Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular disease. A leading hypothesis is that hepatic steatosis may lead to the production of pro-inflammatory cytokines, which accelerate atherosclerosis process and lead to progressive vascular dysfunction. Furthermore, Angiotensin II (Ang II) production, starting from the hepatic precursor angiotensinogen (AGT), seems to play an important role in atherogenic plaque initiation and growth. Using a mouse model of diet induced-obesity (DIO) that develops NAFLD, the impact of a natural diet supplement (kepar, Rikrea, Italy) containing plant extracts such as Curcuma longa, guggul and chlorogenic acid on liver function and atherosclerosis plaque formation was evaluated. Animals, fed high fat diet, were divided into two groups, whose one was treated with oral administration of kepar (1.6 g/die) for 4 months. Expression of genes related to the hepatic dysfunction (Profiler PCR array), plasma Ang II levels (ELISA), hepatic AGT-RNAm expression (RT-PCR), liver steatosis, aortic plaque development and carotid artery thickness (histological analysis), were evaluated and compared to untreated group. In kepar- treated group, the array profile of the liver showed pro-inflammatory mediator downregulation and lipolysis gene upregulation. In treated mice, the liver steatosis was reduced, as well as the AGT-mRNA expression and Agt II plasma levels and histological analysis showed neither atherogenic vascular lesions nor carotid artery thickening. The present study highlights the cooperative action of plant extracts present in kepar as well as the anti-inflammatory properties, resulting protective not only in NAFLD but also against atherogenesis development.
The chronic treatment with a diet supplement containing Curcuma longa, guggul, silymarin and chlorogenic acid counteracts the development of NAFLD and atherosclerosis in a mouse obesity model
D Nuzzo;M Di Carlo;
2015
Abstract
Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular disease. A leading hypothesis is that hepatic steatosis may lead to the production of pro-inflammatory cytokines, which accelerate atherosclerosis process and lead to progressive vascular dysfunction. Furthermore, Angiotensin II (Ang II) production, starting from the hepatic precursor angiotensinogen (AGT), seems to play an important role in atherogenic plaque initiation and growth. Using a mouse model of diet induced-obesity (DIO) that develops NAFLD, the impact of a natural diet supplement (kepar, Rikrea, Italy) containing plant extracts such as Curcuma longa, guggul and chlorogenic acid on liver function and atherosclerosis plaque formation was evaluated. Animals, fed high fat diet, were divided into two groups, whose one was treated with oral administration of kepar (1.6 g/die) for 4 months. Expression of genes related to the hepatic dysfunction (Profiler PCR array), plasma Ang II levels (ELISA), hepatic AGT-RNAm expression (RT-PCR), liver steatosis, aortic plaque development and carotid artery thickness (histological analysis), were evaluated and compared to untreated group. In kepar- treated group, the array profile of the liver showed pro-inflammatory mediator downregulation and lipolysis gene upregulation. In treated mice, the liver steatosis was reduced, as well as the AGT-mRNA expression and Agt II plasma levels and histological analysis showed neither atherogenic vascular lesions nor carotid artery thickening. The present study highlights the cooperative action of plant extracts present in kepar as well as the anti-inflammatory properties, resulting protective not only in NAFLD but also against atherogenesis development.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
