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Updated: Mar 18, 2026
Method of Direct Segmental Intra-hepatic Delivery Using a Rat Liver Hilar Clamp Model
Published on: April 2, 2017
Effect of breviscapine against hepatic ischemia reperfusion injury
Yan-Zhu Lin1, Zhi-Yuan Lu2, Xiao-Hui Liang3
1Clinical Medicine, International School, Jinan University, Guangzhou, China; Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Background:
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.
Methods:
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.
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 (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.
Conclusions:
Breviscapine preconditioning attenuates liver ischemia reperfusion injury via inhibiting liver oxidative stress reaction. The protective mechanism probably inhibits Mfn2 protein and mRNA expression.
