Luteolin Prevents Cardiometabolic Alterations and Vascular Dysfunction in Mice With HFD-Induced Obesity

Gentile, Daniela; Fornai, Matteo; Pellegrini, Carolina; Colucci, Rocchina; Benvenuti, Laura; Duranti, Emiliano; Masi, Stefano; Carpi, Sara; Nieri, Paola; Nericcio, Anna; Garelli, Francesca; Virdis, Agostino; Pistelli, Laura; Blandizzi, Corrado; Antonioli, Luca

doi:10.3389/fphar.2018.01094

Cited by 54 publications

(28 citation statements)

References 51 publications

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“…Upon further investigation, the same group found that this differentiation of CXCR3 + effector memory T cells was partially mediated by the PI3K p110δ-Akt signaling pathway ( 44 ). Apart from infiltration of adipose and vascular tissues by effector T cells, the vascular endothelial dysfunction may also exert a role in the onset and propagation of CVD induced by a HFD ( 45 , 46 ). Evidence for this hypothesis is provided by observations that mice fed with a HFD rich in lard exhibited an inhibition of the L-arginine-NO pathway in red blood cells (RBCs) of mice ( 47 ).…”

Section: Hfd-induced Diseasesmentioning

confidence: 99%

“…For instance, HFD-fed mice treated with Lactobacillus plantarum KY1032 and Lactobacillus curvatus HY7601 exhibited decreased body weight, fat mass, and levels of circulating leptin, insulin, total cholesterol and liver toxicity biomarkers, accompanied by alterations in gut bacterial composition and diversity ( 118 ). In addition, markers of inflammation and obesity are reduced with dietary supplementation with amino acid (especially leucine) and plant components (such as luteolin and flavonoids), alone or in combination, as were performed in HFD-fed mice ( 46 , 119 – 123 ). Although there are additional undefined approaches, the above-mentioned findings give the field a critical boost and may be translated into human studies, thus improving interventional strategies to stem the negative effects of HFDs.…”

Section: Potential Treatment Optionsmentioning

confidence: 99%

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Inflammatory Links Between High Fat Diets and Diseases

et al. 2018

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In recent years, chronic overnutrition, such as consumption of a high-fat diet (HFD), has been increasingly viewed as a significant modifiable risk factor for diseases such as diabetes and certain types of cancer. However, the mechanisms by which HFDs exert adverse effects on human health remains poorly understood. Here, this paper will review the recent scientific literature about HFD-induced inflammation and subsequent development of diseases and cancer, with an emphasis on mechanisms involved. Given the expanding global epidemic of excessive HFD intake, understanding the impacts of a HFD on these medical conditions, gaining great insights into possible underlying mechanisms, and developing effective therapeutic strategies are of great importance.

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Section: Hfd-induced Diseasesmentioning

confidence: 99%

Section: Potential Treatment Optionsmentioning

confidence: 99%

Inflammatory Links Between High Fat Diets and Diseases

et al. 2018

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“…All mice were maintained on the C57BL/ 6JRccHsd background. Animals were group-housed in standard conditions of maintenance 52 . Food and water were provided ad libitum.…”

Section: Cln5 −/− Mouse Model and Tissue Collectionmentioning

confidence: 99%

Proteomic and functional analyses in disease models reveal CLN5 protein involvement in mitochondrial dysfunction

et al. 2020

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CLN5 disease is a rare form of late-infantile neuronal ceroid lipofuscinosis (NCL) caused by mutations in the CLN5 gene that encodes a protein whose primary function and physiological roles remains unresolved. Emerging lines of evidence point to mitochondrial dysfunction in the onset and progression of several forms of NCL, offering new insights into putative biomarkers and shared biological processes. In this work, we employed cellular and murine models of the disease, in an effort to clarify disease pathways associated with CLN5 depletion. A mitochondria-focused quantitative proteomics approach followed by functional validations using cell biology and immunofluorescence assays revealed an impairment of mitochondrial functions in different CLN5 KO cell models and in Cln5 −/− cerebral cortex, which well correlated with disease progression. A visible impairment of autophagy machinery coupled with alterations of key parameters of mitophagy activation process functionally linked CLN5 protein to the process of neuronal injury. The functional link between impaired cellular respiration and activation of mitophagy pathways in the human CLN5 disease condition was corroborated by translating organelle-specific proteome findings to CLN5 patients' fibroblasts. Our study highlights the involvement of CLN5 in activation of mitophagy and mitochondrial homeostasis offering new insights into alternative strategies towards the CLN5 disease treatment.

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“…Polyphenols from several food sources have been increasingly found to favorably affect AT physiology [38], and their modes of action include interaction with cell signaling pathways, modulation of transcription factors activity and gene expression, but also the post-transcriptional regulation of genes via modulation of miRNAs expression [39][40][41].…”

Section: Introductionmentioning

confidence: 99%

The Extra-Virgin Olive Oil Polyphenols Oleocanthal and Oleacein Counteract Inflammation-Related Gene and miRNA Expression in Adipocytes by Attenuating NF-κB Activation

et al. 2019

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Inflammation of the adipose tissue plays an important role in the development of several chronic diseases associated with obesity. Polyphenols of extra virgin olive oil (EVOO), such as the secoiridoids oleocanthal (OC) and oleacein (OA), have many nutraceutical proprieties. However, their roles in obesity-associated adipocyte inflammation, the NF-κB pathway and related sub-networks have not been fully elucidated. Here, we investigated impact of OC and OA on the activation of NF-κB and the expression of molecules associated with inflammatory and dysmetabolic responses. To this aim, fully differentiated Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were pre-treated with OC or OA before stimulation with TNF-α. EVOO polyphenols significantly reduced the expression of genes implicated in adipocyte inflammation (IL-1β, COX-2), angiogenesis (VEGF/KDR, MMP-2), oxidative stress (NADPH oxidase), antioxidant enzymes (SOD and GPX), leukocytes chemotaxis and infiltration (MCP-1, CXCL-10, MCS-F), and improved the expression of the anti-inflammatory/metabolic effector PPARγ. Accordingly, miR-155-5p, miR-34a-5p and let-7c-5p, tightly connected with the NF-κB pathway, were deregulated by TNF-α in both cells and exosomes. The miRNA modulation and NF-κB activation by TNF-α was significantly counteracted by EVOO polyphenols. Computational studies suggested a potential direct interaction between OC and NF-κB at the basis of its activity. This study demonstrates that OC and OA counteract adipocyte inflammation attenuating NF-κB activation. Therefore, these compounds could be novel dietary tools for the prevention of inflammatory diseases associated with obesity.

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Luteolin Prevents Cardiometabolic Alterations and Vascular Dysfunction in Mice With HFD-Induced Obesity

Cited by 54 publications

References 51 publications

Inflammatory Links Between High Fat Diets and Diseases

Inflammatory Links Between High Fat Diets and Diseases

Proteomic and functional analyses in disease models reveal CLN5 protein involvement in mitochondrial dysfunction

The Extra-Virgin Olive Oil Polyphenols Oleocanthal and Oleacein Counteract Inflammation-Related Gene and miRNA Expression in Adipocytes by Attenuating NF-κB Activation

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