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3Departement of Biochemistry, Hospital La Rabta Tunis. Tunisia.

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Presentation on theme: "3Departement of Biochemistry, Hospital La Rabta Tunis. Tunisia."— Presentation transcript:

1 3Departement of Biochemistry, Hospital La Rabta Tunis. Tunisia.
ROLE OF FLAXSEED OIL IN REDUCING INFLAMMATION IN AN EXPERIMENTAL MODEL OF LUNG FIBROSIS INDUCED BY BLEOMYCIN IN RATS Abidi Anouar1, Serairi Raja1 , Kourda Nadia 2, Feki Moncef 3 and Ben Khamsa Saloua1 1Research Unit 03/UR/08-05, Pulmonary Fibrosis: Prevention and Treatment, Faculty of Medicine of Tunis. Tunisia. 2Department of Anatomy and Pathology, Charles Nicole Hospital, Tunis. Tunisia. 3Departement of Biochemistry, Hospital La Rabta Tunis. Tunisia. Abstract Methodology Main Results The purpose of the study was to investigate the effect of flaxseed oil (FO), known by its benefic and therapeutic effects for various diseases on experimental bleomycin (BLM) induced pulmonary fibrosis (PF) in rats. FO was administrated by daily gavage at a dose of 2ml/kg bw during 60 days to rats which underwent fibrosis induction by intratracheal injection of BLM. This treatment decreases inflammation and fibrosis score in the treated group. Also, the profiles of fatty acids composition in the lungs showed an increased rate of Mono Unsatured Fatty Acids (MUFAs) coupled with a decrease of the Poly Unsatured Fatty Acids (PUFAs) in the treated group compared to control one. In red cells, the treatment induced a decrease in SFAS coupled with a high level of PUFAs in the treated group. Keyworlds: flaxseed oil, lung fibrosis, Inflammation, Fatty acids, Lipid mediators, rats Twenty Wistar rats, weighting 180–220g, were divided randomly into 2 groups: control group (G1, n = 10) and a treated group (G2, n = 10). All rats received a distilled water in G1 at dose of 2mL/kg bw and flaxseed oil in G2 at dose of 2mL/kg bw by daily gavages during 60 days. After this period of preventive treatment, pulmonary fibrosis was induced in all rats by bleomycin (4 mg/kg, single dose, intratracheally). Three days later, all rats were sacrificed and lungs were extracted for histological analysis (Inflammatory Index and Score Fibrosis) [1]. FO composition was analyzed by Gas Chromatography (GC). Total Polyunsaturated Fatty Acids (PUFAs) in the lungs and in the red cells (RC), into both groups, were measured also by GC. Data are presented as mean ±standard deviations (S.D), P 0.05 was considered to be significant. Lung sections showed a significant reduction of inflammation (G1 = 3,3±0,48, G2 = 1,9±0,87, P= 0,001) and fibrosis (G1= 3,7±0,948, G2= 2,2±1,39, P = 0,012). Analysis by GC revealed that more than 50% of Flaxseed oil was C18:3, a gamma-linolenic acid. PUFAs in red cells are (16,56%) in G1 and (26 ,12%) in G2 and on the lungs are (24,96%) in G1 and (18,91%) in G2. We noticed that Arachidonic acid was the major component in RC in G2 (14,14±5,04%), decreased almost half in lungs (8,41±3,33%) on the same group compared to control group (RC: 7,96±6,95%, in lungs: 14,03±3,63%) [2, 3]. Based on these results: increasing intake of gamma-linolenic acid leads to an increasing production of arachidonic acid, the major fatty acid precursor of ecosanoids, modulators of inflammatory response observed in the lung fibrosis airways. The results of our studies showed that FO acted on different levels of fibrotic process and may have an important activity in the treatment of pulmonary fibrosis. . Objectives Aim of the study Our study aims to investigate whether Flaxseed (Linum usitatissimum) Oil (FO), used as a preventive treatment, can inhibit bleomycin induced lung fibrosis in rats. Conclusions Fig.1. Effect of FO on the inflammatory index and on the score of fibrois in treated group (G2) and control group (G1) Fig.3. Fatty acids composition in red cells of treated group (G2) and control group (G1) conclusion These results confirm that bleomycin affects the fatty acid composition of lung giving the opportunity to test the effects of substances rich in fatty acids on pulmonary fibrosis models in rats. Fig.2. Fatty acids composition in lungs of treated group (G2) and control group (G1)


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