中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2008年
9期
568-570,封3
,共4页
周满红%汪松%马璇岚%李堂江%刘同英%刘安平
週滿紅%汪鬆%馬璇嵐%李堂江%劉同英%劉安平
주만홍%왕송%마선람%리당강%류동영%류안평
重楼总皂苷%脓毒症%巨噬细胞%肿瘤坏死因子-α%白细胞介素-1β%脂多糖
重樓總皂苷%膿毒癥%巨噬細胞%腫瘤壞死因子-α%白細胞介素-1β%脂多糖
중루총조감%농독증%거서세포%종류배사인자-α%백세포개소-1β%지다당
rhizoma paridis total saponins%sepsis%macrophage%tumor necrosis factor-a%interleukin-1β%liooootvsaccharide
目的 观察重楼总皂苷对脓毒症大鼠的保护作用并探讨其作用机制.方法 采用盲肠结扎穿孔术(CLP)制备大鼠脓毒症模型,观察重楼总皂苷对CLP大鼠死亡率的影响.用酶联免疫吸附法(ELISA)检测术后2、6、12、24和48 h大鼠血清肿瘤坏死因子-a(TNF-a)和白细胞介素-1β(IL-1β)水平;光镜下观察72 h大鼠肺组织病理学变化.分离大鼠腹腔巨噬细胞(PMΦ),用ELISA检测重楼总皂苷对LPS(100/μg/L)诱导大鼠PMΦ释放TNF-a及IL-1β的影响.结果 重楼总皂苷组大鼠死亡率明显低于模型组(50.0%比85.0%,P<0.05).重楼总皂苷各浓度组血清TNF-a和IL-1β水平较模型组相应时间点明显降低(P<0.05或P<0.01);肺组织病理学观察显示肺损伤程度较轻.体外实验表明,5、10、20和40 mg/L重楼总皂苷均可显著降低LPS刺激PMΦ释放TNF-a和IL-1β的水平(P均<0.01);且各浓度组间TNF-a水平差异无统计学意义(P均0.05);而5 mg/L组IL-1β水平显著高于10 mg/L组(P<0.05),但与20 mg/L组和40 mg/L组比较差异无统计学意义(P均0.05).结论 重楼总皂苷能抑制CLP大鼠巨噬细胞活化并减轻肺损伤程度,对CLP大鼠具有保护作用.
目的 觀察重樓總皂苷對膿毒癥大鼠的保護作用併探討其作用機製.方法 採用盲腸結扎穿孔術(CLP)製備大鼠膿毒癥模型,觀察重樓總皂苷對CLP大鼠死亡率的影響.用酶聯免疫吸附法(ELISA)檢測術後2、6、12、24和48 h大鼠血清腫瘤壞死因子-a(TNF-a)和白細胞介素-1β(IL-1β)水平;光鏡下觀察72 h大鼠肺組織病理學變化.分離大鼠腹腔巨噬細胞(PMΦ),用ELISA檢測重樓總皂苷對LPS(100/μg/L)誘導大鼠PMΦ釋放TNF-a及IL-1β的影響.結果 重樓總皂苷組大鼠死亡率明顯低于模型組(50.0%比85.0%,P<0.05).重樓總皂苷各濃度組血清TNF-a和IL-1β水平較模型組相應時間點明顯降低(P<0.05或P<0.01);肺組織病理學觀察顯示肺損傷程度較輕.體外實驗錶明,5、10、20和40 mg/L重樓總皂苷均可顯著降低LPS刺激PMΦ釋放TNF-a和IL-1β的水平(P均<0.01);且各濃度組間TNF-a水平差異無統計學意義(P均0.05);而5 mg/L組IL-1β水平顯著高于10 mg/L組(P<0.05),但與20 mg/L組和40 mg/L組比較差異無統計學意義(P均0.05).結論 重樓總皂苷能抑製CLP大鼠巨噬細胞活化併減輕肺損傷程度,對CLP大鼠具有保護作用.
목적 관찰중루총조감대농독증대서적보호작용병탐토기작용궤제.방법 채용맹장결찰천공술(CLP)제비대서농독증모형,관찰중루총조감대CLP대서사망솔적영향.용매련면역흡부법(ELISA)검측술후2、6、12、24화48 h대서혈청종류배사인자-a(TNF-a)화백세포개소-1β(IL-1β)수평;광경하관찰72 h대서폐조직병이학변화.분리대서복강거서세포(PMΦ),용ELISA검측중루총조감대LPS(100/μg/L)유도대서PMΦ석방TNF-a급IL-1β적영향.결과 중루총조감조대서사망솔명현저우모형조(50.0%비85.0%,P<0.05).중루총조감각농도조혈청TNF-a화IL-1β수평교모형조상응시간점명현강저(P<0.05혹P<0.01);폐조직병이학관찰현시폐손상정도교경.체외실험표명,5、10、20화40 mg/L중루총조감균가현저강저LPS자격PMΦ석방TNF-a화IL-1β적수평(P균<0.01);차각농도조간TNF-a수평차이무통계학의의(P균0.05);이5 mg/L조IL-1β수평현저고우10 mg/L조(P<0.05),단여20 mg/L조화40 mg/L조비교차이무통계학의의(P균0.05).결론 중루총조감능억제CLP대서거서세포활화병감경폐손상정도,대CLP대서구유보호작용.
Objective To investigate the protective effect of rhizoma paridis total saponins (重楼总皂苷) and its mechanism on septic rats. Methods 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-a (TNF-a) and interleukin-1β (IL-1β) levels at 2, 6, 12, 24 and 48 hours after operation by means of enzyme-linked irnmunosorbent assay (ELISA). The pathological changes of lung tissue were observed with light microscope at 72 hours after operation. The peritoneal macrophages (PMΦ) in rats were isolated and the release of TNF-a and IL-1β in PMΦ after exposure to lipopolysaecharide (LPS, 100 μg/L) were measured by ELISA. Results 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-a and IL-1β 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-a and IL-1β from LPS-stimulated PMΦ of rats (all P<0.01). The differences in TNF-a levels among the groups showed no statistically significant difference (all P0.05). The level of IL-1β 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 P0.05). Conclusion Rhizoma paridis total saponins can protect the CLP rats by inhibiting the activation of rat PMΦ to release cytokines and ameliorating acute lung injury.