姜黄素对脓毒症急性肺损伤的炎性反应及Notch2/Hes-1通路的影响

目的探讨姜黄素对脓毒症急性肺损伤的炎症反应及对Notch2/Hes-1通路的影响。方法36只Wistar大鼠随机分为正常对照组、模型组及姜黄素干预组。HE染色观察各组大鼠肺组织病理学改变;测量各组大鼠肺组织湿/干重(W/D)比。酶联免疫吸附法(ELISA)检测各组大鼠血清肿瘤坏死因子-α(TNF-α)与细胞间黏附分子-1(ICAM-1)水平;采用免疫组织化学方法与Western blot方法检测各组大鼠肺组织Notch2与Hes-1蛋白的表达。结果LPS诱导的急性肺损伤大鼠肺组织严重出血且有明显的炎性细胞浸润,血清TNF-α与ICAM-1水平显著升高;而给予姜黄素干预后,急性肺损伤大鼠肺组织炎性明显减轻,血清TNF-α与ICAM-1水平显著降低(P<0.01)。免疫组织化学结果与Western blot结果显示,模型组大鼠肺组织Notch2与Hes-1蛋白表达的平均光密度值显著升高(P<0.01);而给予姜黄素干预后,急性肺损伤大鼠肺组织Notch2与Hes-1蛋白表达的平均光密度值显著降低(P<0.01)。结论姜黄素能够减轻脓毒症急性肺损伤大鼠的炎性反应,其机制可能与Notch2/Hes-1通路相关。

Effect of curcumin on the inflammatory response and notch 2/HES-1 pathway in rats with sepsis-associated acute lung injury

Objective To investigate the effect of curcumin on the inflammatory response and notch 2/HES-1 pathway in rats with sepsis-associated acute lung injury.Methods 36 Wistar rats were randomly divided into control group,LPS group and curcumin intervention group.HE staining was used to observe the pathological changes of lung tissue and the wet/dry(W/D)weight ratio was measured.The levels of TNF-αand ICAM-1 in serum were detected by enzymelinked immunosorbent assay(ELISA),and the expression of Notch2 and HES-1 in lung tissue was detected by immunohistochemistry and Western blot.Results In rats with sepsis-associated acute lung injury,there was severe hemorrhage and inflammatory cell infiltration in lung tissue,and the level of TNF-αand ICAM-1 in serum was increased significantly;after the intervention of curcumin,the inflammation of lung tissue in rats sepsis-associated acute lung injury was significantly reduced,and the level of TNF-αand ICAM-1 in serum was significantly reduced(P<0.01).The results of immunohistochemistry and Western blot showed that the expression of Notch2 and HES-1 protein in the lung tissue of the LPS group was increased significantly(P<0.01),while the expression of Notch2 and HES-1 protein was decreased significantly(P<0.01)after the intervention of curcumin.Conclusion Curcumin could reduce the inflammatory response of sepsis rats with acute lung injury,and its mechanism might be related to notch 2/HES-1 pathway.