Effect of breviscapine against hepatic ischemia reperfusion injury

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• 作者：Yan-zhu Lin ; BD^a ; ^c ; ¹ ; Zhi-yuan Lu ; MD^b ; ¹ ; Xiao-hui Liang ; MD^c ; Kang Li ; MD^d ; Bo Peng ; MD^c ; Jin Gong ; MD ; PhD^c ; ^{gongjin51@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Erigeron breviscapus ; Breviscapine ; Ischemia reperfusion ; Liver ; Mitofusin 2
• 刊名：Journal of Surgical Research
• 出版年：2016
• 出版时间：15 June 2016
• 年：2016
• 卷：203
• 期：2
• 页码：268-274
• 全文大小：631 K

文摘

Breviscapine is an active ingredient extracted from traditional Chinese medicine m>Erigeron breviscapusm>. The purpose of this study was to investigate the effect of breviscapine injection on hepatic ischemia and/or reperfusion injury.

Methods

Forty rats were randomly divided into five groups (m>nm> = 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.

Results

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 (m>Pm> < 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.

Conclusions

Breviscapine preconditioning attenuates liver ischemia reperfusion injury via inhibiting liver oxidative stress reaction. The protective mechanism probably inhibits Mfn2 protein and mRNA expression.