Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China.
Int Immunopharmacol. 2011 Feb;11(2):172-8. doi: 10.1016/j.intimp.2010.11.012. Epub 2010 Nov 19.
Lipopolysaccharide (LPS) plays an important role in Gram-negative bacteria-induced sepsis and multiple organ dysfunction syndrome, which are still the leading cause of high mortality in intensive care units. Although paeoniflorin (Pae) has reportedly exhibited anti-inflammatory effect and protection against immunological liver injury in mice, it is not known whether Pae improve survival in endotoxemic mice. The purpose of this study was to determine the effect of Pae on the mortality, multiple organ dysfunction and cytokine production in lipopolysaccharide (LPS)-treated mice. We found that pretreatment with Pae decreased mortality, reduced lung and kidney injury, decreased serum creatinine level and improve systolic function of heart in mice challenged with LPS. Further experiments showed that Pae inhibited LPS-stimulated tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) release and promoted LPS-induced interleukin-10 (IL-10) production. Our results indicate that Pae protects mice against lethal LPS challenge, at least in part, through inhibiting TNF-α and IL-1β production and accelerating IL-10 expression.
脂多糖（LPS）在革兰氏阴性菌引起的败血症和多器官功能障碍综合征中发挥重要作用，这些疾病仍然是重症监护病房高死亡率的主要原因。虽然芍药苷（Pae）已被报道具有抗炎作用，并能保护小鼠免受免疫性肝损伤，但尚不清楚 Pae 是否能改善内毒素血症小鼠的存活率。本研究旨在确定 Pae 对内毒素（LPS）处理小鼠死亡率、多器官功能障碍和细胞因子产生的影响。我们发现，Pae 预处理可降低 LPS 处理小鼠的死亡率，减轻肺和肾损伤，降低血清肌酐水平，并改善 LPS 攻击小鼠的心脏收缩功能。进一步的实验表明，Pae 抑制了 LPS 刺激的肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）释放，并促进了 LPS 诱导的白细胞介素-10（IL-10）产生。我们的结果表明，Pae 通过抑制 TNF-α 和 IL-1β 的产生并加速 IL-10 的表达，保护小鼠免受致死性 LPS 攻击，至少部分如此。
