Contrast media (meglumine diatrizoate) aggravates renal inflammation, oxidative DNA damage and apoptosis in diabetic rats which is restored by sulforaphane through Nrf2/HO-1 reactivation

Khaleel, Sahar A.; Raslan, Nahed A.; Alzokaky, Amany A.; Ewees, Mohamed G; Ashour, Ahmed; Abdel-Hamied, Hala E.; Abd-Allah, Adel R. A.

doi:10.1016/j.cbi.2019.06.002

Cited by 42 publications

(30 citation statements)

References 68 publications

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“…Like phenolics, several non-phenolic compounds have been shown to protect against DKD (Table 1). Most notable is sulforaphane, which improved kidney morphological and functional alterations in STZ-injected and meglumine diatrizoate-injected diabetic rats through activation of the Nrf2/HO-1 pathway [150]. Sulforaphane treatment also resulted in functional and morphological improvements of CRAD by attenuating OS through inducing the Nrf2-HO-1/Nqo1 signaling pathway [151].…”

Section: Non-phenolic Compoundsmentioning

confidence: 99%

Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling

et al. 2021

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The global burden of chronic kidney disease (CKD) intertwined with cardiovascular disease has become a major health problem. Oxidative stress (OS) plays an important role in the pathophysiology of CKD. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) antioxidant system plays a critical role in kidney protection by regulating antioxidants during OS. Heme oxygenase-1 (HO-1), one of the targets of Nrf2-ARE, plays an important role in regulating OS and is protective in a variety of human and animal models of kidney disease. Thus, activation of Nrf2-HO-1 signaling may offer a potential approach to the design of novel therapeutic agents for kidney diseases. In this review, we have discussed the association between OS and the pathogenesis of CKD. We propose Nrf2-HO-1 signaling-mediated cell survival systems be explored as pharmacological targets for the treatment of CKD and have reviewed the literature on the beneficial effects of small molecule natural products that may provide protection against CKD.

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Section: Non-phenolic Compoundsmentioning

confidence: 99%

Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling

et al. 2021

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“…The NF-kappa B plays a critical role in regulating inflammation, as well as the expression of angiotensin, cytokines, and adhesion molecules [ 87 , 88 ], and Nrf2 can suppress NF-kappa B with negative feedback [ 89 ]. Khaleel et al demonstrated that Nrf2/HO-1 pathway protected CI-AKI in diabetic rats and further demonstrated the protective effect of sulforaphane on CI-AKI [ 90 ].…”

Section: Signaling Pathways Related To Ci-aki and Dmmentioning

confidence: 99%

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Kawaguchi

2020

Contrast Media & Molecular Imaging

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Contrast-induced acute kidney injury (CI-AKI) is the third most common hospital-acquired AKI after AKI induced by renal perfusion insufficiency and nephrotoxic drugs, taking great adverse effects on the prognosis and increasing hospital stay and medical cost. Diabetes nephropathy (DN) is a common chronic complication of DM (diabetes mellitus), and DN is an independent risk factor for chronic kidney disease (CKD) and CI-AKI. The incidence of CI-AKI significantly increases in patients with renal injury, especially in DM-related nephropathy. The etiology of CI-AKI is not fully clear, and research studies on how DM becomes a facilitated factor of CI-AKI are limited. This review describes the mechanism from three aspects. ① Pathophysiological changes of CI-AKI in kidney under high-glucose status (HGS). HGS can enhance the oxidative stress and increase ROS which next causes stronger vessel constriction and insufficient oxygen supply in kidney via vasoactive substances. HGS also aggravates some ion pump load and the latter increases oxygen consumption. CI-AKI and HGS are mutually causal, making the kidney function continue to decline. ② Immunological changes of DM promoting CI-AKI. Some innate immune cells and pattern recognition receptors (PRRs) in DM and/or DN may respond to some damage-associated molecular patterns (DAMPs) formed by CI-AKI. These effects overlap with some pathophysiological changes in hyperglycemia. ③ Signaling pathways related to both CI-AKI and DM. These pathways involved in CI-AKI are closely associated with apoptosis, inflammation, and ROS production, and some studies suggest that these pathways may be potential targets for alleviating CI-AKI. In conclusion, the pathogenesis of CI-AKI and the mechanism of DM as a predisposing factor for CI-AKI, especially signaling pathways, need further investigation to provide new clinical approaches to prevent and treat CI-AKI.

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“…SFN also increased transcriptional activation and protein levels of the antioxidant enzymes NQO1 and HO-1 [102]. In a rat model of STZ-induced diabetic nephropathy with superimposed contrast media injury, treatment with SFN partially abrogated renal injury, lowered renal markers of oxidative stress [malondialdehyde (MDA) and 8-hydroxy-2 -deoxyguanosine (8-OHdG)], and improved renal function [103]. SFN also offered protection in a model of type 2 DM in which mice were fed a high-fat diet followed by STZ injection [104].…”

Section: Potential Role For Sulforaphane (Sfn) In Kidney Diseasementioning

confidence: 99%

Eat Your Broccoli: Oxidative Stress, NRF2, and Sulforaphane in Chronic Kidney Disease

Liebman

2021

Nutrients

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The mainstay of therapy for chronic kidney disease is control of blood pressure and proteinuria through the use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) that were introduced more than 20 years ago. Yet, many chronic kidney disease (CKD) patients still progress to end-stage kidney disease—the ultimate in failed prevention. While increased oxidative stress is a major molecular underpinning of CKD progression, no treatment modality specifically targeting oxidative stress has been established clinically. Here, we review the influence of oxidative stress in CKD, and discuss regarding the role of the Nrf2 pathway in kidney disease from studies using genetic and pharmacologic approaches in animal models and clinical trials. We will then focus on the promising therapeutic potential of sulforaphane, an isothiocyanate derived from cruciferous vegetables that has garnered significant attention over the past decade for its potent Nrf2-activating effect, and implications for precision medicine.

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Contrast media (meglumine diatrizoate) aggravates renal inflammation, oxidative DNA damage and apoptosis in diabetic rats which is restored by sulforaphane through Nrf2/HO-1 reactivation

Cited by 42 publications

References 68 publications

Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling

Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Eat Your Broccoli: Oxidative Stress, NRF2, and Sulforaphane in Chronic Kidney Disease

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