Sulfated polysaccharides from Ulva lactuca were extracted in hot water and precipitated by ethanol then orally gavaged to rats fed on a hypercholesterolemic diet for 21 days to evaluate the antihypercholesterolemic and antioxidant actions. Atorvastatine Ca (Lipitor) was used as a reference drug. The intragastric administration of U. lactuca extract to hypercholesterolemic rats caused significant decrease of serum total lipids, triglycerides, total cholesterol, LDL-cholesterol and vLDL-cholesterol levels. Whereas, HDL-cholesterol concentration was markedly increased by 180%. Aqueous extract showed a significant ameliorative action on elevated atherogenic index, creatine kinase and lactate dehydrogenase activities of hypercholesterolemic group. Furthermore, serum activities of transaminases and alkaline phosphatase were also improved. High fat diet intake caused a highly significantly elevated serum urea, creatinine concentration. These effects were reversed by oral administration of U. lactuca extract. Sulfates polysaccharides extract of U. lactuca ameliorate hepatic enzymatic (catalase, glutathione peroxidase and superoxide dismutase), non-enzymatic (reduced glutathione & total thiol) antioxidant defenses and thiobarbituric acid reactive substances. In conclusion, the tested U. lactuca polysaccharides extract has potent hypocholesterolemic and antioxidant effects in experimentally-induced hypercholesterolemic animal model.

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Introduction: Lambada-cyhalotherin (LCT) caused severe oxidative damage in liver, lung and testis. Aim of the Study: The objective of this research was to evaluate the ameliorative activity and underlying techniques of pure Panax ginseng (G) using rat model of LCT-induced lung damage. Materials and Methods: 36 male adult laboratory rats Rattus norvegicus domestica in weights around 135±10 g were separated into 6 experimental groups: 1 st control group. 2 nd and 3 th groups were G groups (100 and 200 mg G/kg b. wt.) LCT group was given by oral gavage LCT (61.2 mg /kg b. wt.) that is equivalent to 1/10 of LD50. The 5 th and 6 th groups were cotreated with two doses of G. Results: LCT significantly decreased superoxide dismutase (SOD), catalase (CAT) and total thiol (T. thiol) and increased lipid peroxidation (LPO). mRNA and protein expression levels of p53 gene (apoptotic gene) were increased, whereas, Bcl-2 gene (anti-apoptotic gene) mRNA and protein expression levels were decreased in LCT-treated animals. Also, light microscopic and ultrastructure studies for lung tissues of LCT-treated animals showed marked hyperplasia of dilated bronchioles wall, RBCs extravasation in bronchiolium lumen and mononuclear leukocytic infiltration in parenchyma. Additionally, blood vessels congested with thickened walls, alveoli appeared collapsed with compensatory expansion of adjacent alveoli divided by thickened inter-alveolar septa, besides to damage in type 1 and type 2 pneumocytes. G co-treatment attenuated oxidative stress biomarkers. Both tested doses of G significantly decreased p53 and elevate Bcl-2 mRNA and protein expression levels and revealed significant amelioration and restoration of normal histology and ultrastructure of lung. Conclusion:In summary, G has exhibited ameliorative activity against oxidative stress induced by LCT in lung, apoptosis, histopathological and ultrastructural changes in albino rats.