Lin Yan-Zhu, Lu Zhi-Yuan, Liang Xiao-Hui, Li Kang, Peng Bo, Gong Jin
Clinical Medicine, International School, Jinan University, Guangzhou, China; Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Department of Stomatology, Medical College, Jinan University, Guangzhou, China.
J Surg Res. 2016 Jun 15;203(2):268-74. doi: 10.1016/j.jss.2016.02.013. Epub 2016 Feb 19.
Breviscapine is an active ingredient extracted from traditional Chinese medicine Erigeron breviscapus. The purpose of this study was to investigate the effect of breviscapine injection on hepatic ischemia and/or reperfusion injury.
Forty rats were randomly divided into five groups (n = 8): Sham group, Ischemia reperfusion 1 (I/R1) + normal saline (NS) group, I/R1 + breviscapine (Bre), I/R2 + NS group, and I/R2 + Bre group. Group1 and group2 represent ischemia time for 10 min and 30 min, respectively. Breviscapine or normal saline was administered to rats (single dose of 10 mg/Kg, intravenously) 30 min before hepatic ischemia. Serum transaminases, histopathologic changes, malondialdehyde (MDA), and superoxide dismutase (SOD) in liver tissues were evaluated. The expression level of mitochondrial fusion 2 (Mfn2) was also investigated.
After 24-h reperfusion, based on the histopathologic analysis, compared with NS control group, the liver function was improved in breviscapine group. Liver enzymes aspartate and alanine aminotransferase levels were significantly lower in the I/R + Bre group, when compared with the I/R + NS group. Pretreatment with breviscapine reduced MDA level (P < 0.05) and increased SOD activity significantly in I/R + Bre compared with I/R + NS group. Western blot and RT-q polymerase chain reaction showed that Mfn2 was significantly downregulated in breviscapine preconditioning group as compared to normal saline control group.
Breviscapine preconditioning attenuates liver ischemia reperfusion injury via inhibiting liver oxidative stress reaction. The protective mechanism probably inhibits Mfn2 protein and mRNA expression.
灯盏花素是从传统中药灯盏细辛中提取的有效成分。本研究旨在探讨灯盏花素注射液对肝脏缺血和/或再灌注损伤的影响。
40只大鼠随机分为五组（n = 8）：假手术组、缺血再灌注1（I/R1）+生理盐水（NS）组、I/R1 +灯盏花素（Bre）组、I/R2 + NS组和I/R2 + Bre组。第1组和第2组分别代表缺血时间为10分钟和30分钟。在肝脏缺血前30分钟给大鼠静脉注射灯盏花素或生理盐水（单剂量10mg/Kg）。评估血清转氨酶、组织病理学变化、肝组织中的丙二醛（MDA）和超氧化物歧化酶（SOD）。还研究了线粒体融合蛋白2（Mfn2）的表达水平。
再灌注24小时后，基于组织病理学分析，与NS对照组相比，灯盏花素组肝功能得到改善。与I/R + NS组相比，I/R + Bre组的肝酶天冬氨酸和丙氨酸转氨酶水平显著降低。与I/R + NS组相比，灯盏花素预处理降低了I/R + Bre组的MDA水平（P < 0.05）并显著提高了SOD活性。蛋白质免疫印迹法和逆转录-定量聚合酶链反应显示，与生理盐水对照组相比，灯盏花素预处理组中Mfn2显著下调。
灯盏花素预处理通过抑制肝脏氧化应激反应减轻肝脏缺血再灌注损伤。其保护机制可能是抑制Mfn2蛋白和mRNA表达。
