Sirt1 resists advanced glycation end products-induced expressions of fibronectin and TGF-β1 by activating the Nrf2/ARE pathway in glomerular mesangial cells

Huang, Kaipeng; Huang, Juan; Xie, Xi; Wang, Shaogui; Chen, Cheng; Shen, X. Y.; Liu, Peiqing; Huang, Heqing

doi:10.1016/j.freeradbiomed.2013.07.029

Cited by 233 publications

(179 citation statements)

References 40 publications

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“…It has been clarified that AGEs-induced ROS inhibits the translocation of Nrf2 into nucleus, which causes upregulation of antioxidant protein production [27]. In the development of diabetic nephropathy (DN), AGEs induces expressions of fibronectin and TGF-β1, which is attenuated by sirt1 through activating the Nrf2/ARE pathway [28]. One further trial has revealed that AGEs promotes ERK phosphorylation, resulting in a reduction in Nrf-2 and downstream pathway [29].…”

Section: Discussionmentioning

confidence: 99%

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

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Section: Discussionmentioning

confidence: 99%

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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“…Consistent with its dual cellular localization, SIRT1 targets can be found in both the nucleus and the cytoplasm. SIRT1 activation exerts protective effects on multiple organs upon oxidative stress, including kidney (12,(20)(21)(22)(23), whereas SIRT1 knockout (KO) mice show aggravation of renal changes occurring in diabetes and acute kidney injury (12,24).…”

Section: Introductionmentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

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Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

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“…Previous studies have demonstrated that the SIRT1-mediated deacetylation of NRF2 terminated the transcription of antioxidant genes (7). By contrast, SIRT1 is known to protect cells from oxidative stress injury, and silencing its activity results in decreased NRF2 expression levels (8,9). However, the association between SIRT1 and NRF2 and their effect in PQ-induced oxidative stress remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol protects mice from paraquat-induced lung injury: The important role of SIRT1 and NRF2 antioxidant pathways

Zhao

Chen

et al. 2015

Molecular Medicine Reports

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Abstract. Sirtuin 1 (SIRT1) acts via the deacetylation of a number of crucial transcription factors and has been implicated in various biological processes, including oxidative stress. Previous studies have indicated that nuclear factor, erythroid 2-like 2 (NRF2) is an effective target of antioxidant therapy for paraquat (PQ) poisoning. However, the association between SIRT1 and NRF2 and their effects in PQ-induced oxidative stress remains to be elucidated. The current study demonstrated that PQ exposure upregulated the expression of SIRT1 and NRF2 following 6-and 24-h exposure in the lungs of mice. However, long-term exposure to PQ significantly decreased the expression of SIRT1 and NRF2. Resveratrol is a SIRT1 activator, and strongly enhanced SIRT1 expression and attenuated the lung injury resulting from PQ exposure in the current study. Additionally, treatment with resveratrol upregulated the expression of NRF2 and glutathione, increased the activity of heme oxygenase-1, superoxide dismutase and catalase, but depleted the expression of malondialdehyde. The present results demonstrated that resveratrol reduced PQ-induced oxidative stress and lung injury, potentially through the positive feedback signaling loop between SIRT1 and NRF2.

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Sirt1 resists advanced glycation end products-induced expressions of fibronectin and TGF-β1 by activating the Nrf2/ARE pathway in glomerular mesangial cells

Cited by 233 publications

References 40 publications

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Sirtuin 1: A Target for Kidney Diseases

Resveratrol protects mice from paraquat-induced lung injury: The important role of SIRT1 and NRF2 antioxidant pathways

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