Effects of Sesame Oil on Lipopolysaccharide-induced Endotoxemia in Rats

• Main Authors: Hui-Jean Huang, 黃惠靖
• Other Authors: Ming-Yie Liu
• Format: Others
• Language: zh-TW
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/27647776399863906226

碩士 === 國立成功大學 === 環境醫學研究所 === 91 === Lipopolysaccharide (LPS), the main component of the outer cell wall in all Gram-negative bacteria, triggers severe pathologic alternations, such as systemic inflammation, multiple organ dysfunction (MOD), and death in clinical studies. Despite significant advances in the management of sepsis, MOD remains the leading cause of death in septic patients. It was found that sesame oil (SO) could scavenge free radical, reduce lipid peroxidation (LPO), attenuate the LPS-induced MOD, and increase survival rate of sepsis in animal studies. Rats were challenged intraperitoneally with 1 mg/kg LPS. SO (8 ml/kg) was given right after LPS administration. Blood samples were collected at 1, 3, 6, 12, or 24 hrs after LPS-injection. Serum levels of asparate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALKP), total bilirubin (TBIL), LPO, superoxide anion, the activities of superoxide dismutase (SOD) and catalse (CAT), serum levels of glutathione (GSH), nitric oxide, pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-a) and interleukin-1 beta (IL-1b), and anti-inflammatory cytokine interleukin-10 (IL-10) were determined. After LPS injection, SO: (1) up-regulated LPS-induced TNF-a at 1 hr and down-regulated at 3 hrs; (2) reduced IL-1β at 3 hrs, but increased at 12 hrs; (3) slightly but not significantly inhibited IL-10 levels; (4) increased serum levels of nitric oxide at 1, 3, 6, and 12 hrs; (5) reduced LPS-induced superoxide anion at 12 and 24 hrs; (6) failed to affect SOD and CAT activities; (7) up-regulated GSH at 1, 12 and 24 hrs; (8) slightly but not significantly increased LPS-induced LPO; (9) □increased LPS-induced liver injury. It is concluded that SO may not protect against low-dose LPS-induced endotoxemia in rats.