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            ‐Chalcone inhibits high‐fat diet‐induced disturbances in FXR/SREBP‐1c/FAS and FXR/Smad‐3 pathways in the kidney of rats

Alipour, Mohammad Reza; Jeddi, Sajad; Karimi‐Sales, Elham

doi:10.1111/jfbc.13476

Cited by 5 publications

(3 citation statements)

References 48 publications

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“…As shown in a large number of studies, the activated bile acid receptor FXR regulates cholesterol, glucose, and lipid homeostasis, thereby slowing the disease progression of NAFLD, while FXR knockout has the opposite effect. , Insufficient FXR activation leads to a disturbance in bile acid metabolism, resulting in decreased energy expenditure, increased adipogenesis, and increased macrophage activity, by regulating FXR and, thus, glucolipid metabolism, which is a prominent target for the prophylaxis and cure of NAFLD. , So, we examined this key receptor, and as predicted, FXR mRNA levels and its downstream targets BSEP and SHP were significantly upregulated upon overexpression of Clstn3. Immunofluorescence further showed a correlation between Clstn3 and FXR expression.…”

Section: Discussionmentioning

confidence: 97%

Hepatic Clstn3 Ameliorates Lipid Metabolism Disorders in High Fat Diet-Induced NAFLD through Activation of FXR

Guo

Huang

et al. 2023

ACS Omega

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Non-alcoholic fatty liver disease (NAFLD) has become serious liver disease all over the world. At present, NAFLD caused by high calorie and fat diet is increasing. Calsyntenin-3 (Clstn3) is a transmembrane protein that has recently been found to participate in lipid energy metabolism. But whether Clstn3 affects NAFLD lipid metabolism has not been analyzed. We stimulate the mice primary hepatocytes (MPHs) with oleic acid and palmitic acid (OA&PA) to establish a cell model. Then, potential targets, including Clstn3 gene, were validated for improving lipid metabolism disorder in NAFLD model mice (HFD and db/db) by silencing and overexpressing hepatic Clstn3. Moreover, the effects of Clstn3 on lipid homeostasis were determined by functional determination, triglyceride (TG) levels, total cholesterol (TC) levels, ELISA, and qRT-PCR detection. Our results displayed that Clstn3 was decreased in the NAFLD mice model. Also, overexpression of Clstn3 improved lipid metabolism disorders, gluconeogenesis, and energy homeostasis and reduced liver injury, inflammation, and oxidative stress injury. However, opposite results were obtained in Clstn3-silencing mice, suggesting that the Clstn3 gene is closely related to lipid metabolism disorder in NAFLD. RNAseq expression demonstrated that Farnesoid X Receptor (FXR) expression was increased after overexpression of Clstn3. Clstn3 supplementation in FXRKO mice can improve the dysfunction caused by insufficient FXR, suggesting that Clstn3 can improve the NAFLD lipid metabolism disorder to some extent through FXR, which may provide a new method for the treatment of NAFLD.

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Section: Discussionmentioning

confidence: 97%

Hepatic Clstn3 Ameliorates Lipid Metabolism Disorders in High Fat Diet-Induced NAFLD through Activation of FXR

Guo

Huang

et al. 2023

ACS Omega

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“…Plants including Aniba riparia, Piper methysticum, and Didymocarpus corchorijolia can produce trans -chalcone , It targets the expression of TGF-β and ICAM-1, as well as STAT3 and NF-κB modulation, to prevent ischemia-induced retinal neovascularization .…”

Section: Introductionmentioning

confidence: 99%

“… 5 Trans- chalcone, an open-chain flavonoid, has antifibrotic, antioxidant, antidiabetic, hepatoprotective, and anti-inflammatory impacts. 6 , 7 It targets the expression of TGF-β and ICAM-1, as well as STAT3 and NF-κB modulation, to prevent ischemia-induced retinal neovascularization. 8 Trans -chalcone reduces hepatic fibrosis and inflammation driven by acetaminophen and carbon tetrachloride by lowering the generation of nitric oxide, TGF-β, and TNF-α, lipid peroxidation, and diminished glutathione deprivation.…”

Section: Introductionmentioning

confidence: 99%

Trans-Chalcone (1–3-diphenyl-2-propen-1-one) as a Therapeutic Candidate in Joint Inflammation via Reduction of TNF-α, IL-1β, IL-6, and IL-17 in Rodents: An In Vivo Study by RT-PCR and ELISA analysis

Jabbar,

Irfan,

Alamgeer

et al. 2024

ACS Omega

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Autoimmune disorders include vast and distinct illnesses and are characterized by an immune system-mediated attack on the body’s own tissues. Because of their ability to impact any portion of the body, their clinical symptoms are incredibly varied. The variations in symptoms are normally linked with the release and activation of vasoactive, chemotactic substances and cytokines. Cytokines perform a multitude of vital biological tasks, such as immune response control, inflammation, proliferation, and tissue repair. The reversal of inflammatory cytokines and leukocyte infiltration into the inflamed tissue by natural compounds provides an effective remedy for autoimmune diseases. Here, the oral administration of trans-chalcone (TC) for 28 days was tested with gradually increasing doses (30, 60, and 120 mg/kg) in complete Freund’s adjuvant (CFA)-provoked joint tissue stiffness in rats. Paw edema, arthritic index, joint stiffness, thermal and flexion pain, C-reactive protein, and rheumatoid factor (RF) levels were determined to check the tested drug effectiveness in a chronic inflammatory model. Molecular docking studies revealed strong binding affinity with inflammatory cytokines and mediators such as TNF-α, IL-17, COX-2, and iNOS; further, they were quantified at the mRNA level by RT-PCR and ELISA analysis. Oral administration of TC significantly ameliorated paw edema, thymus and spleen indices, joint stiffness, thermal and flexion pain, C-reactive protein, RF, mobility, and stance of the treated animals. This therapeutic effectiveness was linked with a reduction in the mRNA expression of proinflammatory cytokines such as IL-1β, IL-6, and IL-17. The findings of the reported research confirmed the effectiveness of TC in ameliorating joint stiffness and flexion pain by prominently lowering the inflammatory cytokines.

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Wistar rat as an animal model to study high-fat induced kidney damage: a systematic review

Pereira

Correia

Farah

et al. 2021

Archives of Physiology and Biochemistry

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trans ‐Chalcone inhibits high‐fat diet‐induced disturbances in FXR/SREBP‐1c/FAS and FXR/Smad‐3 pathways in the kidney of rats

Cited by 5 publications

References 48 publications

Hepatic Clstn3 Ameliorates Lipid Metabolism Disorders in High Fat Diet-Induced NAFLD through Activation of FXR

Hepatic Clstn3 Ameliorates Lipid Metabolism Disorders in High Fat Diet-Induced NAFLD through Activation of FXR

Trans-Chalcone (1–3-diphenyl-2-propen-1-one) as a Therapeutic Candidate in Joint Inflammation via Reduction of TNF-α, IL-1β, IL-6, and IL-17 in Rodents: An In Vivo Study by RT-PCR and ELISA analysis

Wistar rat as an animal model to study high-fat induced kidney damage: a systematic review

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