Chrysin ameliorates ANTU‐induced pulmonary edema and pulmonary arterial hypertension via modulation of VEGF and eNOs

Wang, Linlin; Wang, Ye; Zhang, Lei

doi:10.1002/jbt.22332

Cited by 21 publications

(10 citation statements)

References 43 publications

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“…The synthesis dysfunction of vasodilator NO is well considered a major reason of PAH [ 5 , 6 ]. Abnormal expression and dysfunction of the endothelial NO synthase (eNOS) in the human pulmonary arterial endothelial cells (HPAECs) leads to decreased NO content and thus contributes to the development and progression of PAH [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] miR‐1226‐3p Promotes eNOS Expression of Pulmonary Arterial Endothelial Cells to Mitigate Hypertension in Rats via Targeting Profilin‐1

Jian

Liang

2021

BioMed Research International

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In pulmonary arterial hypertension (PAH), microRNAs (miRNAs) are related with dysfunction of pulmonary arterial endothelial cells. miR-1226-3p was found to be downregulated in the serum of PAH patients, while few studies have illustrated the regulation mechanism of miR-1226-3p on PAH. In this study, we aimed to systematically investigate the role of miR-1226-3p in PAH. Sprague-Dawley (SD) rats were treated with monocrotaline (MCT) to establish the PAH models. The right ventricular systolic pressure (RVSP), ratio of the right ventricle to the left ventricle with septum (RV/(LV+S) ratio), and nitric oxide (NO) content were used to reflect the symptom of the rats. The rat models were used to observe the regulation mechanism of miR-1226-3p on PAH, and dual-luciferase reporter assay was used to verify the binding effect of miR-1226-3p to Pfn1. Besides, the qRT-PCR and western blot were used to measure the expression levels of miR-1226-3p and some keys proteins such as eNOS and Pfn1, respectively. The results showed that the PAH models were established successfully. The RVSP levels and the RV/(LV+S) ratio of the PAH rats were higher than those indexes in normal rats, while the NO content showed the opposite trends. Besides, the decreased miR-1226-3p and eNOS were, respectively, found in the PAH rats and rPAECs, and overexpressed miR-1226-3p could reverse the disadvantages of the PAH rats including increased RVSP, high RV/(LV+S) ratio, and decreased NO content. Furthermore, miR-1226-3p could directly target the 3 ′ -UTR of Profilin-1 (Pfn1). Overexpressed Pfn1 led to decreased eNOS, while miR-1226-3p could partly inhibit the expression of Pfn1 and increase the expression level of eNOS in rPAECs. In summary, this study suggests miR-1226-3p as a protector to increase eNOS, improve NO content in rPAECs of the PAH rats via targeting Pfn, and finally protect the rats from the injury induced by PAH.

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Section: Introductionmentioning

confidence: 99%

[Retracted] miR‐1226‐3p Promotes eNOS Expression of Pulmonary Arterial Endothelial Cells to Mitigate Hypertension in Rats via Targeting Profilin‐1

Jian

Liang

2021

BioMed Research International

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“…By contrast, chrysin treatment after HLI massively increased eNOS mRNA and NO levels compared with the HLI group. Previous studies reported that chrysin increases eNOS mRNA and protein expression (Mizar et al, 2015; L. Wang et al, 2019). NO, which is constitutively produced by eNOS, plays a substantial role in vascular biology and in the regulation of angiogenesis (Cooke & Losordo, 2002; Moncada et al, 1991).…”

Section: Discussionmentioning

confidence: 92%

Section: Genementioning

confidence: 95%

Chrysin promotes angiogenesis in rat hindlimb ischemia: Impact on PI3K/Akt/mTOR signaling pathway and autophagy

Kamel

Morsy

Elsherbiny

et al. 2022

Drug Development Research

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Limb ischemia occurs due to obstruction of blood perfusion to lower limbs, a manifestation that is associated with peripheral artery disease (PAD). Angiogenesis is important for adequate oxygen delivery. The present study investigated a potential role for chrysin, a naturally occurring flavonoid, in promoting angiogenesis in hindlimb ischemia (HLI) rat model. Rats were allocated into four groups: (1) shamoperated control, (2) HLI: subjected to unilateral femoral artery ligation,(3) HLI + chrysin: received 100 mg/kg, i.p. chrysin immediately after HLI, and (4) HLI + chrysin + rapamycin: received 6 mg/kg/day rapamycin i.p. for 5 days then subjected to HLI and dosed with 100 mg/kg chrysin, i.p. Rats were killed 18 h later and gastrocnemius muscles were collected and divided into parts for (1) immunohistochemistry detection of CD31 and CD105, (2) qRT-PCR analysis of eNOS and VEGFR2, (3) colorimetric analysis of NO, (4) ELISA estimation of TGF-β, VEGF, ATG5 and Beclin-1, and (5) Western blot analysis of p-PI3K, PI3K, p-Akt, Akt, p-mTOR, mTOR, and HIF-1α. Chrysin significantly enhanced microvessels growth in HLI muscles as indicated by increased CD31 and CD105 levels and decreased TGF-β. Chrysin's proangiogenic effect is potentially mediated by increased VEGF, VEGFR2 and activation of PI3K/AKT/mTOR pathway, which promoted eNOS and NO levels as it was reversed by the mTOR inhibitor, rapamycin. Chrysin also inhibited autophagy as it decreased ATG5 and Beclin-1. The current study shows that chrysin possesses a proangiogenic effect in HLI rats and might be useful in patients with PAD.

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“…For HIRT, although it is reported that high-intensity exercise can improve cardiac function, some studies have shown that high-intensity exercise will increase the level of oxidative stress, aggravate endothelial dysfunction, stimulate the increase of ET-1 and inhibit the expression of eNOS. Such changes will affect endothelial function ( Novoa et al, 2017 ; Wang et al, 2019 ). At the same time, the correlation analysis also showed that the correlation between VEGF in myocardium and VEGF in blood was not statistically significant.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Blood Flow-Restricted Low Resistance Training on Microvascular Circulation of Myocardium in Spontaneously Hypertensive Rats

et al. 2022

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Objective: The purpose of this study was to explore the effect of blood flow-restricted low resistance training on microvascular rarefaction in the myocardium of spontaneously hypertensive rats (SHRs).Methods: Four-week-old male SHRs were randomly divided into the following groups: Wistar-Kyoto (WKY), SHR control (SHR-SED), high-intensity resistance training (HIRT), low-intensity resistance training (LIRT), and blood flow-restricted low resistance training (BFRT). The exercise groups began to receive exercise intervention for 8 weeks at the age of 7 weeks. Blood pressure (BP), heart rate (HR), cardiac function, capillary density, and Vascular endothelial growth factor -Phosphatidylinositol 3-kinase-Protein kinase B-Endothelial nitric oxide synthetase (VEGF-Pi3k-Akt-eNOS) were assessed.Results: 1) BP and HR of BFRT decreased significantly, Ejection fraction (EF) and Fraction shortening (FS) increased, and the effect of BFRT on lowering BP and HR was better than that of other groups (p < 0.05); 2) The expression of VEGF, VEGFR2, p-VEGFR2, Pi3k, Akt, p-Akt, eNOS and p-eNOS in the myocardium of the BFRT was significantly upregulated, and eNOS expression was significantly higher than other groups (p < 0 05); 3) the expression of VEGF in the blood of the BFRT was significantly upregulated, higher than SHR-SED, lower than HIRT (p < 0.05), and there was no significant difference between BFRT and LIRT(p > 0.05); 4) the capillary density in the myocardium of BFRT was significantly higher than other exercise groups (p < 0 05).Conclusion: Blood flow-restricted low resistance training can activate the VEGF-Pi3k-Akt-eNOS pathway, upregulate the expression of VEGF in blood, improve microvascular rarefaction, and promote myocardial microvascular circulation, thereby improving cardiac function and lowering blood pressure, achieving the preventive effect of early hypertension.

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Chrysin ameliorates ANTU‐induced pulmonary edema and pulmonary arterial hypertension via modulation of VEGF and eNOs

Cited by 21 publications

References 43 publications

[Retracted] miR‐1226‐3p Promotes eNOS Expression of Pulmonary Arterial Endothelial Cells to Mitigate Hypertension in Rats via Targeting Profilin‐1

[Retracted] miR‐1226‐3p Promotes eNOS Expression of Pulmonary Arterial Endothelial Cells to Mitigate Hypertension in Rats via Targeting Profilin‐1

Chrysin promotes angiogenesis in rat hindlimb ischemia: Impact on PI3K/Akt/mTOR signaling pathway and autophagy

The Effect of Blood Flow-Restricted Low Resistance Training on Microvascular Circulation of Myocardium in Spontaneously Hypertensive Rats

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