Effect of the antioxidant idebenone on maternal diabetes-induced embryo alterations during early organogenesis

Higa, Romina; Roberti, Sabrina Lorena; Mazzucco, María Belén; White, Verónica; Jawerbaum, Alicia

doi:10.1016/j.rbmo.2018.05.006

Cited by 7 publications

(1 citation statement)

References 55 publications

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“…36 TNF-α is negatively influenced by Nrf2, indicating that IDE-induced downregulation of Nrf2 immuno-expression may aim at inactivating T/D-induced inflammatory signaling pathways. 37 The previous studies by Al-Rasheed and his colleagues, 38 Yan and his coworkers, 39 and Shastri et al 32 reporting that IDE reduced the proinflammatory mediators are consistent with the current findings.…”

Section: Discussionsupporting

confidence: 91%

Idebenone regulates sirt1/Nrf2/TNF-α pathway with inhibition of oxidative stress, inflammation, and apoptosis in testicular torsion/detorsion in juvenile rats

et al. 2022

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Testicular torsion is an emergency, mainly in newborn and adolescent males, resulting in testicular ischemia. The current study aimed to evaluate the effect of Idebenone (IDE) on testicular torsion/detorsion (T/D) in juvenile rats. Thirty-two rats were randomized into: (1) the sham group: rats received sham operations with no other interventions; (2) the IDE group: rats received idebenone (100 mg/kg, i. p) without T/D; (3) the T/D group: rats underwent torsion for 2 h and detorsion for 4 h; and (4) the IDE+ T/D group: rats received IDE 1 h before T/D. Testicular malondialdehyde (MDA), total nitrite/nitrate (NOx), total antioxidant capacity (TAC), tumor necrosis factor-α (TNF-α), caspase-3, sirtuin type 1 (Sirt1), serum interleukin-1β (IL-1β), total cholesterol, and testosterone were measured. Histological changes, nuclear factor (erythroid-derived 2)-like-2 factors (Nrf2), and proliferating cell nuclear antigen (PCNA) immuno-expressions were assessed. T/D displayed an increase in MDA, NOx, TNF-α, caspase-3, IL-1β, and total cholesterol with a significant decrease in TAC, Sirt1, and testosterone and strong positive Nrf2 and negative PCNA immuno-expressions. IDE could improve all oxidative, inflammatory, and apoptotic indicators. Therefore, IDE significantly reduced testicular ischemia-reperfusion injury in the juvenile rat testicular T/D model by limiting oxidative stress, inflammation, and apoptosis via the Sirt1/Nrf2/TNF-α pathway.

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Section: Discussionsupporting

confidence: 91%

Idebenone regulates sirt1/Nrf2/TNF-α pathway with inhibition of oxidative stress, inflammation, and apoptosis in testicular torsion/detorsion in juvenile rats

et al. 2022

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Placental mitochondrial dysfunction with metabolic diseases: Therapeutic approaches

Hebert

Myatt

2021

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Maternal diabetes increases FOXO1 activation during embryonic cardiac development

Sato

Leonardi

Roberti

et al. 2023

Molecular and Cellular Endocrinology

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Effect of the antioxidant idebenone on maternal diabetes-induced embryo alterations during early organogenesis

Abstract: Maternal idebenone treatment ameliorates altered parameters related to the prooxidant-proinflammatory environment found in embryos from mild diabetic rats, suggesting a putative treatment to prevent diabetes-induced embryo alterations.

Cited by 7 publications

References 55 publications

Idebenone regulates sirt1/Nrf2/TNF-α pathway with inhibition of oxidative stress, inflammation, and apoptosis in testicular torsion/detorsion in juvenile rats

Idebenone regulates sirt1/Nrf2/TNF-α pathway with inhibition of oxidative stress, inflammation, and apoptosis in testicular torsion/detorsion in juvenile rats

Placental mitochondrial dysfunction with metabolic diseases: Therapeutic approaches

Maternal diabetes increases FOXO1 activation during embryonic cardiac development

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