Hesperetin attenuates the expression of markers of adipose tissue fibrosis in pre-adipocytes.

Adipose tissue fibrosis Collagen Hesperetin Matrix metalloproteinase Obesity Osteopontin

Journal

BMC complementary medicine and therapies
ISSN: 2662-7671
Titre abrégé: BMC Complement Med Ther
Pays: England
ID NLM: 101761232

Informations de publication

Date de publication:
11 Sep 2023
Historique:
received: 12 03 2023
accepted: 04 09 2023
medline: 13 9 2023
pubmed: 12 9 2023
entrez: 11 9 2023
Statut: epublish

Résumé

Excessive extracellular matrix (ECM) deposition in adipose tissue is a hallmark of fibrosis, leading to disrupted adipose tissue homeostasis and metabolic dysfunction. Hesperetin, a flavonoid compound, has shown promising anti-inflammatory, anti-obesity and anti-diabetic properties. Therefore, we investigated the anti-fibrotic effects of hesperetin, through targeting ECM components and matrix metalloproteinase enzymes. 3T3-L1 cells were cultured in DMEM, containing 10% FBS and 1% penicillin/streptomycin. Cells were treated with a range of hesperetin concentrations, and the cell viability was determined using MTT assay. Subsequently, the expression of genes encoding collagen VI, osteopontin, matrix metalloproteinase-2 (Mmp-2) and Mmp-9 was analyzed using specific primers and real-time PCR technique. To evaluate protein levels of collagen VI and osteopontin, Western blotting was performed. Hesperetin affected the viability of 3T3-L1 adipocytes with IC50 of 447.4 µM, 339.2 µM and 258.8 µM (24 h, 48 and 72 h, respectively). Hesperetin significantly reduced the gene and protein expression of both collagen VI and osteopontin in 3T3-L1 pre-adipocytes, in a time- and dose-dependent manner. Hesperetin was also able to cause a remarkable decline in gene expression of Mmp2 and Mmp9. Hesperetin could potently reduce the production of markers of adipose tissue fibrosis and might be considered a potential anti-fibrotic compound in obesity. Thus, hesperetin has the potency to be used for the treatment of obesity-associated fibrosis.

Sections du résumé

BACKGROUND BACKGROUND
Excessive extracellular matrix (ECM) deposition in adipose tissue is a hallmark of fibrosis, leading to disrupted adipose tissue homeostasis and metabolic dysfunction. Hesperetin, a flavonoid compound, has shown promising anti-inflammatory, anti-obesity and anti-diabetic properties. Therefore, we investigated the anti-fibrotic effects of hesperetin, through targeting ECM components and matrix metalloproteinase enzymes.
METHODS METHODS
3T3-L1 cells were cultured in DMEM, containing 10% FBS and 1% penicillin/streptomycin. Cells were treated with a range of hesperetin concentrations, and the cell viability was determined using MTT assay. Subsequently, the expression of genes encoding collagen VI, osteopontin, matrix metalloproteinase-2 (Mmp-2) and Mmp-9 was analyzed using specific primers and real-time PCR technique. To evaluate protein levels of collagen VI and osteopontin, Western blotting was performed.
RESULTS RESULTS
Hesperetin affected the viability of 3T3-L1 adipocytes with IC50 of 447.4 µM, 339.2 µM and 258.8 µM (24 h, 48 and 72 h, respectively). Hesperetin significantly reduced the gene and protein expression of both collagen VI and osteopontin in 3T3-L1 pre-adipocytes, in a time- and dose-dependent manner. Hesperetin was also able to cause a remarkable decline in gene expression of Mmp2 and Mmp9.
CONCLUSION CONCLUSIONS
Hesperetin could potently reduce the production of markers of adipose tissue fibrosis and might be considered a potential anti-fibrotic compound in obesity. Thus, hesperetin has the potency to be used for the treatment of obesity-associated fibrosis.

Identifiants

pubmed: 37697354
doi: 10.1186/s12906-023-04152-z
pii: 10.1186/s12906-023-04152-z
pmc: PMC10496229
doi:

Substances chimiques

hesperetin Q9Q3D557F1
Matrix Metalloproteinase 2 EC 3.4.24.24
Osteopontin 106441-73-0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

315

Subventions

Organisme : Iran University of Medical Sciences
ID : 1400-1-4-19488

Informations de copyright

© 2023. BioMed Central Ltd., part of Springer Nature.

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Auteurs

Alemeh Taheri (A)

Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Hemmat Highway, Tehran, 1449614535, Iran.

Samira Ezzati Mobaser (SE)

Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular- Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

Pegah Golpour (P)

Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Mona Nourbakhsh (M)

Hazrat Aliasghar Children Hospital, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Masoumeh Tavakoli-Yaraki (M)

Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Hemmat Highway, Tehran, 1449614535, Iran.

Sahar Yarahmadi (S)

Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Hemmat Highway, Tehran, 1449614535, Iran.

Mitra Nourbakhsh (M)

Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Hemmat Highway, Tehran, 1449614535, Iran. Nourbakhsh.m@iums.ac.ir.
Finetech in Medicine Research Center, Iran University of Medical Sciences, Tehran, Iran. Nourbakhsh.m@iums.ac.ir.

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Classifications MeSH