中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2014年
6期
65-68,75
,共5页
阮琼%张海英%杨爱东%王利霞%吴中华%符胜光%庞慧芳
阮瓊%張海英%楊愛東%王利霞%吳中華%符勝光%龐慧芳
원경%장해영%양애동%왕리하%오중화%부성광%방혜방
宣肺通腑方%急性肺损伤%髓样分化蛋白-2%核因子-κB%蛋白表达%基因表达%大鼠
宣肺通腑方%急性肺損傷%髓樣分化蛋白-2%覈因子-κB%蛋白錶達%基因錶達%大鼠
선폐통부방%급성폐손상%수양분화단백-2%핵인자-κB%단백표체%기인표체%대서
Xuanfeitongfufang Decoction%acute lung injury%MD-2%NF-κB%protein expression%mRNA expression%rats
目的:观察宣肺通腑方对脂多糖(LPS)诱导的急性肺损伤(ALI)大鼠肺组织髓样分化蛋白-2(MD-2)、核因子-κB(NF-κB)蛋白及其基因表达的影响,并探讨其作用机制。方法 Wistar大鼠随机分为正常组、模型组、地塞米松组和宣肺通腑方大、中、小剂量组,每组8只。尾静脉注射LPS 6 mg/kg制备大鼠ALI模型。宣肺通腑方各组于造模前以15.12、7.56、3.78 g原药材/kg宣肺通腑方水煎液灌胃,1次/d,连续3 d;地塞米松组在造模前1 h按5 mg/kg腹腔注射地塞米松。造模后9 h麻醉取材,采用免疫组化ABC法和实时荧光定量聚合酶链反应检测MD-2、NF-κB蛋白及其基因表达,光镜下观察大鼠肺组织病理变化。结果与正常组比较,模型组MD-2、NF-κB蛋白及其基因表达均明显上调(P<0.05,P<0.01);与模型组比较,地塞米松组和宣肺通腑方各组MD-2、NF-κB蛋白及其基因表达明显降低(P<0.05,P<0.01);地塞米松组和宣肺通腑方各剂量组比较差异无统计学意义(P>0.05)。病理观察结果显示,与正常组比较,模型组大鼠肺组织出现大片出血及坏死,炎症细胞大量浸润;宣肺通腑方各剂量组和地塞米松组大鼠肺组织病理改变明显轻于模型组,肺细支气管偶见炎症改变,水肿较轻,炎性细胞渗出较少。结论宣肺通腑方能减轻ALI大鼠肺组织损伤,对肺损伤有保护作用,其机制可能与其降低ALI大鼠MD-2、NF-κB蛋白及其基因表达有关。
目的:觀察宣肺通腑方對脂多糖(LPS)誘導的急性肺損傷(ALI)大鼠肺組織髓樣分化蛋白-2(MD-2)、覈因子-κB(NF-κB)蛋白及其基因錶達的影響,併探討其作用機製。方法 Wistar大鼠隨機分為正常組、模型組、地塞米鬆組和宣肺通腑方大、中、小劑量組,每組8隻。尾靜脈註射LPS 6 mg/kg製備大鼠ALI模型。宣肺通腑方各組于造模前以15.12、7.56、3.78 g原藥材/kg宣肺通腑方水煎液灌胃,1次/d,連續3 d;地塞米鬆組在造模前1 h按5 mg/kg腹腔註射地塞米鬆。造模後9 h痳醉取材,採用免疫組化ABC法和實時熒光定量聚閤酶鏈反應檢測MD-2、NF-κB蛋白及其基因錶達,光鏡下觀察大鼠肺組織病理變化。結果與正常組比較,模型組MD-2、NF-κB蛋白及其基因錶達均明顯上調(P<0.05,P<0.01);與模型組比較,地塞米鬆組和宣肺通腑方各組MD-2、NF-κB蛋白及其基因錶達明顯降低(P<0.05,P<0.01);地塞米鬆組和宣肺通腑方各劑量組比較差異無統計學意義(P>0.05)。病理觀察結果顯示,與正常組比較,模型組大鼠肺組織齣現大片齣血及壞死,炎癥細胞大量浸潤;宣肺通腑方各劑量組和地塞米鬆組大鼠肺組織病理改變明顯輕于模型組,肺細支氣管偶見炎癥改變,水腫較輕,炎性細胞滲齣較少。結論宣肺通腑方能減輕ALI大鼠肺組織損傷,對肺損傷有保護作用,其機製可能與其降低ALI大鼠MD-2、NF-κB蛋白及其基因錶達有關。
목적:관찰선폐통부방대지다당(LPS)유도적급성폐손상(ALI)대서폐조직수양분화단백-2(MD-2)、핵인자-κB(NF-κB)단백급기기인표체적영향,병탐토기작용궤제。방법 Wistar대서수궤분위정상조、모형조、지새미송조화선폐통부방대、중、소제량조,매조8지。미정맥주사LPS 6 mg/kg제비대서ALI모형。선폐통부방각조우조모전이15.12、7.56、3.78 g원약재/kg선폐통부방수전액관위,1차/d,련속3 d;지새미송조재조모전1 h안5 mg/kg복강주사지새미송。조모후9 h마취취재,채용면역조화ABC법화실시형광정량취합매련반응검측MD-2、NF-κB단백급기기인표체,광경하관찰대서폐조직병리변화。결과여정상조비교,모형조MD-2、NF-κB단백급기기인표체균명현상조(P<0.05,P<0.01);여모형조비교,지새미송조화선폐통부방각조MD-2、NF-κB단백급기기인표체명현강저(P<0.05,P<0.01);지새미송조화선폐통부방각제량조비교차이무통계학의의(P>0.05)。병리관찰결과현시,여정상조비교,모형조대서폐조직출현대편출혈급배사,염증세포대량침윤;선폐통부방각제량조화지새미송조대서폐조직병리개변명현경우모형조,폐세지기관우견염증개변,수종교경,염성세포삼출교소。결론선폐통부방능감경ALI대서폐조직손상,대폐손상유보호작용,기궤제가능여기강저ALI대서MD-2、NF-κB단백급기기인표체유관。
Objective To investigate the effects of Xuanfeitongfufang Decoction on expressions of MD-2, NF-κB protein and its mRNA in lung of the rats with acute lung injury caused by LPS. Methods Wistar rats were randomly divided into normal group, model group, dexamethasone group and Xuanfeitongfufang Decoction large-, medium-, small-dose group, each group had eight rats. The ALI rat model was established by LPS tail-intravenous injection (6 mg/kg). The rats in Xuanfeitongfufang Decoction groups were pretreated by Xuanfeitongfufang Decoction (15.12, 7.56, 3.78 g/kg) for 3 days before LPS induced ALI. The rats in dexamethasone group were pretreated by dexamethasone (5 mg/kg). MD-2, NF-κB protein and its mRNA were measured by immunohistochemistry and PCR. The histopathology of the lung injury was observed by light microscope. Results Compared with normal group, the expression of MD-2, NF-κB protein and its mRNA were obviously increased in model group (P<0.01). Compared with model group, the expression of MD-2, NF-κB protein and its mRNA were obviously decreased in Xuanfeitongfufang Decoction groups and dexamethasone group (P<0.01), and there was no obvious difference between Xuanfeitongfufang Decoction groups and dexamethasone group. Light microscope observation indicates that there were large areas of pulmonary hemorrhage and necrosis in model group. While in Xuanfeitongfufang Decoction group and dexamethasone group, the pathological manifestations were much more ameliorated than those of the model group. The lung bronchiale inflammation appeared occasionally, and the edema was lightly. Conclusion Xuanfeitongfufang Decoction can lessen the injury of lung tissue and has protective effects on rats with ALI, the mechanism is possibly related to the inhibition of the expressions of MD-2 and NF-κB protein and its mRNA in injured lung tissues.