Engeletin Attenuates Aβ1–42-Induced Oxidative Stress and Neuroinflammation by Keap1/Nrf2 Pathway

Huang, Zhixiong; Ji, Hu; Shi, Junfeng; Zhu, Xinchen; Zhi, Zhongwen

doi:10.1007/s10753-020-01250-9

Cited by 35 publications

(21 citation statements)

References 31 publications

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“…Engeletin, which is also referred to as rhamnoside of dihydrokaempferol, is a bioactive derivative of Smilax glabra rhizomilax . In prior research, engeletin has shown anti-inflammatory and antioxidant activity in vitro ( 15 ) and ability to further suppress the growth of cervical and lung cancer cells ( 16 , 17 ). Herein, we explored the protective activity of engeletin in the context of CI/R injury and assessed the underlying mechanisms whereby it regulates angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Liu

et al. 2021

Braz J Med Biol Res

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Engeletin is a natural derivative of Smilax glabra rhizomilax that exhibits anti-inflammatory activity and suppresses lipid peroxidation. In the present study, we sought to elucidate the mechanistic basis for the neuroprotective and pro-angiogenic activity of engeltin in a human umbilical vein endothelial cells (HUVECs) oxygen-glucose deprivation and reoxygenation (OGD/R) model system and a middle cerebral artery occlusion (MCAO) rat model of cerebral ischemia and reperfusion injury. These analyses revealed that engeletin (10, 20, or 40 mg/kg) was able to reduce the infarct volume, increase cerebral blood flow, improve neurological function, and bolster the expression of vascular endothelial growth factor (VEGF), vasohibin-2 (Vash-2), angiopoietin-1 (Ang-1), phosphorylated human angiopoietin receptor tyrosine kinase 2 (p-Tie2), and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) in MCAO rats. Similarly, engeletin (100, 200, or 400 nM) markedly enhanced the migration, tube formation, and VEGF expression of HUVECs in an OGD/R model system, while the VEGF receptor (R) inhibitor axitinib reversed the observed changes in HUVEC tube formation activity and Vash-2, VEGF, and CD31 expression. These data suggested that engeletin exhibited significant neuroprotective effects against cerebral ischemia and reperfusion injury in rats, and improved cerebrovascular angiogenesis by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways.

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Section: Introductionmentioning

confidence: 99%

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Liu

et al. 2021

Braz J Med Biol Res

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“…4E ). Engeletin is a flavanonol glycoside extracted from hymenaea martiana , and its antioxidant function has been uncovered recently [ 21 , 22 ]. Engeletin administration reduced the level of ROS, rescued ATP generation, and increased the viability in GC cells with CDO1 overexpression (Fig.…”

Section: Resultsmentioning

confidence: 99%

Cysteine dioxygenase 1 attenuates the proliferation via inducing oxidative stress and integrated stress response in gastric cancer cells

Zhao

et al. 2022

Cell Death Discov.

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Whereas cysteine dioxygenase 1 (CDO1) expression is lost due to its hypermethylated promoter across a range of cancer types including gastric cancer (GC), its functions and molecular underpinnings remain largely unknown. Here we demonstrate that reduced CDO1 expression is indicative of unfavorable prognosis in patients with GC. CDO1 overexpression in GC cells markedly inhibits cellular proliferation in vitro and in vivo. Mechanistically, CDO1 exerts this cytostatic effect via increasing oxidative stress and thus activating integrated stress response (ISR) in GC cells. High throughput screening (HTS) of antioxidants library identifies that Engeletin, a flavanonol glycoside, blunts oxidative stress and the ISR to relieve the inhibitory effect of CDO1 on the proliferation in GC cells. Additionally, genetic disruption or pharmaceutical inhibition of the ISR boosts the growth in the GC cells with CDO1 expression. Our data uncover the molecular mechanisms underlying the cytostatic function of CDO1 in the proliferation of GC cells.

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“…Oxidative stress is a result of imbalance between the generation of ROS and the antioxidant defense systems ( 32 ). LDH and MDA are the important indicators of cellular oxidative stress, and SOD is a protective indicator ( 33 , 34 ). The results of the present study demonstrated that 20, 40 and 60 µg/ml ozone decreased LDH and MDA levels and increased SOD release, and that 20 µg/ml ozone was the most effective.…”

Section: Discussionmentioning

confidence: 99%

Ozone induces tolerance against cardiomyocytes oxygen‑glucose deprivation/reperfusion through inhibition of autophagy pathway

Zhu

Liu

et al. 2021

Exp Ther Med

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Previous studies have reported that excess activation of autophagy in cardiomyocytes is associated with an increase in myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury. Ozone therapy affords significant cardio-protection against myocardial OGD/R injury. The present study was designed to determine whether ozone-induced tolerance to myocardial OGD/R injury was mediated by inhibiting autophagy. Subsequently, the rat cardio myoblast H9C2 cell line was used in the present study. A model of H9C2 cells under OGD/R was established. The cells were incubated with different concentrations of ozone (10-60 µg/ml) during reperfusion. Furthermore, to investigate the role of autophagy in OGD/R-induced injury, the autophagy inducer and inhibitor were applied. Cell viability was detected by Cell Counting kit-8 assay. Cell apoptosis was evaluated by flow cytometry. Oxidative stress was examined by superoxide dismutase, lactate dehydrogenase and malondialdehyde levels. The expressions of apoptosis regulator B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (BAX), cleaved caspase-3, markers of autophagy microtuble-associated protein 1 light chain 3 (LC3), autophagy-related protein 5 (Atg5) and Beclin-1 were measured by western blot analysis. As a result, OGD/R notably decreased cell viability and induced apoptosis in H9C2 cells, while ozone (10-40 µg/ml) reversed the noxious effects of OGD/R on H9C2 cells, and 20 µg/ml ozone was the most effective. Ozone inhibited the decrease in the ratio of Bcl-2/BAX and the expression of cleaved caspase-3, and inhibited the increase in the ratio of LC3-II/LC3-I and the expression of Atg5 and Beclin-1 elicited by OGD/R, as well as dose-dependently preventing OGD/R-induced oxidative stress. Furthermore, rapamycin markedly reversed the effects of ozone (20 µg/ml) on OGD/R-induced expression of autophagy marker proteins and 3-methyladenine further improved the effect of ozone. Taken together, the results of the present study provided a credible mechanism by which ozone treatment at low concentrations could protect the myocardium from OGD/R-induced injury by inhibiting autophagy.

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Engeletin Attenuates Aβ1–42-Induced Oxidative Stress and Neuroinflammation by Keap1/Nrf2 Pathway

Cited by 35 publications

References 31 publications

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Engeletin protects against cerebral ischemia/reperfusion injury by modulating the VEGF/vasohibin and Ang-1/Tie-2 pathways

Cysteine dioxygenase 1 attenuates the proliferation via inducing oxidative stress and integrated stress response in gastric cancer cells

Ozone induces tolerance against cardiomyocytes oxygen‑glucose deprivation/reperfusion through inhibition of autophagy pathway

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