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目的:探讨玉郎伞(YLS)提取物对大鼠急性肺损伤(ALI)的影响。方法:将Wistar大鼠随机分为7组,分别为正常组,模型组,阳性对照组(地塞米松,3 mg·kg-1),玉郎伞水提物(TYLS)高、低剂量组(按生药量计60,30 g·kg-1),YLS总黄酮(FYLS)高、低剂量组(0.1,0.05 g·kg-1),每组动物连续灌胃给药7 d,于末次给药后30 min,采用腹腔注射20%酵母混悬液5 mL·kg-12次诱发大鼠急性肺损伤模型。最后测定肺组织的湿干比重(W/D)和肺组织髓过氧化物酶(MPO)的活性,免疫组化法测定大鼠肺组织中核因子-κB p65(NF-κB p65)的表达、ELISA法测定肺组织白介素-1β(IL-1β)的含量,并HE染色观察肺组织病理形态改变。结果:与正常组比较,模型组肺W/D和MPO活性增大、肺组织IL-1β含量增加、NF-κB p65表达升高(均P<0.01),肺组织有炎性病理改变。与模型组比较,TYLS高、低剂量组(4.31±0.15),(4.72±0.35)及FYLS高剂量组(4.74±0.23)肺W/D低于模型组(5.01±0.33)(P<0.05,P<0.01);TYLS高剂量组及FYLS高剂量组的肺MPO活性为(1.000±0.304),(0.956±0.139)U·g湿片-1,肺IL-1β含量为(265.58±47.05),(222.31±53.99)ng·L-1,肺组织细胞NF-κB p65阳性率为(51.00±8.62)%,(48.88±11.80)%,均比模型组明显降低(P<0.05,P<0.01);另外,从组织病理学角度上看,TYLS及FYLS组肺损伤程度也有所减轻,以高剂量组较为明显。结论:预先给予TYLS或FYLS可明显减轻ALI大鼠肺组织炎症反应及肺水肿程度,其机制可能是通过干扰NF-κB途径从而抑制IL-1β生成。
Objective: To investigate the effects of YLS on acute lung injury (ALI) in rats. Methods: Wistar rats were randomly divided into 7 groups: normal group, model group, positive control group (dexamethasone, 3 mg · kg -1), TYLC, low dose group (60,30 g · kg-1), YLS total flavonoids (FYLS) and low dose group (0.1,0.05 g · kg-1). The animals in each group were given gavage for 7 days, At 30 min after administration, acute lung injury model was induced by intraperitoneal injection of 5 mL · kg-12 20% yeast suspension. Finally, the wet / dry weight (W / D) and the activity of myeloperoxidase (MPO) in lung tissue were measured. The expression of NF-κB p65 in lung tissue was detected by immunohistochemistry, The content of interleukin-1β (IL-1β) in lung tissue was measured by ELISA. The pathological changes of lung tissue were observed by HE staining. Results: Compared with the normal group, the activity of W / D and MPO in the model group increased, the content of IL-1β in the lung tissue increased, the expression of NF-κB p65 increased (all P <0.01), and the inflammatory pathological changes in the lung tissue. Compared with the model group, the lung W / D of TYLS high and low dose group (4.31 ± 0.15), (4.72 ± 0.35) and FYLS high dose group (4.74 ± 0.23) were lower than that of model group (5.01 ± 0.33) (1.000 ± 0.304), (0.956 ± 0.139) U · g wet tablet-1, and lung IL-1β content was (265.58 ± 47.05), P <0.01) (222.31 ± 53.99) ng · L-1, the positive rates of NF-κB p65 in lung tissue were (51.00 ± 8.62)% and (48.88 ± 11.80)%, respectively, In addition, from the histopathological point of view, TYLS and FYLS group also reduced the extent of lung injury, high-dose group was more obvious. CONCLUSION: Pretreatment with TYLS or FYLS can significantly reduce the lung inflammation and the degree of pulmonary edema in ALI rats. The mechanism may be that it inhibits IL-1β production by interfering with NF-κB pathway.