Naringin protects endothelial cells from apoptosis and inflammation by regulating the Hippo-YAP Pathway

Zhao, Hui; Liu, Meirong; Liu, Hui; Suo, Rong; Lu, Chengzhi

doi:10.1042/bsr20193431

Cited by 65 publications

(58 citation statements)

References 28 publications

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“…In pulmonary hypertension, EndMT causes matrixgenerating fibroblasts and contributes to the progression of extracellular matrix productions and collagen depositions, and subsequently causes the pulmonary vascular remodeling (Xiong, 2015). Naringin are found to produce protective effects against End MT in atherosclerosis (Zhao et al, 2020). Here in this study, our data indicated significantly decreased endothelial markers, increased mesenchymal markers, and EndMT-related transcription factors in the lung tissue of an MCT-induced rat model of PAH.…”

Section: Discussionsupporting

confidence: 59%

“…Naringin is a flavanone glycoside synthesized from the flavanone naringenin and the disaccharide neohesperidose. Previous studies have demonstrated the potential protective effects of Naringin on diseases including osteoporosis, atherosclerosis, hypertension, and alcoholic hepatic steatosis (Zhao et al, 2020;Akintunde et al, 2020;Zhou et al, 2019). However, the efficacies of Naringin to the pathogenesis of PAH is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence has indicated that cardiac function is damaged by pulmonary interstitial fibrosis, contributing to the formation of pulmonary hypertension and causing RV failure (Andersen et al, 2019). Naringin attenuates damages in vascular endothelial caused by Oxidized low-density lipoprotein (ox-LDL) and alleviates paraquat-induced acute lung injury in mice through the suppression of collagen synthesis (Zhao et al, 2020;Chen et al, 2013). Naringenin, a conversion of naringin, can increase the protective effect of L-arginine against monocinine induced pulmonary hypertension in rats (Ahmed et al, 2014), therefore potentially participating in the protective effects of naringin on PAH.…”

Section: Discussionmentioning

confidence: 99%

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Naringin Ameliorates Monocrotaline-Induced Pulmonary Arterial Hypertension Through Endothelial-To-Mesenchymal Transition Inhibition

Cai

Xiang

et al. 2021

Front. Pharmacol.

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Pulmonary arterial hypertension (PAH) caused by enhanced arterial pressure increases vessel resistance in the lung. Endothelial-to-mesenchymal transition (EndMT) plays key roles in the vascular remodeling in PAH. Naringin, a protective gaseous mediator is commonly extracted from tomatoes and citrus fruits (such as grapefruits), and demonstrates anti-inflammation, anti-oxidant, anti-proliferation, and anti-tumor effects. Meanwhile, the association of Naringin and the process of EndMT is still unclear. In this study, monocrotaline (MCT) administration (60 mg/kg) was delivered for the induction of PAH in rats. Following this, Naringin (concentrations: 25, 50, and 100 mg/kg/day) was used for treatments. Human Umbilical Vein Endothelial Cells (HUVECs) were stimulated with Naringin and transforming growth factor β1 (TGFβ1, 10 ng/ml). As the result, Naringin was demonstrated to inhibit EndMT and alleviate PAH progression. In particular, in HUVECs, Naringin significantly suppressed the mesenchymal marker expression induced by TGFβ1 treatment, enhanced the endothelial marker expression, and inhibited the activation of ERK and NF-κB signaling pathways. To conclude, this study provided novel evidence suggesting the beneficial effects of Naringin in PAH through the inhibition of the ERK and NF-κB signaling pathways and the EndMT progression in pulmonary arteries.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Naringin Ameliorates Monocrotaline-Induced Pulmonary Arterial Hypertension Through Endothelial-To-Mesenchymal Transition Inhibition

Cai

Xiang

et al. 2021

Front. Pharmacol.

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“…Naringin, a polymethoxylated flavonoid glycoside, is the main bioactive flavonoid extracted from citrus fruits [ 6 , 7 ] and has a positive effect on osteoporosis caused by postmenopause, glucocorticoid, orchidectomy, and aging [ 8 ]. Studies have shown that naringin can promote the differentiation and proliferation of various types of cells [ 9 – 12 ] and improve the bone mass in an osteoporotic rat model [ 9 ]. Naringin also promotes osteoclast apoptosis through the mitochondrial-mediated apoptotic pathway, so as to inhibit bone loss in OVX rat models and exhibit antiosteoporotic pharmacological activity [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of Naringin Treatment on Postmenopausal Osteoporosis in Ovariectomized Rats: A Meta-Analysis and Systematic Review

Zhu

Xie

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Background. Osteoporosis is a major disease that affects the quality of life of middle-aged and old people, so it is very important to find efficient and safe drugs to treat osteoporosis. The purpose of this study was to investigate the therapeutic effect of naringin on postmenopausal osteoporosis in ovariectomized (OVX) rats. Methods. Chinese biomedical databases, CNKI, PubMed, EMBASE, and Wan Fang were searched for articles from inception to March 2020. Two independent researchers screened articles according to inclusion criteria. RevMan 5.3 was used for data analysis. Results. Ten studies were included in the systematic review. The bone mineral density (BMD) significantly increased after naringin treatment (weighted mean difference, 0.06; 95% CI, 0.03–0.09; P < 0.01). There was no significant increase in BMD after estrogen treatment compared with naringin (weighted mean difference, 0.00; 95% CI, −0.00 to 0.01; P = 0.06). The trabecular bone volume (BV/TV) (weighted mean difference, 2.09; 95% CI, 1.85–2.34; P < 0.01) and trabecular thickness (Tb.Th) (weighted mean difference, 6.65; 95% CI, 6.55–6.74; P < 0.01) significantly increased after using naringin. Conclusions. Naringin had been shown to promote bone formation in OVX rats. However, the mechanism of naringin needs more research to confirm.

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“…Inactivated Hippo pathway rarely could make phosphorylation to YAP protein. The unphosphorylated YAP protein enriches in the nucleus via translocating into the nucleus to promote the expression of related genes that contribute to cell proliferation and survival [8]. Therefore, the activation of Hippo pathway determines the phosphorylation level and subcellular localization of YAP protein, which also determines the role of this pathway in tumorigenesis and development.…”

Section: Introductionmentioning

confidence: 99%

LTBP4 Inhibits the Proliferation and Metastasis in Melanoma by Activating Hippo-YAP Signaling

Wang¹,

Tang²,

Wu³

et al. 2020

Preprint

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Background: Malignant melanoma is the deadliest of skin cancer. The present study aimed to elucidate potential key candidate genes in melanoma and its molecular mechanism. Methods: Three gene expression profile data sets (GSE46517, GSE52882 and GSE54493) were downloaded from the GEO database, which included data from melanoma tissue samples and cell lines. DEGs were subsequently investigated by GO analysis via using DAVID website. PPI network was constructed using the STRING database and visualized by Cytoscape software and MCODE were utilized to PPI network to pick out meaningful DEGs. Cell proliferation, apoptosis, migration and invasion were measured using CCK-8, colony formation, flow cytometry, transwell and wound healing assays. RT-PCR, western blotting and immunohistochemistry assays were used to detect mRNA and protein expressions. TCGAportal and GEPIA databases were used to perform the bioinformatics analysis of LTBP4 in melanoma. Results: LTBP4 both is the DEG and a key gene from the most significant module of the PPI network. LTBP4 expression was down-regulation in melanoma tissues and cells relative to controls, which showed positive correlation with invasion, TNM stage, distal metastasis and lymph node metastasis, and predicted the poor prognosis for patients with melanoma. Cox analysis identified LTBP4 low-expression as an independent prognostic variable for overall survival (OS) in patients with melanoma. The results revealed that LTBP4 inhibition reduced cell apoptosis, promoted cell proliferation and metastasis. These changes were correlated caspase-3, ki67 and E-cadherin expressions by western blotting assay. Further in vivo tumor formation study in nude mice indicated that LTBP4 inhibition promoted the progress of tumor formation. LTBP4 gene knockout reduced the phosphorylation level of YAP, MST1 and MOB1 and promoted the nuclear translocation of YAP to inhibit the activation of Hippo signaling pathway. The functions of LTBP4 overexpression (OE) inhibiting the expressions of CTGF, Cyr61 and Birc5, promoting the apoptosis, and inhibiting the metastasis and proliferation of melanoma cells were reversed by YAP/or MST1 OE.Conclusions: LTBP4 OE suppressed the proliferation and metastasis in melanoma via inhibiting the nuclear translocation of YAP to activating Hippo signaling pathway, thereby inhibiting the development and progression of melanoma.

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Naringin protects endothelial cells from apoptosis and inflammation by regulating the Hippo-YAP Pathway

Cited by 65 publications

References 28 publications

Naringin Ameliorates Monocrotaline-Induced Pulmonary Arterial Hypertension Through Endothelial-To-Mesenchymal Transition Inhibition

Naringin Ameliorates Monocrotaline-Induced Pulmonary Arterial Hypertension Through Endothelial-To-Mesenchymal Transition Inhibition

Effect of Naringin Treatment on Postmenopausal Osteoporosis in Ovariectomized Rats: A Meta-Analysis and Systematic Review

LTBP4 Inhibits the Proliferation and Metastasis in Melanoma by Activating Hippo-YAP Signaling

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