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灯盏花素对大鼠肝脏缺血再灌注损伤的实验研究 被引量:1

Experimental study on possible effect of breviscapin in the ischemia-reperfusion injury of rat liver
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摘要 目的探讨灯盏花素(erigeron breviscapus)对大鼠肝脏缺血再灌注损伤的保护作用及其机制。方法 SD大鼠45只随机分为假手术组、缺血再灌注组和灯盏花素组。分别检测各组大鼠肝脏缺血60分钟,再灌注120分钟时血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、肿瘤坏死因子α(TNF-α)水平,以及肝组织中超氧化物岐化酶(SOD)活性和bcl-2蛋白表达的变化;并观察肝脏病理组织学改变。结果与假手术组比较,缺血再灌注组血清中ALT、AST、TNF-α含量显著增加,肝组织SOD活性显著降低(均P<0.05);与缺血再灌注组比较,灯盏花素组血清中ALT、AST、TNF-α含量显著降低(均P<0.05),但SOD活性及bcl-2蛋白表达增加(均P<0.05)。灯盏花素组肝脏炎症反应较缺血再灌注组明显减轻。结论灯盏花素对大鼠肝脏缺血再灌注损伤有保护作用,其机制可能与其增强SOD活性和上调bcl-2蛋白表达有关。 Objective To study the effect of Breviscapin during ischemia-reperfusion injury of rat liver and assess the possible mechanism. Mothods Forty five SD rats were randomly divided into pseud-operation group, ischemia-reperfusion group and breviscapin group. During the liver ischemia sixty minutes and reperfusion one hundred and twenty minutes, the level of ALT, AST and TNF-α in the serum were determined.The change of SOD activity of the hepatic tissue and expression of bcl-2 in liver cells were studied. Liver histopathology was observed respectively. Results The level of ALT、AST and TNF-α in ischemia-reperfusion group were obviously higher than pseud-operation group(all P〈0.05). SOD activity of the hepatic tissue in ischemia-reperfusion group was lower than pseud-operation group(P〈0.05). The level of ALT、AST and TNF-αin breviscapin group were lower than that in ischemia-reperfusion group. But SOD activity and the expression of bcl-2 in breviscapin group were higher than that in ischemia-reperfusion group. Inflammation of the liver in breviscapin group was significantly reduced than that in ischemia reperfusion group(P〈0.05). Conclusions Breviscapin has protective effects on rat liver ischemia-reperfusion injury. The protective effect of breviscapine might be attributed to the enhanced SOD activity and the up-regulation of bcl-2 expression.
出处 《消化肿瘤杂志(电子版)》 2016年第3期176-180,共5页 Journal of Digestive Oncology(Electronic Version)
关键词 灯盏花素 缺血再灌注 肝脏 细胞凋亡 Breviscapin Ischemia reperfusion Liver Apoptosis
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