Feprazone Displays Antiadipogenesis and Antiobesity Capacities in in Vitro 3 T3-L1 Cells and in Vivo Mice.


Journal

ACS omega
ISSN: 2470-1343
Titre abrégé: ACS Omega
Pays: United States
ID NLM: 101691658

Informations de publication

Date de publication:
16 Mar 2021
Historique:
received: 09 11 2020
accepted: 09 02 2021
entrez: 22 3 2021
pubmed: 23 3 2021
medline: 23 3 2021
Statut: epublish

Résumé

Excessive lipid accumulation in adipose tissues and deregulation of adipogenesis-induced obesity affect millions of people worldwide. Feprazone, a nonsteroidal anti-inflammatory drug, has a wide clinical use. However, it is unknown whether Feprazone possesses an antiadipogenic ability. The aim of this study is to investigate whether Feprazone possesses an antiadipogenic ability in 3 T3-L1 cells and an antiobesity capacity in mouse models. An MTT assay was used to determine the optimized incubation concentrations of Feprazone in 3 T3-L1 cells. The lipid accumulation was evaluated using Oil Red O staining. The concentrations of triglyceride and glycerol release were detected to check the lipolysis during 3 T3-L1 adipogenesis. A quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of sterol regulatory element-binding protein-1C (SREBP-1C) and fatty acid binding protein 4 (FABP4) in treated cells. The expressions of peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer-binding protein α (C/EBP-α), adipose triglyceride lipase (ATGL), and aquaporin-7 (AQP-7) were detected using qRT-PCR and Western blot analysis. After the high-fat diet (HFD) mice were treated with Feprazone, the pathological state of adipocyte tissues was evaluated using HE staining. The adipocyte size, visceral adipocyte tissue weight, and bodyweights were recorded. According to the proliferation result, 30 and 60 μM Feprazone were used as the optimized concentrations of Feprazone. In the in vitro study, lipid accumulation, elevated production of triglycerides, the release of glycerol, upregulated SREBP-1C, FABP4, PPAR-γ, and C/EBP-α and downregulated ATGL and AQP-7 in the 3 T3-L1 adipocytes induced by the adipocyte differentiation cocktail medium were significantly reversed by treatment with Feprazone. In the in vivo experiment, we found that the increased adipocyte size, visceral adipocyte tissue weight, and body weights induced by HFD feeding in mice were significantly suppressed by the administration of Feprazone. Feprazone might display anti-adipogenic and antiobesity capacities in in vitro 3 T3-L1 cells and in vivo mice.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
Excessive lipid accumulation in adipose tissues and deregulation of adipogenesis-induced obesity affect millions of people worldwide. Feprazone, a nonsteroidal anti-inflammatory drug, has a wide clinical use. However, it is unknown whether Feprazone possesses an antiadipogenic ability. The aim of this study is to investigate whether Feprazone possesses an antiadipogenic ability in 3 T3-L1 cells and an antiobesity capacity in mouse models.
METHODS METHODS
An MTT assay was used to determine the optimized incubation concentrations of Feprazone in 3 T3-L1 cells. The lipid accumulation was evaluated using Oil Red O staining. The concentrations of triglyceride and glycerol release were detected to check the lipolysis during 3 T3-L1 adipogenesis. A quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of sterol regulatory element-binding protein-1C (SREBP-1C) and fatty acid binding protein 4 (FABP4) in treated cells. The expressions of peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer-binding protein α (C/EBP-α), adipose triglyceride lipase (ATGL), and aquaporin-7 (AQP-7) were detected using qRT-PCR and Western blot analysis. After the high-fat diet (HFD) mice were treated with Feprazone, the pathological state of adipocyte tissues was evaluated using HE staining. The adipocyte size, visceral adipocyte tissue weight, and bodyweights were recorded.
RESULTS RESULTS
According to the proliferation result, 30 and 60 μM Feprazone were used as the optimized concentrations of Feprazone. In the in vitro study, lipid accumulation, elevated production of triglycerides, the release of glycerol, upregulated SREBP-1C, FABP4, PPAR-γ, and C/EBP-α and downregulated ATGL and AQP-7 in the 3 T3-L1 adipocytes induced by the adipocyte differentiation cocktail medium were significantly reversed by treatment with Feprazone. In the in vivo experiment, we found that the increased adipocyte size, visceral adipocyte tissue weight, and body weights induced by HFD feeding in mice were significantly suppressed by the administration of Feprazone.
CONCLUSION CONCLUSIONS
Feprazone might display anti-adipogenic and antiobesity capacities in in vitro 3 T3-L1 cells and in vivo mice.

Identifiants

pubmed: 33748580
doi: 10.1021/acsomega.0c05470
pmc: PMC7970497
doi:

Types de publication

Journal Article

Langues

eng

Pagination

6674-6680

Informations de copyright

© 2021 The Authors. Published by American Chemical Society.

Déclaration de conflit d'intérêts

The authors declare no competing financial interest.

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Auteurs

Liqun Che (L)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Bo Ren (B)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Yuanyuan Jia (Y)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Yujia Dong (Y)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Yanbing Wang (Y)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Jie Shan (J)

Department of Endocrinology Ward 3, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Yuchun Wang (Y)

Department of pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.

Classifications MeSH