SIRT3-mediated deacetylation protects inner hair cell synapses in a H2O2-induced oxidative stress model in vitro

Zhao, Chunli; Liang, Wenqi; Zhan, Yɑnɡ; Chen, Zhong-Rui; Du, Zhongtao; Gong, Shusheng

doi:10.1016/j.yexcr.2022.113280

Cited by 9 publications

(7 citation statements)

References 45 publications

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“…The excess ROS leads to the formation of oxidized biomolecules, DNA mutation, protein denaturation, and enhanced lipid peroxidation, resulting in oxidative damage to cells, apoptosis, and necrosis [ 6 ]. ROS are mainly produced in the mitochondria and endoplasmic reticulum [ 7 ]. The liver is a major organ for metabolism and detoxification in mammals and is one of the richest in terms of mitochondrial number and density, making it susceptible to a number of stressors [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, changes in those trace elements in the body can reflect antioxidant levels on the other hand. Mitochondrial deacetylase sirtuin 3 (SIRT3) is an important regulator of ROS production [ 7 ]. Under conditions of stress, it maintains mitochondrial function by deacetylating proteins, specifically superoxide dismutase (SOD2) at lysine 68.…”

Section: Introductionmentioning

confidence: 99%

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Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size

Zou

Bian

et al. 2023

IJMS

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Microplastics have become a new type of environmental pollutant that can accumulate in various tissues and organs of the body and cause chronic damage. In this study, two different size polystyrene microplastics (PS-MPs, 5 μm and 0.5 μm) exposure models were established in mice to investigate the effects of PS-MPs with different particle sizes on oxidative stress in the liver. The results showed that PS-MPs exposure caused a decrease in body weight and liver-to-body weight. The hematoxylin and eosin staining and transmission electron microscopy results showed that exposure to PS-MPs led to the disorganized cellular structure of liver tissue, nuclear crinkling, and mitochondrial vacuolation. The extent of damage in the 5 μm PS-MP exposure group was more extensive when compared with the other group. The evaluation of oxidative-stress-related indicators showed that PS-MPs exposure exacerbated oxidative stress in hepatocytes, especially in the 5 μm PS-MPs group. The expression of oxidative-stress-related proteins sirtuin 3(SIRT3) and superoxide dismutase (SOD2) was significantly reduced, and the reduction was more pronounced in the 5 μm PS-MPs group. In conclusion, PS-MPs exposure led to oxidative stress in mouse hepatocytes and caused more severe damage in the 5 μm PS-MPs group when compared with the 0.5 μm PS-MPs group.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size

Zou

Bian

et al. 2023

IJMS

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“…In the cardiac ischemia reperfusion injury that occurs in the post-stroke condition, the excessive production of free radicals, the increase of circulating HSP60, the increase of intracellular calcium, the leakage of H into the mitochondrial surfaces, and inflammation lead to the opening of the mitochondrial permeability transition pores. This can lead to the reduction of ATP, irreversible oxidation of protein, fat, and DNA in cardiomyocytes, and initiation of apoptosis (30). In this way, most researchers have considered the increase of HSP60 as a risk factor and aggravating damage, but in a new study, therapeutic benefits of protein-protein interactions between various types of HSPs, including HSP60, in the treatment of heart attack and damage caused by ischemia-reinjection have been supported.…”

Section: Discussionmentioning

confidence: 99%

The Effect of high-intensity interval training with caloric restriction on gene expression of apoptosis indices HSP70 and HSP60 in the myocardium of male rats

Mazhari,

Matinhomaee,

Fatolahi

2024

J Shahrekord Univ Med Sci

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Background and aims: The purpose of this study was to investigate the effect of high-intensity interval training combined with calorie restriction on the expression of HSP70 and HSP60 in the myocardium of male rats. Methods: A total of 27 male rats were randomly divided into three groups (9 rats in each group): control, caloric restriction, and caloric restriction with high-intensity interval training. During the study, the control group had free access to water and food, but the amount of food in the food restriction group was limited to 50% and the calorie restriction-exercise group was limited to 25% of the control group. The restriction-exercise group was subjected to intense interval training for eight weeks. The gene expression of apoptotic indicators HSP70 and HSP60 was assessed using the real-time PCR method. The data were analyzed using Shapiro-Wilk test and ANOVA test. Results: Body weight in both calorie restriction groups significantly decreased (P=0.001). The results of the post hoc test showed a significant increase in the expression of HSP70 and HSP60 genes in the myocardium of male rats in the calorie-restricted-exercise group compared to the calorie-restricted and control groups (P=0.001). Additionally, no significant difference was observed between the two restriction and control groups in terms of HSP70 and HSP60 (P=0.102). Conclusion: The combination of high-intensity interval training and mild food restriction significantly increased HSP60 and HSP70 expression.

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“…Sirtuin (SIRT3), a deacetylase whose primary function is to regulate mitochondrial electron transport chain activity, maintains ATP homeostasis by stimulating β‐oxidation through deacetylation of long‐chain acyl coenzyme A dehydrogenase 14 . As a positive regulator of mitochondrial activity, SIRT3 regulates antioxidant enzymes, cell survival, and longevity 15,16 . Therefore, it has cytoprotective properties associated with the regulation of antioxidant effects in a variety of disease models, including neurological disorders such as persistent epilepsy.…”

Section: Introductionmentioning

confidence: 99%

“…14 As a positive regulator of mitochondrial activity, SIRT3 regulates antioxidant enzymes, cell survival, and longevity. 15,16 Therefore, it has cytoprotective properties associated with the regulation of antioxidant effects in a variety of disease models, including neurological disorders such as persistent epilepsy. SIRT3 is also involved in the autophagy induction process.…”

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confidence: 99%

SIRT3 enhances the protective effect of Xyloketal B on seizure‐induced brain injury by regulating AMPK/mTOR signaling‐mediated autophagy

Chen,

Liu,

Zhou

2023

The Kaohsiung J of Med Scie

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Brain damage in children due to seizures is irreversible and has been a major public health concern. The herbal monomer Xyloketal B (Xyl‐B) can be used as a neuroprotective drug because of its antioxidant, antiapoptotic, and anti‐inflammatory effects but with few adverse effects. In this article, we constructed a rat developmental convulsion model and a primary hippocampal neuronal cell convulsion model, through which we studied hippocampal neuronal morphology and neuronal apoptosis using H&E staining and TUNEL staining, respectively. Moreover, we measured TNF‐α, IL‐6, and IL‐1β inflammatory factor levels using ELISA, MDA, and SOD kits. The expression of SIRT3 in hippocampal tissues was determined by qPCR and Western blotting. The expression of autophagy‐related proteins such as LC3, p62, and Beclin‐1 was evaluated by Western blotting or immunohistochemistry. The role of SIRT3 and autophagic activity with Xyl‐B in convulsive seizure‐induced brain injury was investigated by knocking down SIRT3 expression levels. Our results showed that Xyl‐B plays a neuroprotective role in convulsive seizure‐induced brain injury by increasing SIRT3 expression and activating the autophagy pathway. The regulatory role of SIRT3 in the autophagy pathway with Xyl‐B treatment was explored by knocking down SIRT3 expression and inhibiting autophagy. Our results revealed that SIRT3 enhances the protective effect of Xyl‐B against postconvulsive brain injury by regulating AMPK/mTOR signaling‐mediated autophagy.

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SIRT3-mediated deacetylation protects inner hair cell synapses in a H2O2-induced oxidative stress model in vitro

Cited by 9 publications

References 45 publications

Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size

Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size

The Effect of high-intensity interval training with caloric restriction on gene expression of apoptosis indices HSP70 and HSP60 in the myocardium of male rats

SIRT3 enhances the protective effect of Xyloketal B on seizure‐induced brain injury by regulating AMPK/mTOR signaling‐mediated autophagy

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