (iso-abbrev): Sci Prog

Journal ID (publisher-id): SCI

Journal ID (hwp): spsci

Title: Science Progress

Publisher: SAGE Publications (Sage UK: London, England )

ISSN (Print): 0036-8504

ISSN (Electronic): 2047-7163

Publication date (Electronic): 26 May 2022

Publication date Collection: Apr-Jun 2022

Volume: 105

Issue: 2

Electronic Location Identifier: 00368504221102751

Affiliations

[1 ]Nutrition and Food Science, Department of Physical Sport Science, Ringgold 112893, universityPrincess Nourah bint Abdulrahman University; , Riyadh, Saudi Arabia

[2 ]Department of Food Science and Nutrition, College of Food and Agricultural Sciences, Ringgold 37850, universityKing Saud University; , Riyadh, Saudi Arabia

[3 ]Department of Food Science and Technology, Faculty of Agriculture and Food Science, Ringgold 341207, universityIbb University; , Ibb, Yemen

Author notes

[*]Jozaa Z. ALTamimi, Nutrition and Food Science, Department of Physical Sport Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia. Email: jaltamimi@ 123456pnu.edu.sa

Author information

Nora A AlFaris https://orcid.org/0000-0002-9135-5725

Muneer M Alsayadi https://orcid.org/0000-0002-6892-0765

Jozaa Z ALTamimi https://orcid.org/0000-0002-5510-0768

Article

Publisher ID: 10.1177_00368504221102751

DOI: 10.1177/00368504221102751

PMC ID: 10358522

PubMed ID: 35619568

SO-VID: 9a533cc2-e25e-4f7d-9343-3014ef533526

License:

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

History

Funding

Funded by: The authors are grateful to the Deanship of Scientific Research at Princess Nourah bint Abdulrahman University, through the Research Funding Program (RGP-1442 - 6), for funding this work.;