EVALUATION OF ROSMARIC ACID EFFECTS ON HYPERLIPIDIC DIET-INDUCED NON-ALCOHOLIC FATTY LIVER DISEASE IN WISTAR RATS.

• Grant number: 12/25358-2
• Support Opportunities: Scholarships in Brazil - Master
• Start date: August 01, 2013
• End date: June 30, 2015
• Field of knowledge: Health Sciences - Nutrition
• Principal Investigator: Raquel Alves dos Santos
• Grantee: Carolina Cristina de Freitas
• Host Institution: Pró-Reitoria Adjunta de Pesquisa e Pós-Graduação. Universidade de Franca (UNIFRAN). Franca , SP, Brazil

Abstract

The non-alcoholic fatty liver disease (NAFLD), which hallmark is the accumulation of fat in the liver, has been described since 80's as the hepatic component of metabolic syndrome. NAFLD has progressed to epidemiological proportions and has multifactorial etiology with well defined environmental. If not treated this disease can result in non-alcoholic steatohepatitis (NASH) caracterized by the presence of fibrosis and inflammation. The genetic component of NAFLD includes a great range of genes that affect its susceptibility and severity, including the peroxisome proliferator-activated receptor gene gamma (PPAR³). PPAR³ is a transcriptional factor that regulates the expression of other genes such as CD36, ADRP and LPL involved in the control of lipid metabolism. The prevention as well as the treatment of NAFLD include the change of life style as a balanced diet and physical exercises; however the complete adherence to this treatment sometimes is not well succeed compromising the success of the treatment. Thus, the searching for therapeutic alternatives is of great interest. Rosmarinic acid (RA) is a phenolic compound able to modulate the antioxidant defense. Literature reports that (RA) can affect the carbohydrate metabolism and modulate the expression of PPAR³. Therefore, the present study aims to evaluate the effects of RA in Wistar rats submitted to a hiperlipidic diet experimentally. For this purpose the histopatological analysis of liver tissue will be performed, as well the detection of the extension of DNA damage. Transcriptional expression of PPAR³, CD36, ADRP and LPL will be evaluated by qPCR, and levels of ±-tocopherol, reduced glutathione, tiobarbituric reactive substances, AST, ALT, TAG, LDL, total cholesterol and glucose tolerance will be determined by biochemical methods.