Teneligliptin protects against ischemia/reperfusion-induced endothelial permeabilityin vivoandin vitro

Zhang, Lei; Yuan, Weiqiong; Kong, Xiangli; Zhang, Bei

doi:10.1039/c9ra08810e

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…[ 36 ] Herein, KLF2 was found to be markedly downregulated in both MCAO mice and OGD/R‐stimulated HBMVECs, in line with results presented by Chen [ 37 ] and Lei. [ 38 ] The KLF2 level was found to be remarkably increased by Netrin‐1 in both MCAO mice and OGD/R‐stimulated HBMVECs, suggesting that the function of Netrin‐1 might be regulated by KLF2 upregulation. Furthermore, the alleviation of Netrin‐1 on endothelial monolayer permeability in HBMVECs was abrogated by KLF2 knockdown, verifying that KLF2 was an important mediator responsible for the protective function of Netrin‐1.…”

Section: Discussionmentioning

confidence: 99%

Netrin‐1 protects blood–brain barrier (BBB) integrity after cerebral ischemia‐reperfusion by activating the Kruppel‐like factor 2 (KLF2)/occludin pathway

Li,

Liu,

Chen

et al. 2024

J Biochem & Molecular Tox

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Ischemia/reperfusion (I/R)‐induced neural damage and neuroinflammation have been associated with pathological progression during stroke. Netrin‐1 is an important member of the family of laminin‐related secreted proteins, which plays an important role in governing axon elongation. However, it is unknown whether Netrin‐1 possesses a beneficial role in stroke. Here, we employed the middle cerebral artery occlusion (MCAO) model to study the function of Netrin‐1 in alleviating brain injuries. Our results demonstrate that Netrin‐1 rescued poststroke neurological deficits and inhibited production of the inflammatory cytokines such as interleukin 6 (IL‐6) and endothelial chemokine (C‐X‐C motif) ligand 1 (Cxcl1). Importantly, Netrin‐1 protected against MCAO‐induced dysfunction of the blood–brain barrier (BBB) in mice and a reduction in the expression of the tight junction (TJ) protein occludin. Additionally, we report that Netrin‐1 could ameliorate oxygen‐glucose deprivation/reoxygenation (OGD/R)‐induced injury and prevent aggravation in endothelial monolayer permeability in bEnd.3 human brain microvascular endothelial cells (HBMVECs). Mechanistically, Netrin‐1 ameliorated OGD/R‐induced decrease in occludin and Kruppel‐like factor 2 (KLF2) in HBMVECs. Notably, silencing of KLF2 abolished the beneficial effects of Netrin‐1 in protecting endothelial permeability and occludin expression, suggesting that these effects are mediated by KLF2. In conclusion, our findings suggest that Netrin‐1 could constitute a novel therapeutic strategy for ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Netrin‐1 protects blood–brain barrier (BBB) integrity after cerebral ischemia‐reperfusion by activating the Kruppel‐like factor 2 (KLF2)/occludin pathway

Li,

Liu,

Chen

et al. 2024

J Biochem & Molecular Tox

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“…21 Moreover, recent studies demonstrated that teneligliptin rescues endothelial cell viability through the ERK5/KLF2 signaling pathway. 22,23 However, it would still be necessary to investigate whether the differences in binding modes between teneligliptin and other DPP-4 inhibitors are clinically meaningful.…”

Section: A B Cmentioning

confidence: 99%

Effect of Switching from Linagliptin to Teneligliptin Dipeptidyl Peptidase-4 Inhibitors in Older Patients with Type 2 Diabetes Mellitus

Han¹,

Lee²,

Lee

et al. 2020

DMSO

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Introduction Dipeptidyl peptidase-4 (DPP-4) inhibitors are widely prescribed for type 2 diabetes (T2D) and their glycemic control effects are well studied. However, information regarding the effects of switching DPP-4 inhibitors is limited, especially in older patients. Research Design and Methods We investigated whether switching from linagliptin to teneligliptin decreases blood glucose in older (≥65 years) T2D patients. In total, 164 patients with T2D who switched from linagliptin to teneligliptin for >12 weeks were included and the primary outcome was glycemic changes. Results Switching from linagliptin to teneligliptin ameliorated fasting blood glucose (148.1 ± 47.1 to 139.6 ± 43.4 mg/dL), glycated hemoglobin (HbA1c; 7.9 ± 1.3 to 7.5 ± 1.2%), and postprandial blood glucose (224.8 ± 77.4 to 205.8 ± 70.8 mg/dL) levels (all P < 0.05). Low-density lipoprotein cholesterol concentration was reduced while liver and kidney functions were maintained. Subgroup analysis showed that glucose control improved more in patients with uncontrolled hyperglycemia (HbA1c > 8.0%) and chronic kidney disease (estimated glomerular filtration rate <90 mL/min/1.73m 2 ). Multiple logistic analysis indicated higher baseline HbA1c was the strongest predictor of teneligliptin switching response. Conclusion Switching from linagliptin to teneligliptin helps maintain kidney function and reduce blood glucose safely in older patients with T2D.

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Finding the most cost-effective option from commonly used Dipeptidyl peptidase-4 inhibitors in India: a systematic study

Singh,

Arora,

Narula

et al. 2023

Expert Review of Endocrinology & Metabolism

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Teneligliptin protects against ischemia/reperfusion-induced endothelial permeabilityin vivoandin vitro

Abstract: Ischemic stroke is a leading cause of disability and mortality worldwide, especially among the elderly population.

Cited by 3 publications

References 34 publications

Netrin‐1 protects blood–brain barrier (BBB) integrity after cerebral ischemia‐reperfusion by activating the Kruppel‐like factor 2 (KLF2)/occludin pathway

Netrin‐1 protects blood–brain barrier (BBB) integrity after cerebral ischemia‐reperfusion by activating the Kruppel‐like factor 2 (KLF2)/occludin pathway

<p>Effect of Switching from Linagliptin to Teneligliptin Dipeptidyl Peptidase-4 Inhibitors in Older Patients with Type 2 Diabetes Mellitus</p>

Finding the most cost-effective option from commonly used Dipeptidyl peptidase-4 inhibitors in India: a systematic study

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