医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2015年
8期
993-997
,共5页
刘振宁%高嵩岚%张红雷%赵敏
劉振寧%高嵩嵐%張紅雷%趙敏
류진저%고숭람%장홍뢰%조민
罗格列酮%百草枯%损伤,肺%核因子-κB%激活蛋白-1%炎症
囉格列酮%百草枯%損傷,肺%覈因子-κB%激活蛋白-1%炎癥
라격렬동%백초고%손상,폐%핵인자-κB%격활단백-1%염증
Rosiglitazone%Paraquat%Injury,lung%Nuclear factor-kappa B%Activating protein-1%Inflammation
目的：研究罗格列酮对百草枯致大鼠肺损伤过程中的炎症抑制作用机制。方法将72只SD雄性大鼠随机分成3组,每组24只。模型对照组：腹腔注射百草枯20 mg·kg-1；罗格列酮组：腹腔注射百草枯前1 h,腹腔注射罗格列酮10 mg·kg-1；空白对照组：腹腔注射0.9％氯化钠溶液1 mL。注射百草枯后4,8 h及1,3 d,收集各组大鼠血清和肺组织标本,组织切片苏木精-伊红( HE)染色进行肺损伤评分,采用酶联免疫吸附法( ELISA)检测血清白细胞介素-1β( IL-1β)和肿瘤坏死因子-α( TNF-α)含量,采用免疫组化方法检测NF-κB蛋白在肺组织的表达,利用Western blot法检测肺组织核因子-κB (NF-κB)和激活蛋白(AP-1)蛋白表达水平。结果模型对照组大鼠血清炎性细胞因子IL-1β和TNF-α含量明显增加。罗格列酮组肺组织损伤程度明显降低,血清IL-1β和TNF-α含量减少,肺组织NF-κB和AP-1蛋白的表达降低。结论罗格列酮可以抑制百草枯中毒大鼠肺组织NF-κB和AP-1蛋白表达,减少IL-1β和TNF-α分泌,对百草枯所致大鼠肺损伤炎症有抑制作用。
目的：研究囉格列酮對百草枯緻大鼠肺損傷過程中的炎癥抑製作用機製。方法將72隻SD雄性大鼠隨機分成3組,每組24隻。模型對照組：腹腔註射百草枯20 mg·kg-1；囉格列酮組：腹腔註射百草枯前1 h,腹腔註射囉格列酮10 mg·kg-1；空白對照組：腹腔註射0.9％氯化鈉溶液1 mL。註射百草枯後4,8 h及1,3 d,收集各組大鼠血清和肺組織標本,組織切片囌木精-伊紅( HE)染色進行肺損傷評分,採用酶聯免疫吸附法( ELISA)檢測血清白細胞介素-1β( IL-1β)和腫瘤壞死因子-α( TNF-α)含量,採用免疫組化方法檢測NF-κB蛋白在肺組織的錶達,利用Western blot法檢測肺組織覈因子-κB (NF-κB)和激活蛋白(AP-1)蛋白錶達水平。結果模型對照組大鼠血清炎性細胞因子IL-1β和TNF-α含量明顯增加。囉格列酮組肺組織損傷程度明顯降低,血清IL-1β和TNF-α含量減少,肺組織NF-κB和AP-1蛋白的錶達降低。結論囉格列酮可以抑製百草枯中毒大鼠肺組織NF-κB和AP-1蛋白錶達,減少IL-1β和TNF-α分泌,對百草枯所緻大鼠肺損傷炎癥有抑製作用。
목적：연구라격렬동대백초고치대서폐손상과정중적염증억제작용궤제。방법장72지SD웅성대서수궤분성3조,매조24지。모형대조조：복강주사백초고20 mg·kg-1；라격렬동조：복강주사백초고전1 h,복강주사라격렬동10 mg·kg-1；공백대조조：복강주사0.9％록화납용액1 mL。주사백초고후4,8 h급1,3 d,수집각조대서혈청화폐조직표본,조직절편소목정-이홍( HE)염색진행폐손상평분,채용매련면역흡부법( ELISA)검측혈청백세포개소-1β( IL-1β)화종류배사인자-α( TNF-α)함량,채용면역조화방법검측NF-κB단백재폐조직적표체,이용Western blot법검측폐조직핵인자-κB (NF-κB)화격활단백(AP-1)단백표체수평。결과모형대조조대서혈청염성세포인자IL-1β화TNF-α함량명현증가。라격렬동조폐조직손상정도명현강저,혈청IL-1β화TNF-α함량감소,폐조직NF-κB화AP-1단백적표체강저。결론라격렬동가이억제백초고중독대서폐조직NF-κB화AP-1단백표체,감소IL-1β화TNF-α분비,대백초고소치대서폐손상염증유억제작용。
Objective To study inhibition effect of rosiglitazone on lung injury induced by paraquat. Methods 72 male SD rats were randomly divided into three groups ( n=24 ): model control group, paraquat ( PQ ) was administered intraperitoneally at the dose of 20 mg·kg-1;rosiglitazone group, rosiglitazone (10 mg·kg-1 , ip) was administered 1 h before PQ administration; blank control group, 1 mL 0. 9% sodium chloride solution was administered intraperitoneally. The concentration of TNF-α and IL-1β in serum was measured by ELISA at 4, 8 h and 1, 3 day(s) after PQ exposure. The lung injury scores and nuclear factor-kappa B( NF-κB) positive signal were investigated 3 days after PQ exposure by HE staining and immunohistochemistry, respectively. Protein expression levels of NF-κB and activating protein-1(AP-1) were also determined by using Western blotting. Results The levels of IL-1β and TNF-α in serum of PQ-treated rats were significantly increased as compared with blank control group. Rosiglitazone pretreatment reduced the degree of lung tissue injury, the levels of IL-1β and TNF-α in serum, and the protien expression levels of NF-κB and AP-1 as compared with the model control group. Conclusion Rosiglitazone can inhibit NF-κB and AP-1 protein expression in lung tissue, reduce the levels of IL-1β and TNF-α in serum after PQ exposure, and exert an inhibition effect on inflammation in PQ-induced lung injury of rats.
