Shi Yaoping, Qiu Xiaoxia, Dai Mengjun, Zhang Xuebin, Jin Guangxin
Department of Interventional Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Department of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Transplant Proc. 2019 Jul-Aug;51(6):2051-2059. doi: 10.1016/j.transproceed.2019.04.066.
Hepatic ischemia-reperfusion (IR) injury is a serious complication of many clinical conditions, which may lead to liver or multiple organ failure. Hyperoside, a flavonoid compound, has been reported to protect against myocardial and cerebral injury induced by IR. This study aimed to investigate the protective effects of hyperoside on hepatic IR injury in rats.
Using the 70% hepatic IR injury model, we divided 32 male Wistar rats into 4 groups (n = 8): sham-operated, IR+saline (saline/p.o.), IR+vehicle (carboxy methyl cellulose/p.o.), and IR+hyperoside (50 mg/kg/d/p.o.). At 24 hours after reperfusion, blood and liver tissue were collected. The effects of hyperoside on hepatic IR injury were assessed through tests of serum transaminase, hepatic histopathology, and measurement of markers of oxidative stress and apoptosis.
Pretreatment with hyperoside protected the liver from IR injury by a reduction in serum aspartate aminotransferase/alanine aminotransferase levels and a decrease in the severity of histologic changes. Hyperoside treatment also decreased the activity of malondialdehyde, increased the activities of superoxide dismutase and glutathione peroxidase, up-regulated the expression of heme oxygenase 1 and NAD(P)H:quinone oxidoreductase 1, and reduced the apoptotic index after IR injury. A decrease in the expression of caspase-3 and an increase in the ratio of B cell lymphoma 2 to B cell lymphoma 2-associated X also were observed.
Hyperoside has a protective effect on hepatic IR injury in rats, which may be due to its antioxidant and antiapoptotic properties.
肝缺血再灌注（IR）损伤是许多临床病症的严重并发症，可能导致肝衰竭或多器官衰竭。据报道，黄酮类化合物金丝桃苷可预防IR诱导的心肌和脑损伤。本研究旨在探讨金丝桃苷对大鼠肝IR损伤的保护作用。
采用70%肝IR损伤模型，将32只雄性Wistar大鼠分为4组（n = 8）：假手术组、IR+生理盐水组（生理盐水/口服）、IR+赋形剂组（羧甲基纤维素/口服）和IR+金丝桃苷组（50 mg/kg/d/口服）。再灌注24小时后，采集血液和肝组织。通过检测血清转氨酶、肝脏组织病理学以及测量氧化应激和凋亡标志物来评估金丝桃苷对肝IR损伤的影响。
金丝桃苷预处理可通过降低血清天冬氨酸转氨酶/丙氨酸转氨酶水平以及减轻组织学变化的严重程度来保护肝脏免受IR损伤。金丝桃苷治疗还降低了丙二醛的活性，增加了超氧化物歧化酶和谷胱甘肽过氧化物酶的活性，上调了血红素加氧酶1和NAD(P)H：醌氧化还原酶1的表达，并降低了IR损伤后的凋亡指数。还观察到半胱天冬酶-3表达降低以及B细胞淋巴瘤-2与B细胞淋巴瘤-2相关X蛋白的比例增加。
金丝桃苷对大鼠肝IR损伤具有保护作用，这可能归因于其抗氧化和抗凋亡特性。
