Oxygen–Glucose Deprivation/Reperfusion-Induced Sirt3 Reduction Facilitated Neuronal Injuries in an Apoptosis-Dependent Manner During Prolonged Reperfusion

Wan, Rongqi; Fan, Jiahui; Song, Huimeng; Sun, Weiyi; Yin, Yanling

doi:10.1007/s11064-021-03502-y

Cited by 6 publications

(3 citation statements)

References 48 publications

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“…SIRT3, a mitochondrial histone deacetylation enzyme, is primarily localized in mitochondria. It can directly deacetylate and activate the major mitochondrial antioxidant enzymes and mitochondrial metabolic enzymes downstream [29], as well as apoptosis-related proteins [30]. Burgeoning studies have reported that SIRT3 can alleviate CP-induced renal tubule epithelial cell injury by maintaining mitochondrial integrity, further suggesting that improving mitochondrial dynamics by increasing SIRT3 expression has become a potential therapeutic strategy to alleviate CP-induced renal injury [31].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Liquiritigenin against Cisplatin-Induced Nephrotoxicity via NRF2/SIRT3-Mediated Improvement of Mitochondrial Function

Zhou

Dai

et al. 2022

Molecules

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Acute kidney injury (AKI) induced by cisplatin (CP), a first-line anticancer drug for chemotherapy, is common. To date, there is an urgent need to find effective treatments to reduce the nephrotoxicity caused by CP. Meanwhile, the restoration of mitochondrial dysfunction shows potential to be used as an adjunct to conventional therapeutic strategies. This study found that liquiritigenin can ameliorate mitochondrial dysfunction and acute kidney injury induced by CP in mice. The intraperitoneal injection of 15 mg/kg body weight liquiritigenin for 2 days markedly protected against CP-induced mitochondrial dysfunction, restored renal tubule and mitochondrial morphology, decreased blood Scr and BUN levels, and decreased cell apoptosis. Furthermore, the elevated expression of SIRT3 induced by liquiritigenin, which can be upregulated by NRF2, was confirmed in vivo and in vitro. The underlying protective mechanisms of liquiritigenin in CP-induced nephrotoxicity were then investigated. Molecular docking results showed that liquiritigenin has potent binding activities to KEAP1, GSK-3β and HRD1. Further results showed that liquiritigenin induced the nuclear translocation of NRF2 and increased the levels of mitochondrial bioenergetics-related protein such as PGC-1α, and TFAM, which are related to NRF2 activity and mitochondrial biogenesis. In addition, liquiritigenin was found to possibly reverse the decrease in BCL2/BAX ratio induced by CP in live cultured renal tubule epithelial cells. Collectively, these results indicated that liquiritigenin could be used as a potential nephroprotective agent to protect against cisplatin-induced acute kidney injury in a NRF2-dependent manner by improving mitochondria function.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Liquiritigenin against Cisplatin-Induced Nephrotoxicity via NRF2/SIRT3-Mediated Improvement of Mitochondrial Function

Zhou

Dai

et al. 2022

Molecules

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“…BACE1, a key regulatory enzyme in the generation of Aβ peptide, is decreased by honokiol [ 126 ]. Hippocampal neuronal injuries caused by oxygen-glucose deprivation/reperfusion OGD/R are moderately rescued by honokiol treatment via SIRT3 activation [ 166 ]. Honokiol also ameliorates surgery-induced memory loss and decreases Sirt3 expression and neuroinflammatory injury in the hippocampus [ 167 ].…”

Section: Translational Significance Of Sirt3 Activationmentioning

confidence: 99%

A Promising Strategy to Treat Neurodegenerative Diseases by SIRT3 Activation

Tyagi

Pugazhenthi

2023

IJMS

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SIRT3, the primary mitochondrial deacetylase, regulates the functions of mitochondrial proteins including metabolic enzymes and respiratory chain components. Although SIRT3’s functions in peripheral tissues are well established, the significance of its downregulation in neurodegenerative diseases is beginning to emerge. SIRT3 plays a key role in brain energy metabolism and provides substrate flexibility to neurons. It also facilitates metabolic coupling between fuel substrate-producing tissues and fuel-consuming tissues. SIRT3 mediates the health benefits of lifestyle-based modifications such as calorie restriction and exercise. SIRT3 deficiency is associated with metabolic syndrome (MetS), a precondition for diseases including obesity, diabetes, and cardiovascular disease. The pure form of Alzheimer’s disease (AD) is rare, and it has been reported to coexist with these diseases in aging populations. SIRT3 downregulation leads to mitochondrial dysfunction, neuroinflammation, and inflammation, potentially triggering factors of AD pathogenesis. Recent studies have also suggested that SIRT3 may act through multiple pathways to reduce plaque formation in the AD brain. In this review, we give an overview of SIRT3’s roles in brain physiology and pathology and discuss several activators of SIRT3 that can be considered potential therapeutic agents for the treatment of dementia.

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“…The activities of sirtuins are regulated in response to multiple external stimulation and stress responses, such as drug exposure, glucose deprivation and metabolic stress. 18 , 19 , 20 SIRT3 is reported to be localized in the mitochondrial matrix and promotes deacetylation of multiple metabolic enzymes in response to metabolic changes. 21 Hyperacetylation of several mitochondrial proteins are observed in SIRT3 −/− mice.…”

Section: Introductionmentioning

confidence: 99%

Honokiol ameliorates cigarette smoke‐induced damage of airway epithelial cells via the SIRT3/SOD2 signalling pathway

Li,

Ye,

Wang

et al. 2023

J Cellular Molecular Medi

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Cigarette smoking can cause damage of airway epithelial cells and contribute to chronic obstructive pulmonary disease (COPD). Honokiol is originally isolated from Magnolia obovata with multiple biological activities. Here, we investigated the protective effects of honokiol on cigarette smoke extract (CSE)‐induced injury of BEAS‐2B cells. BEAS‐2B cells were treated with 300 mg/L CSE to construct an in vitro cell injury model, and cells were further treated with 2, 5 and 10 μM honokiol, then cell viability and LDH leakage were analysed by CCK‐8 and LDH assay kits, respectively. Apoptosis was detected by flow cytometry analysis. ELISA was used to measure the levels of tumour necrosis factor (TNF)‐ɑ, IL‐1β, IL‐6, IL‐8 and MCP‐1. The results showed that honokiol (0.5–20 μM) showed non‐toxic effects on BEAS‐2B cells. Treatment with honokiol (2, 5 and 10 μM) reduced CSE (300 mg/L)‐induced decrease in cell viability and apoptosis in BEAS‐2B cells. Honokiol also decreased CSE‐induced inflammation through inhibiting expression and secretion of inflammatory cytokines, such as TNF‐ɑ, IL‐1β, IL‐6, IL‐8 and MCP‐1. Moreover, honokiol repressed CSE‐induced reactive oxygen species (ROS) production, decrease of ATP content and mitochondrial biogenesis, as well as mitochondrial membrane potential. Mechanistically, honokiol promoted the expression of SIRT3 and its downstream target genes, which are critical regulators of mitochondrial function and oxidative stress. Silencing of SIRT3 reversed the protective effects of honokiol on CSE‐induced damage and mitochondrial dysfunction in BEAS‐2B cells. These results indicated that honokiol attenuated CSE‐induced damage of airway epithelial cells through regulating SIRT3/SOD2 signalling pathway.

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Oxygen–Glucose Deprivation/Reperfusion-Induced Sirt3 Reduction Facilitated Neuronal Injuries in an Apoptosis-Dependent Manner During Prolonged Reperfusion

Cited by 6 publications

References 48 publications

Protective Effects of Liquiritigenin against Cisplatin-Induced Nephrotoxicity via NRF2/SIRT3-Mediated Improvement of Mitochondrial Function

Protective Effects of Liquiritigenin against Cisplatin-Induced Nephrotoxicity via NRF2/SIRT3-Mediated Improvement of Mitochondrial Function

A Promising Strategy to Treat Neurodegenerative Diseases by SIRT3 Activation

Honokiol ameliorates cigarette smoke‐induced damage of airway epithelial cells via the SIRT3/SOD2 signalling pathway

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