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

Liu, Hui; Li, Shucui; Xu, Yangyang; Wang, Xin; Ren, Rui; Zhu, Haibo; Zhang, Shuping

doi:10.1590/1414-431x2020e11028

Cited by 13 publications

(24 citation statements)

References 37 publications

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“…Rutin is a flavonoid from the same class of Q3G, which corroborates its antiangiogenic activity. Furthermore the literature reported that kaempferol interferes with VASH1 expression [ 36 ] and that engeletin regulates VASH2 [ 54 ], which is consistent with the regulation of both angiogenic factors by flavonoids.…”

Section: Discussionsupporting

confidence: 68%

“…Flavonoids such as FAA [ 33 ] and vadimezan [ 34 ] interfere with tubulin; thus, they are grouped as VDAs. We speculate that Q3G is a VDA mainly because of its interference with VASH expression, similar to kaempferol [ 36 ] which regulates VASH1 and Engeletin [ 54 ] that acts on VASH2.…”

Section: Discussionmentioning

confidence: 99%

“…It has an antiproliferative effect in vitro on CC cells (SW480, DLD-1, and HCT116) no significant effect on non-tumor colon cells (IEC-18) [ 52 ]. Considering this antiproliferative effect of Q3G on CC [ 52 , 53 ], the evidence from flavonols as promising angiogenic agents, and also its relationship with VASHs [ 35 , 54 ], we evaluated the antitumoral effect of Q3G in vivo and its relationship with vascularization in a xenogeneic CC animal model.…”

Section: Introductionmentioning

confidence: 99%

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Antitumor effect of isoquercetin on tissue vasohibin expression and colon cancer vasculature

et al. 2022

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Tumor cells trigger angiogenesis through the expression of angiogenic factors. Vasohibins (VASHs) are a family of peptides that regulate angiogenesis. Flavonoids have antiproliferative antitumor properties; however, few studies have highlighted their antiangiogenic potential. This study evaluated the flavonoid isoquercetin (Q3G) as an antitumor compound related to colon cancer vascularization and regulation of VASH1 and 2. Mice bearing xenogeneic colon cancer ( n = 15) were divided into 3 groups: Q3G-treated (gavage, daily over a week), bevacizumab-treated (intraperitoneal, single dose), or untreated animals. Tumor growth, histological characteristics, blood vessel volume, and VASH1 and 2 expressions were analyzed. Q3G impaired tumor growth and vascularization, upregulated VASH1, and downregulated VASH2 in comparison to untreated animals. Mice treated with Q3G showed approximately 65% fewer blood vessels than untreated animals and 50% fewer blood vessels than mice treated with bevacizumab. Thus, we show that Q3G has antitumor activity, impairs vascularization, and differentially modulates VASH1 and 2 expressions in colon cancer.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antitumor effect of isoquercetin on tissue vasohibin expression and colon cancer vasculature

et al. 2022

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“…In addition, atherosclerosis is also the pathological basis of cerebral infarction and peripheral vascu- lar disease, and HCG11 is dramatically increased in AS patients [25]. Human umbilical vein colorectal cells are involved in CI/R injury [24], and HCG11 can regulate the proliferation of these cells and inhibit angiogenesis [12]. However, the role of HCG11 in CI/R injury remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through microRNA miR-381-3p to regulate tumour protein p53

Gao¹,

Gao²,

Du³

et al. 2022

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Introduction: Long non-coding RNA (LncRNA) plays a critical role in cerebral ischemia-reperfusion (CI/R) injury. The purpose of the current research was to investigate the regulatory role of the LncRNA human leukocyte antigen complex group 11 (HCG11) in CI/R injury and explore its potential mechanism. Material and methods: The rat middle cerebral artery occlusion (MCAO) model was established to simulate CI/R injury in vivo. mRNA levels of HCG11, microRNA (miR)-381-3p, tumour protein p53, and neuro-inflammatory factors were detected by quantitative reverse transcription PCR (RT-qPCR). Bederson score and Longa score were assessed for neurological deficits. Triphenyl tetrazolium chloride (TTC) staining was used to examine the cerebral infarct volume. What is more, oxidative stress was evaluated by the commercial kit. Finally, the relationship between HCG11, miR-381-3p, and p53 was verified by a dual-luciferase reporter assay. Results: HCG11 was elevated in MCAO rats. And it competitively bound miR-381-3p and down-regulated the expression of p53. Inhibition of HCG11 inhibited cerebral infarct volume and neurological deficits in MCAO rats, and inhibited the secretion of neuro-inflammation and the over-activation of oxidative stress, exerting the protective effect of CI/R injury. However, inhibition of miR-381-3p in rats significantly weakened the protective effect of depression of HCG11 in MCAO rats, resulting in increased cerebral infarction volume and neurological deficits, elevated neuro-inflammatory secretion, and oxidative stress activation. Conclusions: The present research shows that LncRNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through miR-381-3p to regulate p53.

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“…Infarct brain tissues appear white, while normal brain tissues appear red. The sections were digitized, and the infarct areas were measured using Image Pro Plus software to calculate the percentage of cerebral infarct areas [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Cornin protects against cerebral ischemia/reperfusion injury by preventing autophagy via the PI3K/Akt/mTOR pathway

Lan

et al. 2022

BMC Pharmacol Toxicol

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Background Ischemia stroke is the leading cause of disability, which is a consequence of vascular occlusion. The purpose of this study is to investigate the effect of cornin which is isolated from the fruit of Verbena officinalis L, against astrocytes autophagy induced by cerebral ischemia/reperfusion (CI/R) injury in vitro and in vivo and its potential mechanism. Methods Cornin at dose of 2.5, 5 and 10 mg/kg were intravenously injected to MCAO rats at 15 min after reperfusion. The infarction volume, blood–brain barrier (BBB), neurological severity score (mNSS), and autophagy related protein were used to evaluated the protective effects and potential mechanism of cornin in autophagy with or without phosphoinositide-3 kinase (PI3K)inhibitor LY294002 and mammalian target of rapamycin (mTOR) small interfering RNA (siRNA) at 24 h after CI/R injury. The potential protective effects and mechanism of cornin at concention of 10 ~ 1000 nM were also evaluated in oxygen glucose deprivation/reperfusion (OGD/R) in U87 cells. Results The results suggest that cornin at dose of 5 or 10 mg/kg significantly reduce the cerebral infarction volume and blood–brain barrier (BBB) leakage, and improve neurological recovery in MCAO rats. Cleaved caspase-3 and Bax levels were significantly decreased, while B-cell lymphoma-2 (Bcl-2) and the apoptosis regulator ratio (Bcl-2/Bax) were markedly increased when treated with 2.5–10 mg/kg cornin. The obvious decreased expressions of glial fibrillary acidic protein (GFAP), myosin-like BCL2 interacting protein (Beclin-1) and microtubule-associated protein light chain 3 II (LC3-II) and increased of neuronal nuclei (NeuN), sequestosome-1 (p62), phosphorylated mTOR (p-mTOR), and phosphorylated Akt (p-Akt) were observed in MCAO rats treated with 10 mg/kg cornin, which was counteracted by LY294002. The expression of autophagy-related proteins with or without LY294002 and mTOR siRNA presented the similar results as in vitro in OGD/R in U87 cells. Conclusions These results indicate that cornin improved neurological recovery after cerebral ischemia injury by preventing astrocytes autophagy induced by CI/R via the PI3K/Akt/mTOR signaling pathway.

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

Cited by 13 publications

References 37 publications

Antitumor effect of isoquercetin on tissue vasohibin expression and colon cancer vasculature

Antitumor effect of isoquercetin on tissue vasohibin expression and colon cancer vasculature

Long non-coding RNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through microRNA miR-381-3p to regulate tumour protein p53

Cornin protects against cerebral ischemia/reperfusion injury by preventing autophagy via the PI3K/Akt/mTOR pathway

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