Sirt3 mediates the protective effect of hydrogen in inhibiting ROS-induced retinal senescence

Li, Ruichan; Li, Yanli; Xie, Jing; Huang, Xudong; Zhang, Li; Liu, Hua; Li, Lihua

doi:10.1016/j.freeradbiomed.2019.02.005

Cited by 28 publications

(19 citation statements)

References 56 publications

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“…The antioxidant defense mechanism of SIRT3 is mainly achieved by regulating the deacetylation of superoxide dismutase 2 (SOD2) to enhance the activity of SOD2 to scavenge ROS (Katwal et al, 2018). A recent study confirmed that SIRT3 has a significant antisenescence effect on ROS‐induced retinal senescence (Li et al, 2019). In addition, a work by Geng et al (2018) illustrated that adjudin delays the senescence of mouse fibroblasts induced by hydroxyurea by promoting SIRT3 expression.…”

Section: Introductionmentioning

confidence: 74%

SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress‐induced senescence of nucleus pulposus cells

Lin

et al. 2021

Journal Cellular Physiology

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Senescence of nucleus pulposus (NP) cells (NPC) is a major cause of intervertebral disc degeneration (IVDD), so delay NPC senescence may be beneficial for mitigating IVDD. We studied the effect and mechanism of silent information regulator 2 homolog 3 (SIRT3) on NPC senescence in vivo and in vitro. First, we observed SIRT3 expression in normal and degenerated NPC with immunohistochemical and immunofluorescence staining. Second, using SIRT3 lentivirus transfection, reactive oxygen species probe, senescence-associated β-galactosidase staining, polymerase chain reaction, and western blot to observe the oxidative stress, senescence, and degeneration degree among groups. Subsequently, pretreatment with adenosine monophosphate-activated protein kinase (AMPK) agonists and inhibitors, observing oxidative stress, senescence, and degeneration degree among groups. Finally, the IVDD model was constructed and divided into Ctrl, Vehicle, LV-shSIRT3, and LV-SIRT3 groups. X-ray and magnetic resonance imaging scans were performed on rat's tails after 1 week; hematoxylin and eosin and safranin-O staining were used to evaluate the degree of IVDD; immunofluorescence staining was used to observe SIRT3 expression; immunohistochemical staining was used to observe oxidative stress, senescence, and degeneration degree of NP. We found that SIRT3 expression is reduced in degenerated NP tissues but increased in H 2 O 2 -induced NPC. Moreover, SIRT3 upregulation decreased oxidative stress, delayed senescence, and degeneration of NPC. In addition, activation of the AMPK/PGC-1α pathway can partially mitigate the NPC oxidative stress, senescence, and degeneration caused by SIRT3 knockdown. The study in vivo revealed that local SIRT3 overexpression can significantly reduce oxidative stress and ECM degradation of NPC, delay NPC senescence, thereby mitigating IVDD. In summary, SIRT3 mediated by the AMPK/PGC-1α pathway mitigates IVDD by delaying oxidative stress-induced NPC senescence.

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Section: Introductionmentioning

confidence: 74%

SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress‐induced senescence of nucleus pulposus cells

Lin

et al. 2021

Journal Cellular Physiology

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“…As previously described [ 28 ], the frozen tissue sections were stained with DHE reaction mixture to detect ROS generation in the myocardium. Each sample was examined with an Olympus FV10C-W3 laser confocal microscope, and the fluorescent intensity in different groups was determined by the ImageJ software.…”

Section: Methodsmentioning

confidence: 99%

Bakuchiol Alleviates Hyperglycemia-Induced Diabetic Cardiomyopathy by Reducing Myocardial Oxidative Stress via Activating the SIRT1/Nrf2 Signaling Pathway

Shang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Bakuchiol (BAK), a monoterpene phenol reported to have exerted a variety of pharmacological effects, has been related to multiple diseases, including myocardial ischemia reperfusion injury, pressure overload-induced cardiac hypertrophy, diabetes, liver fibrosis, and cancer. However, the effects of BAK on hyperglycemia-caused diabetic cardiomyopathy and its underlying mechanisms remain unclear. In this study, streptozotocin-induced mouse model and high-glucose-treated cell model were conducted to investigate the protective roles of BAK on diabetic cardiomyopathy, in either the presence or absence of SIRT1-specific inhibitor EX527, SIRT1 siRNA, or Nrf2 siRNA. Our data demonstrated for the first time that BAK could significantly abate diabetic cardiomyopathy by alleviating the cardiac dysfunction, ameliorating the myocardial fibrosis, mitigating the cardiac hypertrophy, and reducing the cardiomyocyte apoptosis. Furthermore, BAK achieved its antifibrotic and antihypertrophic actions by inhibiting the TGF-β1/Smad3 pathway, as well as decreasing the expressions of fibrosis- and hypertrophy-related markers. Intriguingly, these above effects of BAK were largely attributed to the remarkable activation of SIRT1/Nrf2 signaling, which eventually strengthened cardiac antioxidative capacity by elevating the antioxidant production and reducing the reactive oxygen species generation. However, all the beneficial results were markedly abolished with the administration of EX527, SIRT1 siRNA, or Nrf2 siRNA. In summary, these novel findings indicate that BAK exhibits its therapeutic properties against hyperglycemia-caused diabetic cardiomyopathy by attenuating myocardial oxidative damage via activating the SIRT1/Nrf2 signaling.

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“…After fixing with 50% OTC at -80˚C for 2 h, the sections were washed three times with PBS for 5 min each time and dHe (50 µM) was applied to each tissue section, which was incubated in a light-protected humidified chamber at 37˚C for 30 min. Sections were washed three times with PBS for 5 min each time (48). Subsequently, the sections were sealed with neutral balsam (cat.…”

Section: Detection Of Rosmentioning

confidence: 99%

Ameliorative effects and mechanism of crocetin in arsenic trioxide‑induced cardiotoxicity in rats

Zhao

Zheng

et al. 2020

Mol Med Rep

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arsenic trioxide (aTo) is commonly used to treat patients with acute promyelocytic leukemia since it was authorized by the u.S. Food and drug administration in the 1970s, but its applicability has been limited by its cardiotoxic effects. Therefore, the aim of the present study was to investigate the cardioprotective effects and underlying mechanism of crocetin (crT), the critical ingredient of saffron. Sprague-dawley rats were then randomly divided into four groups (n=10/group): i) control group; ii) aTo group, iii) crT-low (20 mg/kg) group; and iv) crT-high (40 mg/kg) group. rats in the control and aTo groups were intraperitoneally injected with equal volumes of 0.9% sodium chloride solution, and crT groups were administered with either 20 and 40 mg/kg crT. Following 6 h, all groups except the control group were intraperitoneally injected with 5 mg/kg aTo over 10 days. cardiotoxicity was indicated by changes in electrocardiographic (ecG) patterns, morphology and marker enzymes. Histomorphological changes in the heart tissue were observed by pathological staining. The levels of superoxide dismutase, glutathione peroxidase, malondialdehyde and catalase in the serum were analyzed using colometric commercial assay kits, and the levels of reactive oxygen species in the heart tissue were detected using the fluorescent probe dihydroethidium. The expression levels of inflammatory factors and activities of apoptosis-related proteins were analyzed using immunohistochemistry. The protein expression levels of silent information regulator of transcription 1 were measured using western blotting. cardiotoxicity was induced in male Sprague-dawley rats with aTo (5 mg/kg). crT (20 and 40 mg/kg) and aTo were co-administered to evaluate possible cardioprotective effects. CRT significantly reduced the heart rate and J-point elevation induced by aTo in rats. Histological changes were evaluated via hematoxylin and eosin staining. crT decreased the levels of creatine kinase and lactate dehydrogenase, increased the activities of superoxide dismutase, glutathione-peroxidase and catalase, and decreased the levels of malondialdehyde and reactive oxygen species. Moreover, crT downregulated the expression levels of the pro-inflammatory factors IL-1, TnF-α, il-6, Bax and p65, as well as increased the expression of Bcl-2. It was also identified that CRT enhanced silent information regulator of transcription 1 protein expression. Thus, the present study demonstrated that crT treatment effectively ameliorated aTo-induced cardiotoxicity. The protective effects of crT can be attributed to the inhibition of oxidative stress, inflammation and apoptosis. Therefore, CRT represents a promising therapeutic method for improving the cardiotoxic side effects caused by aTo treatment, and additional clinical applications are possible, but warrant further investigation.

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Sirt3 mediates the protective effect of hydrogen in inhibiting ROS-induced retinal senescence

Cited by 28 publications

References 56 publications

SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress‐induced senescence of nucleus pulposus cells

SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress‐induced senescence of nucleus pulposus cells

Bakuchiol Alleviates Hyperglycemia-Induced Diabetic Cardiomyopathy by Reducing Myocardial Oxidative Stress via Activating the SIRT1/Nrf2 Signaling Pathway

Ameliorative effects and mechanism of crocetin in arsenic trioxide‑induced cardiotoxicity in rats

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