Zhou Man-hong, Wang Song, Ma Xuan-lan, Li Tang-jiang, Liu Tong-ying, Liu An-ping
Department of Emergency, The Affiliated Hospital of Zunyi Medical College, Zunyi 563003, Guizhou, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2008 Sep;20(9):568-70.
To investigate the protective effect of rhizoma paridis total saponins and its mechanism on septic rats.
Septic model was reproduced by cecal ligation and puncture (CLP) in Wistar rats. Rhizoma paridis total saponins was administered to observe its protective effects on septic rats. Blood was collected to determine serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta(IL-1 beta)levels at 2, 6, 12, 24 and 48 hours after operation by means of enzyme-linked immunosorbent assay (ELISA). The pathological changes of lung tissue were observed with light microscope at 72 hours after operation. The peritoneal macrophages (PMPhi) in rats were isolated and the release of TNF-alpha and IL-1 beta in PMPhi after exposure to lipopolysaccharide (LPS, 100 microg/L) were measured by ELISA.
Mortality in the rhizoma paridis total saponins group was significantly lower than the CLP group (50.0% vs. 85.0%, P < 0.05). The levels of TNF-alpha and IL-1 beta in serum were significantly lower than those of the CLP group at the same time (P < 0.05 or P < 0.01). The degree of inflammatory injury to the lung was much milder than that in the CLP group. In the in vitro experiment, it was shown that rhizoma paridis total saponins in concentrations of 5, 10, 20 and 40 mg/L could inhibit remarkably the release of TNF-alpha and IL-1 beta from LPS-stimulated PMPhi of rats (all P < 0.01). The differences in TNF-alpha levels among the groups showed no statistically significant difference(all P > 0.05). The level of IL-1 beta in 5 mg/L group was significantly higher than that of the 10 mg/L group (P < 0.05), but showed no difference with those of 20 mg/L and 40 mg/L groups (both P > 0.05).
Rhizoma paridis total saponins can protect the CLP rats by inhibiting the activation of rat PMPhi to release cytokines and ameliorating acute lung injury.
探讨重楼总皂苷对脓毒症大鼠的保护作用及其机制。
采用盲肠结扎穿孔法(CLP)复制Wistar大鼠脓毒症模型。给予重楼总皂苷,观察其对脓毒症大鼠的保护作用。术后2、6、12、24和48小时采集血液,采用酶联免疫吸附测定法(ELISA)检测血清肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)水平。术后72小时用光镜观察肺组织的病理变化。分离大鼠腹腔巨噬细胞(PMPhi),用ELISA检测脂多糖(LPS,100μg/L)刺激后PMPhi中TNF-α和IL-1β的释放。
重楼总皂苷组死亡率显著低于CLP组(50.0%对85.0%,P<0.05)。血清中TNF-α和IL-1β水平在同一时间显著低于CLP组(P<0.05或P<0.01)。肺组织炎症损伤程度比CLP组轻得多。体外实验表明,5、10、20和40mg/L浓度的重楼总皂苷能显著抑制LPS刺激的大鼠PMPhi释放TNF-α和IL-1β(均P<0.01)。各组间TNF-α水平差异无统计学意义(均P>0.05)。5mg/L组IL-1β水平显著高于10mg/L组(P<0.05),但与20mg/L和40mg/L组无差异(均P>0.05)。
重楼总皂苷可通过抑制大鼠PMPhi激活释放细胞因子及改善急性肺损伤来保护CLP大鼠。