Saxagliptin protects against hypoxia-induced damage in H9c2 cells

Zhang, Lili; Qi, Xiaogui; Zhang, Guowei; Zhang, Yingying; Tian, Jiali

doi:10.1016/j.cbi.2019.108864

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…This decrease in antioxidant activity (both SOD and T-AOC) in hypoxia-treated microglia is consistent with previous studies [9,44]. In addition, overproduction of ROS also results in the loss of mitochondrial membrane potential and aggravates mitochondrial dysfunction [8,45,46]. Furthermore, the effect of propofol on mitochondrial membrane potential and mitochondrial function is related to dose, cell type, and administration route [12,47].…”

Section: Discussionsupporting

confidence: 90%

Propofol Attenuates Hypoxia‐Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF‐κB/Hif‐1α Signaling

Peng

et al. 2020

BioMed Research International

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Hypoxia-induced neuroinflammation typically causes neurological damage and can occur during stroke, neonatal hypoxic-ischemic encephalopathy, and other diseases. Propofol is widely used as an intravenous anesthetic. Studies have shown that propofol has antineuroinflammatory effect. However, the underlying mechanism remains to be fully elucidated. Thus, we aimed to investigate the beneficial effects of propofol against hypoxia-induced neuroinflammation and elucidated its potential cellular and biochemical mechanisms of action. In this study, we chose cobalt chloride (CoCl2) to establish a hypoxic model. We found that propofol decreased hypoxia-induced proinflammatory cytokines (TNFα, IL-1β, and IL-6) in BV2 microglia, significantly suppressed the excessive production of reactive oxygen species, and increased the total antioxidant capacity and superoxide dismutase activity. Furthermore, propofol attenuated the hypoxia-induced decrease in mitochondrial membrane potential andy 2 strongly inhibited protein expression of nuclear factor-kappa B (NF-κB) subunit p65 and hypoxia inducible factor-1α (Hif-1α) in hypoxic BV2 cells. To investigate the role of NF-κB p65, specific small interfering RNA (siRNA) against NF-κB p65 were transfected into BV2 cells, followed by exposure to hypoxia for 24 h. Hypoxia-induced Hif-1α production was downregulated after NF-κB p65 silencing. Further, propofol suppressed Hif-1α expression by inhibiting the upregulation of NF-κB p65 after exposure to hypoxia in BV2 microglia. In summary, propofol attenuates hypoxia-induced neuroinflammation, at least in part by inhibiting oxidative stress and NF-κB/Hif-1α signaling.

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Section: Discussionsupporting

confidence: 90%

Propofol Attenuates Hypoxia‐Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF‐κB/Hif‐1α Signaling

Peng

et al. 2020

BioMed Research International

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“…HMGB1 is a key inflammatory cytokine involved in kidney diseases, and Nrf2 is considered a master regulator of cellular redox signaling, inflammatory pathway. Inhibition of the inflammatory mediator HMGB1 along with upregulation of Nrf2/HO-1 has been demonstrated to significantly improve hypoxia-induced cell injury [41,42]. Another study also shows that increased Nrf2 activity can attenuate hyperoxiainduced inflammatory by inhibiting the accumulation of extracellular HMGB1 [43].…”

Section: Keap1mentioning

confidence: 97%

Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway

Zhao

Feng

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Contrast-induced acute kidney injury (CI-AKI) is the third common cause of acute kidney injury (AKI), which is associated with poor short- and long-term outcomes. Currently, effective therapy strategy for CI-AKI remains lacking. Stanniocalcin-1 (STC1) is a conserved glycoprotein with antiapoptosis and anti-inflammatory functions, but the role of STC1 in controlling CI-AKI is unknown. Here, we demonstrated a protective role of STC1 in contrast-induced injury in cultured renal tubular epithelial cells and CI-AKI rat models. Recombinant human STC1 (rhSTC1) regulated mitochondrial quality control, thus suppressing contrast-induced mitochondrial damage, oxidative stress, inflammatory response, and apoptotic injury. Mechanistically, activation of the Nrf2 signaling pathway contributes critically to the renoprotective effect of STC1. Together, this study demonstrates a novel role of STC1 in preventing CI-AKI and reveals Nrf2 as a molecular target of STC1. Therefore, this study provides a promising preventive target for the treatment of CI-AKI.

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“…However, some studies have shown promising results. For instance, saxagliptin has been found to moderate hypoxia-induced cell death, ROS production, and NOX-4 expressions, while also rescuing mitochondrial membrane potential in rat cardiomyocytes [115]. In addition, sitagliptin reduced TNF-α and S100A12-induced cellular oxidative stress, NADPH oxidase, and NF-κB activation in human aortic smooth muscle cells.…”

Section: Dpp-4imentioning

confidence: 96%

An Overview of the Cardioprotective Effects of Novel Antidiabetic Classes: Focus on Inflammation, Oxidative Stress, and Fibrosis

Balogh

Wagner

Fekete

2023

IJMS

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Metabolic diseases, particularly diabetes mellitus (DM), are significant global public health concerns. Despite the widespread use of standard-of-care therapies, cardiovascular disease (CVD) remains the leading cause of death among diabetic patients. Early and evidence-based interventions to reduce CVD are urgently needed. Large clinical trials have recently shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) ameliorate adverse cardiorenal outcomes in patients with type 2 DM. These quite unexpected positive results represent a paradigm shift in type 2 DM management, from the sole importance of glycemic control to the simultaneous improvement of cardiovascular outcomes. Moreover, SGLT2i is also found to be cardio- and nephroprotective in non-diabetic patients. Several mechanisms, which may be potentially independent or at least separate from the reduction in blood glucose levels, have already been identified behind the beneficial effect of these drugs. However, there is still much to be understood regarding the exact pathomechanisms. This review provides an overview of the current literature and sheds light on the modes of action of novel antidiabetic drugs, focusing on inflammation, oxidative stress, and fibrosis.

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Saxagliptin protects against hypoxia-induced damage in H9c2 cells

Cited by 6 publications

References 39 publications

Propofol Attenuates Hypoxia‐Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF‐κB/Hif‐1α Signaling

Propofol Attenuates Hypoxia‐Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF‐κB/Hif‐1α Signaling

Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway

An Overview of the Cardioprotective Effects of Novel Antidiabetic Classes: Focus on Inflammation, Oxidative Stress, and Fibrosis

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