Background: Arthrospira maxima has been widely used for nutritional purposes. Additionally, A. maxima has shown immunomodulator, antiviral, antioxidant, vasomotor and hypolipidemic effects in laboratory and animal studies. A. maxima prevents fatty liver induced by either carbon tetrachloride (CCl4) or fructose-rich diet; however, the liver lipid composition in these models is not clearly known yet. The aim of this study was to evaluate the effects of A. maxima on the liver lipid profile in CCl4-induced steatohepatitis.
Methods: A single sublethal, intraperitoneal dose of CCl4 was administered to male Wistar rats fed a diet with or without 5% A. maxima. Liver lipids: total lipids, triacylglycerols, total cholesterol, free fatty acids, and thiobarbituric acid reactive substances were assessed 24 and 48 h after injury with CCl4. Additionally, triacylglycerols, total cholesterol and aspartate aminotransferase were evaluated in blood.
Results: Forty eight hours after CCl4 treatment, rats fed a diet without A. maxima had serum aspartate aminotransferase and liver triacylglycerols values that were, respectively, 2.2 and 1.4 times higher than those of animals receiving 5% A. maxima in their diet. The same pattern was observed for liver free fatty acids and thiobarbituric acid reactive substances. The groups fed a diet with A. maxima and treated with CCl4 showed a higher saturated fatty acid liver content than the groups without A. maxima in their diet. The percentage of unsaturated fatty acids increased 48 h after CCl4 treatment, but its value was 0.5 times lower in the group receiving A. maxima than in the group fed without A. maxima. In the liver, all animals receiving A. maxima showed a trend towards a lower percentage of unsaturated fatty acids, despite the mentioned increase 48 h after CCl4 treatment.
Conclusions: The results suggest that, in the fatty liver induced by CCl4, the hepatoprotective effect of A. maxima involves (a) an antioxidant mechanism and (b) a lower unsaturation of the liver fatty acids. The preventive effect of A. maxima on the liver lipid changes induced by CCl4 could be partially explained by its antioxidant action and the ability to increase the synthesis/release of nitric oxide, but not by its soluble dietary fiber.