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Sesame oil potently protects rats against sepsis, and sesamol appears to be the protective ingredient in sesame oil. The aims of the present study were to examine the effects of sesamol on mortality and reactive oxygen species-associated liver injury in Wistar rats with cecal-ligation-and-puncture-induced sepsis (septic rats). After sepsis was induced, sesamol was administered every 6 h. The survival rate was determined during the ensuing 48 h. Hepatic injury was assessed using blood biochemistry and histological examination. Hepatic oxidative stress was assessed by determining the levels of liver lipid peroxidation, hydroxyl radical, and superoxide anion generation, and nitric oxide production 12 h after cecal ligation and puncture. Inducible nitric oxide synthase expression was also determined. Sesamol delayed mortality and attenuated hepatic injury in septic rats. Hepatic lipid peroxidation, hydroxyl radical, and superoxide anion levels were significantly lower in sesamol-treated septic rats. Furthermore, sesamol inhibited the production of nitrite and the expression of inducible nitric oxide synthase in the liver in septic rats. Therefore, sesamol may delay mortality and attenuate oxidative stress-associated liver injury by inhibiting the production of nitric oxide, at least partially, in septic rats.

Endotoxin is a potent inducer of lipid peroxidation (LPO), which is associated with the development of endotoxemia. 3,4-Methylenedioxyphenol (sesamol) is one of the sesame oil lignans with a high anti-LPO effect. Whether sesamol can attenuate endotoxin-induced LPO and multiple organ injury is unknown. After a dose response for sesamol in endotoxin-challenged rats was established, experiments were conducted to assess its effects on hydroxyl radical, peroxynitrite, and superoxide anion counts, activities of superoxide dismutase, catalase, and glutathione peroxidase, as well as the production of nitric oxide (NO) and the expression of inducible NO synthase. In addition, the effects of sesamol on endotoxin-induced hepatic and renal injuries were assessed. Sesamol (a) dose dependently reduced serum LPO inendotoxin-challenged rats, (b) decreased hydroxyl radical and peroxynitrite, but not superoxide anion counts, (c)increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in endotoxin-treated rats, (d)reduced NO production and inducible NO synthase expression, and (e) attenuated hepatic and renal injuries induced by endotoxin in rats. We concluded that sesamol might protect against organ injury by decreasing NO-associated LPO in endotoxemic rats.