Hydroxytyrosol (HT) is among the main bioactive ingredients isolated from olive tree with a variety of biological and pharmacological activities. In the current study, the antioxidative and anti-inflammatory activities of HT were distinguished in the splenic tissue following lipopolysaccharide (LPS)-mediated septic response. Thirty-five Swiss mice were divided into five groups (n = 7): control, HT (40 mg/kg), LPS (10 mg/kg), HT 20 mg+LPS and HT 40 mg+LPS. HT was administered for 10 days, while a single LPS dose was applied. The obtained findings demonstrate that HT administration enhanced the survival rate and decreased lactate dehydrogenase level in LPS-challenged mice. Treatment with HT inhibited the incidence of oxidative damage in splenic tissue through decreasing lipoperoxidation and increasing antioxidant molecules, namely glutathione, superoxide dismutase and catalase. HT also decreased total leukocytes count, C-reactive protein, monocyte chemoattractant protein-1, and myeloperoxidase levels. Additionally, HT suppressed the production levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6. Moreover, mRNA expression of inducible nitric oxide synthase and nitric oxide production were increased after HT administration. Furthermore, HT supplementation resulted in a downregulation of p38 mitogen-activated protein kinase, inhibited the activation of the nuclear factor kappa-B from the nucleus to the cytoplasm, and attenuated infiltration of activated immune cells and tissue injury following LPS injection. Collectively, these findings demonstrate the antioxidative and anti-inflammatory properties of HT against LPS-mediated inflammation and sepsis. Therefore, HT could be applied as an alternative anti-inflammatory agent to minimize or prevent the development of systemic inflammatory response associated with septic shock.

羟基酪醇（HT）是从橄榄树中分离出的主要生物活性成分之一，具有多种生物和药理活性。在目前的研究中，HT 在脂多糖 (LPS) 介导的脓毒症反应后的脾组织中具有抗氧化和抗炎活性。三十五只瑞士小鼠被分为五组 (n = 7)：对照、HT (40 mg/kg)、LPS (10 mg/kg)、HT 20 mg+LPS 和 HT 40 mg+LPS。HT 给药 10 天，同时应用单一 LPS 剂量。获得的研究结果表明，HT 给药提高了 LPS 攻击小鼠的存活率并降低了乳酸脱氢酶水平。HT 治疗通过减少脂质过氧化和增加抗氧化分子，即谷胱甘肽，抑制脾组织氧化损伤的发生。超氧化物歧化酶和过氧化氢酶。HT 还降低了白细胞总数、C 反应蛋白、单核细胞趋化蛋白 1 和髓过氧化物酶水平。此外，HT 抑制肿瘤坏死因子-α、白细胞介素-1β 和白细胞介素-6 的产生水平。此外，HT 给药后诱导型一氧化氮合酶的 mRNA 表达和一氧化氮产生增加。此外，HT 补充导致 p38 丝裂原活化蛋白激酶的下调，抑制从细胞核到细胞质的核因子 kappa-B 的活化，并减轻 LPS 注射后活化免疫细胞的浸润和组织损伤。总的来说，这些发现证明了 HT 对 LPS 介导的炎症和败血症的抗氧化和抗炎特性。所以，