Protective Effect of Silymarin on Lipopolysaccharide- Induced on Learning and Memory Deficiency in Male Rat

Lipopolysaccharide (LPS) or bacterial endotoxin triggers production of ROS and inflammatory cytokines. LPS is a major constituent of the outer membrane of gram-negative bacteria. Several studies have shown that, LPS induce oxidative stress in the hippocampus. Nowadays S. marianum have been shown to treat on the learning, memory deficiency and other organ toxicity. The purpose of this study is to verify theprotective effect of S. marianum against LPS -inducedmemory deficiency in male rat. Materials and Methods:In this research, 40 male Wistar rats were divided into 4 groups (n=9 in each) in standard conditions: The animals were treated with S. marianum for a 2 weeksbefore the biochemical tests, includes measurements of inflammatory and oxidative stress. Finally, initial (acquisition index) and step-through latencies (retention and recall index) were measured using passive avoidance test and alternation behavior percentage as an index ofspatial memory was determined using Y maze. The level of malondialdehyde (MDA) in the homogenate hippocampus tissue of the animal’s brains was measured. Results: The results of our investigation show that, LPS induced motor deficit as evidenced by histopathologicaldamages and biochemical abnormalities (P<0.01). Data showed that MDA level was significantly increasedin the hippocampus of LPS-treated rats but protectivegroup’s adjusted MDA level content (P<0.05). In addition, destructive effects of LPS on histopathological and biochemical parameters were improved. Western blot analysis show that S. marianum treatment inhibitedapoptosis stimulated by LPS through decreasing the caspase 3, 8, 9 ratio level in the hippocampus tissue.Conclusion: The results of this research demonstrated that S. marianum could exert protective effects against toxic effects of LPS in rat hippocampus tissue. Antiinflammatory drug can play a protective role in attenuating of the hippocampus inflammation induced by LPS injection.