探讨落新妇苷对大鼠肝脏缺血再灌注损伤（HIRI）的保护作用及自噬的影响。

将54只SD大鼠随机分为假手术组（Sham组）、缺血再灌注组（HIRI组）以及落新妇苷组（40 mg·kg^-1·d^-1，连续7 d），每组18只。建立大鼠HIRI模型，于再灌注4、8、16 h后取下腔静脉血及肝左外叶组织。全自动生化分析仪检测血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）水平；光学显微镜下观察肝细胞显微结构变化；Western blotting分析肝组织中自噬相关蛋白LC3、Beclin-1的表达；电镜下观察肝脏组织内自噬小体数量情况。

同检测时间点比较，Sham组和落新妇苷组的血清ALT和AST水平均低于HIRI组（P<0.05），且肝细胞肿胀、炎性细胞浸润、汇管区结构损伤明显较轻。落新妇苷组LC3-Ⅱ/ LC3-Ⅰ灰度值比值及Beclin-1蛋白灰度值在术后4、8、16 h明显低于HIRI组（P<0.05）。落新妇苷组肝组织的自噬小体数量较HIRI组有所减少（3.68±0.42 vs 7.12±0.60，t=36.382，P<0.01）。

落新妇苷预处理可减轻大鼠HIRI，其作用机制可能与其抑制自噬有关。

To explore the protective effect of Astilbin in hepatic ischemia-reperfusion injury (HIRI).

Fifty-four SD rats were divided into Sham group (control group), HIRI group (ischemia-reperfusion group) and Astilbin group (40 mg·kg^-1·d^-1 for continuous 7 days) with 18 in each group, to establish the model of rat HIRI. After the liver was reperfused with blood (in 4, 8, 16 h), the specimens of blood and liver tissues were collected. Serum alanine aminotransferase (ALT) and aspertate aminotransferase (AST) were detected by automatic biochemical analyzer. The changes of liver cell microstructure were observed under the optical microscope. The expression of autophagy related protein LC3 and Beclin-1 in liver tissue were detected by Western blotting analysis. The number of autophagosome was observed using electron microscope.

Compared with the HIRI group at each detection time point, serum ALT and AST levels of the sham group and Astilbin group were significantly lower (P<0.05), with less liver cell swelling, inflammatory cell infiltration, and the structural damage of the sinks. LC3- / LC3-ratio and the gray value of Beclin-1 protein in the Astilbin group were lower than that of group HIRI at 4, 8, 16 h after operation (P<0.05). The number of autophagosomes in liver tissue of Astilbin group was also less than the HIRI group (3.68±0.42 vs 7.12±0.60, t=36.382, P<0.01).

Astilbin pretreatment can reduce HIRI and its mechanism may be associated with inhibiting the autophagy.