E1231/SR647 Protects Against Unilateral Renal Ischemia-Reperfusion Injury by Modulating SIRT1/FOXO3 Interactions with Nrf2 and NFκB Pathways DOI Creative Commons
Sameh Saber, Rabab S. Hamad, Elsayed A. Elmorsy

и другие.

European Journal of Pharmaceutical Sciences, Год журнала: 2025, Номер unknown, С. 107099 - 107099

Опубликована: Апрель 1, 2025

Ischemia is a major contributor to acute kidney injury (AKI), for which current treatment options remain limited. One NAD+-dependent deacetylase that can preserve renal cells SIRT1. To date, no research has directly explored the effects of E1231, SIRT1 activator, in context ischemia-reperfusion (IR) injury. Enhancing NAD+ levels essential sustaining activity. Hence, combined use E1231 and SR647, precursor, could potentially amplify protective by supporting prolonged activation. This study first investigate therapeutic potential combining SR647 mitigating unilateral IR Rats treated with E1231/SR647 effectively demonstrated reduced tubular damage, inflammation, necrosis. These improvements correlated kidney-to-body weight ratio increased urine output flow rate. Additionally, rats reductions serum creatinine, BUN, UAER, cystatin C, as well urinary NGAL both KIM-1 levels. On other hand, elevations creatinine CL were recorded. alone provided moderate functional recovery, was negated when co-administered inhibitor. upregulated activity, subsequently enhancing FOXO3 It also boosted Nrf2 upregulating antioxidant protein expression HO-1 NQO1. Furthermore, inflammatory response inhibiting NFκB In conclusion, promising therapy may protect function during ischemic events through modulation SIRT1/FOXO3 control over pathways.

Язык: Английский

Activation of SIRT1 by SRT1720 Alleviates Dyslipidemia, Improves Insulin Sensitivity and Exhibits Liver-Protective Effects in Diabetic Rats on a High-Fat Diet: New Insights into the SIRT1/Nrf2/NFκB Signaling Pathway DOI Creative Commons
Elsayed A. Elmorsy, Hossam A. Elsisi, Abdullah S. Alkhamiss

и другие.

European Journal of Pharmaceutical Sciences, Год журнала: 2025, Номер 206, С. 107002 - 107002

Опубликована: Янв. 6, 2025

Insulin resistance and diabetes are associated with non-alcoholic fatty liver disease (NAFLD) steatohepatitis (NASH) conditions, which distinguished by metabolic dysfunction, oxidative stress inflammation. Sirtuin 1 (SIRT1), a NAD

Язык: Английский

Процитировано

4
The dual missions of FoxO3a in inflammatory diseases: Regulation of antioxidant enzymes and involvement in programmed cell death DOI

Xiangli Ma,

Yujie Lin,

Ling Zhang

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 151, С. 114369 - 114369

Опубликована: Март 2, 2025

Язык: Английский

Процитировано

0
E1231/SR647 Protects Against Unilateral Renal Ischemia-Reperfusion Injury by Modulating SIRT1/FOXO3 Interactions with Nrf2 and NFκB Pathways DOI Creative Commons
Sameh Saber, Rabab S. Hamad, Elsayed A. Elmorsy

и другие.

European Journal of Pharmaceutical Sciences, Год журнала: 2025, Номер unknown, С. 107099 - 107099

Опубликована: Апрель 1, 2025

Ischemia is a major contributor to acute kidney injury (AKI), for which current treatment options remain limited. One NAD+-dependent deacetylase that can preserve renal cells SIRT1. To date, no research has directly explored the effects of E1231, SIRT1 activator, in context ischemia-reperfusion (IR) injury. Enhancing NAD+ levels essential sustaining activity. Hence, combined use E1231 and SR647, precursor, could potentially amplify protective by supporting prolonged activation. This study first investigate therapeutic potential combining SR647 mitigating unilateral IR Rats treated with E1231/SR647 effectively demonstrated reduced tubular damage, inflammation, necrosis. These improvements correlated kidney-to-body weight ratio increased urine output flow rate. Additionally, rats reductions serum creatinine, BUN, UAER, cystatin C, as well urinary NGAL both KIM-1 levels. On other hand, elevations creatinine CL were recorded. alone provided moderate functional recovery, was negated when co-administered inhibitor. upregulated activity, subsequently enhancing FOXO3 It also boosted Nrf2 upregulating antioxidant protein expression HO-1 NQO1. Furthermore, inflammatory response inhibiting NFκB In conclusion, promising therapy may protect function during ischemic events through modulation SIRT1/FOXO3 control over pathways.

Язык: Английский

Процитировано

0