Abstract:

Objective To explore the effect of vitexin on hepatic ischemia-reperfusion injury（HIRI）by regulating autophagy in mice. Methods Eighteen male C57BL/6 mice weigh 20-25 g were selected anddivided into Sham group，Ischemia-Reperfusion（I/R）group and Vitexin group，respectively，with 6 mice in eachgroup. Vitexin group received intraperitoneal injection of vitexin 10 mg/kg 6 h preoperatively. Sham group and I/R group received equal amount of normal saline. HIRI model was constructed in I/R group and Vitexin group. Sham group received abdomen open and closure only. Serum alanine transaminase（ALT）and aspartate aminotransferase （AST）levels were detected in all groups，histopathological features were observed by hematoxylin-eosin（HE）staining，apoptosis was detected by Terminal-deoxynucleoitidyl Transferase Mediate Nick End Labeling （TUNEL）assay and expression of Beclin1，Bcl-2，LC3，caspase-3 proteins were detected by WesternBlot. Results Compared with I/R group，Vitexin group had a significantly lower levels of ALT and AST inserum〔ALT（U/L）：201.57±77.12 vs. 444.31±92.61，AST（U/L）：311.72±90.91 vs. 623.54±112.05，

all P ＜ 0.05〕，decreased injury of liver cells were shown in microscope and apoptotic cells marked by TUNEL assay，and the expressions of Beclin1，LC3，caspase-3 proteins weredecreased while

The expressionofBcl-2proteinincreased at the same time. Conclusion Vitexin canattenuate HIRI

inmice，whichmaybe related to theinhibitionof hepatocyteautophagy

摘要：

目的 探讨牡荆素（Vitexin）对小鼠肝缺血 / 再灌注损伤（HIRI）的作用并阐述可能的机制。方法 选取 18 只体重为 20 ～ 25 g 的健康雄性 C57BL/6 小鼠，随机分为假手术组（Sham 组）、缺血 / 再灌注组（I/R 组）和牡荆素组（Vitexin 组），每组 6 只小鼠。Vitexin 组于术前 6 h 腹腔注射 10 mg/kg 牡荆素。Sham 组与 I/R 组腹腔注射等量生理盐水。I/R 组和 Vitexin 组建立小鼠肝脏 HIRI 模型，Sham 组仅进行开腹和关腹操作。检测各组小鼠血清中丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）水平，光镜下观察肝组织病理学改变，TUNEL 法检测肝细胞凋亡情况 ；通过蛋白质免疫印迹试验（Western Blot）检测自噬调控因子 Beclin1、抗凋亡相关基因 Bcl-2、微管相关蛋白轻链 3（LC3）与天冬氨酸特异性半胱氨酸蛋白酶 3（caspase-3）的表达水平。结果 与 I/R 组相比较，Vitexin 组小鼠血清 ALT 和 AST 水平明显降低〔ALT（U/L）：201.57±77.12比 444.31±92.61，AST（U/L）：311.72±90.91 比 623.54±112.05，均 P ＜ 0.05〕，且在光镜下可见肝细胞损伤减轻 ；同时凋亡的肝细胞数量明显减少 ；肝组织中 Beclin1、LC3 和 caspase-3 蛋白的表达水平明显降低，而 Bcl-2 蛋白的表达水平明显增加。结论 牡荆素能够减轻小鼠 HIRI，其机制可能与牡荆素抑制再灌注时肝细胞自噬有关。