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RESEARCH PRODUCT

NAFLD and Atherosclerosis Are Prevented by a Natural Dietary Supplement Containing Curcumin, Silymarin, Guggul, Chlorogenic Acid and Inulin in Mice Fed a High-Fat Diet

Marta Di CarloPasquale PiconeFlavia MulèManfredi RizzoGaetano-felice CaldaraSara BaldassanoAntonella AmatoDomenico Nuzzo

subject

0301 basic medicineMaleAngiotensinogenAdministration OralSettore BIO/09 - Fisiologiachemistry.chemical_compoundMice0302 clinical medicineNon-alcoholic Fatty Liver DiseasePlant GumsCommiphorachemistry.chemical_classificationNutrition and Dieteticsnon-alcoholic fatty liver disease; atherogenic lesions; diet-induced obesity; natural dietary supplement; renin-angiotensin system imbalance; Profiler PCR arrayAngiotensin IIFatty liverInulinNeoplasm Proteinsrenin-angiotensin system imbalance030211 gastroenterology & hepatologyatherogenic lesionmedicine.symptomChlorogenic AcidSilymarinmedicine.medical_specialtynatural dietary supplementCurcumindiet-induced obesityProfiler PCR array; atherogenic lesions; diet-induced obesity; natural dietary supplement; non-alcoholic fatty liver disease; renin-angiotensin system imbalanceInflammationBiologyDiet High-FatFatty Acid-Binding ProteinsArticle03 medical and health sciencesInternal medicineRenin–angiotensin systemmedicineAnimalsRNA MessengerProfiler PCR arrayatherogenic lesionsPlant ExtractsFatty acidLipid metabolismmedicine.diseaseAtherosclerosisLipid MetabolismMice Inbred C57BL030104 developmental biologyEndocrinologychemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinDietary SupplementsCurcuminSteatosisDyslipidemiaFood Science

description

Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular diseases. NAFDL is associated with atherogenic dyslipidemia, inflammation and renin-angiotensin system (RAS) imbalance, which in turn lead to atherosclerotic lesions. In the present study, the impact of a natural dietary supplement (NDS) containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin on NAFLD and atherosclerosis was evaluated, and the mechanism of action was examined. C57BL/6 mice were fed an HFD for 16 weeks; half of the mice were simultaneously treated with a daily oral administration (os) of the NDS. NAFLD and atherogenic lesions in aorta and carotid artery (histological analysis), hepatic expression of genes involved in the NAFLD (PCR array), hepatic angiotensinogen (AGT) and AT1R mRNA expression (real-time PCR) and plasma angiotensin (ANG)-II levels (ELISA) were evaluated. In the NDS group, steatosis, aortic lesions or carotid artery thickening was not observed. PCR array showed upregulation of some genes involved in lipid metabolism and anti-inflammatory activity (Cpt2, Ifng) and downregulation of some genes involved in pro-inflammatory response and in free fatty acid up-take (Fabp5, Socs3). Hepatic AGT, AT1R mRNA and ANG II plasma levels were significantly lower with respect to the untreated-group. Furthermore, NDS inhibited the dyslipidemia observed in the untreated animals. Altogether, these results suggest that NDS prevents NAFLD and atherogenesis by modulating the expression of different genes involved in NAFLD and avoiding RAS imbalance.

10.3390/nu9050492http://europepmc.org/articles/PMC5452222