Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs

Zhang, Huaping; Yang, Xiaorong; Pang, Xue-Fen; Zhao, Zhenxiang; Hou, Yu; Zhou, Hui

doi:10.1007/s11010-018-3476-8

Cited by 43 publications

(30 citation statements)

References 41 publications

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“…The present study demonstrated that the expression levels of SIRT1 and AMPK were downregulated in the BLM‐induced pulmonary fibrosis group compared to the control animals. Previous studies reported that the knockdown of SIRT1 promoted the profibrogenic activity of TGF‐ß1 in lung fibroblasts and contribute to the development of vascular dysfunction 28,29 . Furthermore, the present study demonstrated that a decrease in the SIRT1 levels was associated with a high oxidative stress in the BLM‐treated rats, indicating the involvement of the ROS/SIRT1 pathway in the mechanism of BLM‐induced pulmonary fibrosis 12 .…”

Section: Discussionsupporting

confidence: 68%

Modulation of bleomycin‐induced oxidative stress and pulmonary fibrosis by N‐acetylcysteine in rats via AMPK/SIRT1/NF‐κβ

Mansour

Omran

Hasan

et al. 2020

Clin Exp Pharma Physio

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The efficacy of bleomycin (BLM) as an antineoplastic drug is limited to the development of dose and time‐dependent pulmonary fibrosis. This study was intended to investigate the effect of N‐acetylcysteine (NAC) on BLM‐induced pulmonary fibrosis in rats. Twenty rats were randomly divided to the following four groups: Group one served as control; group two received BLM (15 mg/kg, intraperitoneal (ip)) for five consecutive days; group three received NAC (200 mg/kg, ip) for five consecutive days; and group four received NAC 1 hour before BLM for 5 days. The expression of connective tissue growth factor (CTGF), platelet‐derived growth factor (PDGF), silent information regulator l (SIRT1), AMP‐activated protein kinase (AMPK) were determined by qRT‐PCR in lung tissues. The changes in transforming growth factor‐beta1 (TGF‐β1), tumour necrosis factor‐α (TNF‐α), interleukin‐β1 (IL‐β1) and nuclear factor kappa‐β (NF‐κβ) in serum were measured by ELISA. The tissue antioxidant status was determined biochemically. BLM administration caused pulmonary fibrosis as evidenced by increased levels of inflammatory mediators (TGF‐β1, TNF‐α, IL‐β1 and NF‐κβ) in serum (P < .05), elevated lipid peroxidation and nitric oxide and depleted endogenous antioxidants in lung tissue (P < .05). The expression levels of SIRT1 and AMPK were significantly decreased (P < .05), while the expression levels of CTGF and PDGF were increased significantly in the BLM group as compared to the control group (P < .05). These alterations were normalized by NAC intervention. NAC markedly attenuated the lung histopathological changes and reduced collagen deposition. These results suggest that NAC exerted an ameliorative effect against BLM‐induced oxidative damage and pulmonary fibrosis via SIRT1/ AMPK/ NF‐κβ pathways.

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Section: Discussionsupporting

confidence: 68%

Modulation of bleomycin‐induced oxidative stress and pulmonary fibrosis by N‐acetylcysteine in rats via AMPK/SIRT1/NF‐κβ

Mansour

Omran

Hasan

et al. 2020

Clin Exp Pharma Physio

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“…proposed that autophagy deficiency is a predisposing factor for inflammatory disease. Additionally, GEN protects against oxidized low-density lipoprotein (ox-LDL)-induced senescence by enhancing sirtuin 1 (SIRT1)/liver kinase B1/AMP kinase-mediated autophagy flux (14), and reverses ox-LDLor lipopolysaccharide (LPS)-induced inflammatory responses via miR-34a/SIRT1/FOXO3a (15) and MyD88/NF-κB/BCL-2 signaling pathways in VECs (16). These findings suggest that GEN regulates microRNAs (miRNAs/miRs), autophagy and apoptosis, thus alleviating VEC injury triggered by various inducers; however, the underlying mechanisms are yet to be clearly defined.…”

Section: Genistein Alleviates Chronic Vascular Inflammatory Response mentioning

confidence: 99%

Genistein alleviates chronic vascular inflammatory response via the miR‑21/NF‑κB p65 axis in lipopolysaccharide‑treated mice

Xie

Liu

et al. 2021

Mol Med Rep

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“…AMPK can regulate apoptosis and autophagy during coronary artery disease (300), endothelial dysfunction during hyperglycemia (54), and oxidative stress cell injury (301,302). Anti-senescence activity also can be fostered through mTOR inhibition, AMPK activation, and the acceleration of autophagic flux (303). In addition to nicotinamide, other agents rely upon the ability of AMPK to modulate cellular metabolism.…”

Section: Nicotinamide and The Downstream Pathways Of Mtormentioning

confidence: 99%

“…Inhibition of mTOR activity with activation of autophagy can reduce markers of senescence and aging in the skin of patients (326). Blockade of mTOR also can prevent aging and cell injury with extension of cell longevity through AMPK in endothelial cells (303). Additional work suggests that a balance is required during embryogenesis for autophagy and apoptosis that can affect body axis formation (327).…”

Section: Nicotinamide and The Necessary Modulation Of Autophagy With mentioning

confidence: 99%

New Insights for nicotinamide Metabolic disease autophagy and mTOR

Maiese

2020

Front Biosci

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Metabolic disorders, such as diabetes mellitus (DM), are increasingly becoming significant risk factors for the health of the global population and consume substantial portions of the gross domestic product of all nations. Although conventional therapies that include early diagnosis, nutritional modification of diet, and pharmacological treatments may limit disease progression, tight serum glucose control cannot prevent the onset of future disease complications. With these concerns, novel strategies for the treatment of metabolic disorders that involve the vitamin nicotinamide, the mechanistic target of rapamycin (mTOR), mTOR Complex 1 (mTORC1), mTOR Complex 2 (mTORC2), AMP activated protein kinase (AMPK), and the cellular pathways of autophagy and apoptosis offer exceptional promise to provide new avenues of treatment. Oversight of these pathways can promote cellular energy homeostasis, maintain mitochondrial function, improve glucose utilization, and preserve pancreatic β-cell function. Yet, the interplay among mTOR, AMPK, and autophagy pathways can be complex and affect desired clinical outcomes, necessitating further investigations to provide efficacious treatment strategies for metabolic dysfunction and DM.

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Genistein protects against ox-LDL-induced senescence through enhancing SIRT1/LKB1/AMPK-mediated autophagy flux in HUVECs

Cited by 43 publications

References 41 publications

Modulation of bleomycin‐induced oxidative stress and pulmonary fibrosis by N‐acetylcysteine in rats via AMPK/SIRT1/NF‐κβ

Modulation of bleomycin‐induced oxidative stress and pulmonary fibrosis by N‐acetylcysteine in rats via AMPK/SIRT1/NF‐κβ

Genistein alleviates chronic vascular inflammatory response via the miR‑21/NF‑κB p65 axis in lipopolysaccharide‑treated mice

New Insights for nicotinamide Metabolic disease autophagy and mTOR

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