Background High levels of serum lipopolysaccharide (LPS) were observed in sepsis patients with liver injury and high mortality. However, the role of liver in modulation LPS induced inflammatory injury was ill investigated. In the present study, the severity of LPS induced inflammatory response was observed after liver resection or portal branch occlusion to decreasing functional liver mass. The local and systemic damage was observed to investigate the role of liver in modulation inflammatory injury. Methods First, 30%, 70%, and 90% partial hepatectomy (PH) were performed, and serum TNF-α, survival rate, and hepatic LPS uptake was observed. Second, LPS-exposure of the functional liver mass was decreased by selectively blocking the RL prior to LPS-injection, which was given 30 min before a 70% PH, and the inflammatory response was compared in the occluded and the non-occluded liver. The control group was subjected to LPS injection 30 min prior to liver resection without blocking the RL transiently. The serum TNF-α, ALT, AST, creatinine levels, and urea levels, survival rate, hepatic LPS uptake, and hepatic inflammatory cytokines was observed. Results The decreasing of functional liver mass after 90%, 70%, and 30% PH was associated with decreased serum TNF-α, survival rate, and increased hepatic LPS uptake after LPS injection. Occluding the right lobes (RL) prior to LPS administration reversed the liver injury caused by 70% PH, indicated by 100% survival rate and decreased liver and kidney injury, and systemic inflammatory response. The induction of inflammatory response in occluding liver lobes were lower than un-occluding liver lobes. Conclusions The severity of the LPS-induced systemic inflammatory injury is determined by functional liver volume. This observation suggests that the liver is the central organ for the initiation of the inflammatory response, and is involved in causing a severe SIRS with systemic damage and death.

中文翻译：

---

在大鼠模型中，LPS 诱导的炎症损伤的严重程度与 LPS 注射后的功能性肝块呈负相关。

背景 在伴有肝损伤和高死亡率的脓毒症患者中观察到高水平的血清脂多糖 (LPS)。然而，肝脏在调节 LPS 诱导的炎症损伤中的作用尚未得到充分研究。在本研究中，观察到 LPS 诱导的炎症反应的严重程度在肝切除或门静脉分支闭塞以减少功能性肝块后。观察局部和全身损伤，探讨肝脏在调节炎症损伤中的作用。方法首先进行30%、70%和90%的肝部分切除术（PH），观察血清TNF-α、存活率和肝LPS摄取情况。其次，通过在 LPS 注射前选择性阻断 RL 来减少功能性肝块的 LPS 暴露，在 70% PH 前 30 分钟给予，比较闭塞和非闭塞肝脏的炎症反应。对照组在肝切除前30分钟注射LPS，不暂时阻断RL。观察血清TNF-α、ALT、AST、肌酐水平和尿素水平、存活率、肝LPS摄取和肝炎性细胞因子。结果 90%、70% 和 30% PH 后功能性肝质量的减少与 LPS 注射后血清 TNF-α、存活率和肝 LPS 摄取增加有关。在 LPS 给药之前封闭右叶 (RL) 可逆转 70% PH 引起的肝损伤，100% 的存活率和减少的肝肾损伤和全身炎症反应表明。闭塞肝叶中炎症反应的诱导低于未闭塞肝叶。结论 LPS诱导的全身性炎症损伤的严重程度取决于功能性肝体积。这一观察结果表明，肝脏是引发炎症反应的中心器官，并参与导致严重的 SIRS 系统性损伤和死亡。