Salidroside pretreatment attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting the mitogen-activated protein kinase pathway in mice.
Salidroside pretreatment attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting the mitogen-activated protein kinase pathway in mice.
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红景天苷预处理通过抑制小鼠丝裂原激活蛋白激酶途径减轻肝缺血再灌注损伤期间的细胞凋亡和自噬
DOI：
10.2147/dddt.s136792
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Guo C
中科院分区：
文献类型：
--
作者：
Feng J;Zhang Q;Mo W;Wu L;Li S;Li J;Liu T;Xu S;Fan X;Guo C
缺血再灌注损伤（IRI）在许多临床情况下，如肝切除术和肝移植，都会导致肝损伤。在本研究中，我们研究了抗氧化剂、抗炎剂和抗癌剂红景天苷（Sal）对小鼠肝脏IRI的影响。将小鼠随机分为6组：正常对照组、假手术组、Sal（20 mg/kg）组、IRI组、IRI + Sal（10 mg/kg）组和IRI + Sal（20 mg/kg）组。我们在再灌注后2、8和24小时测定了肝酶、促炎细胞因子、TNF-α和白细胞介素-6以及凋亡和自噬相关标志物蛋白。丝裂原活化蛋白激酶（MAPK）信号的组成部分，包括P-38，jun N-末端激酶（JNK），和细胞外信号调节激酶（ERK），也使用MAPK激活剂茴香霉素来推断它们在肝IRI中的作用。我们的研究结果表明，Sal通过降低血清中肝酶的水平来安全地保护肝细胞免受IRI的影响。这些发现得到了组织病理学的证实。我们的结论是，Sal保护肝细胞免受IRI部分通过抑制MAPK信号转导，包括P38，JNK和ERK的磷酸化。这改善了小鼠肝脏中的炎症反应、细胞凋亡和自噬。
Ischemia–reperfusion injury (IRI) contributes to liver damage in many clinical situations, such as liver resection and liver transplantation. In the present study, we investigated the effects of the antioxidant, anti-inflammatory, and anticancer agent salidroside (Sal) on hepatic IRI in mice. The mice were randomly divided into six groups: normal control, Sham, Sal (20 mg/kg), IRI, IRI + Sal (10 mg/kg), and IRI + Sal (20 mg/kg). We measured liver enzymes, proinflammatory cytokines, TNF-α and interleukin-6, and apoptosis- and autophagy-related marker proteins at 2, 8, and 24 hours after reperfusion. Components of mitogen-activated protein kinase (MAPK) signaling, including P-38, jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK), were also measured using an MAPK activator anisomycin to deduce their roles in hepatic IRI. Our results show that Sal safely protects hepatocytes from IRI by reducing levels of liver enzymes in the serum. These findings were confirmed by histopathology. We concluded that Sal protects hepatocytes from IRI partly by inhibiting the activation of MAPK signaling, including the phosphorylation of P38, JNK, and ERK. This ameliorates inflammatory reactions, apoptosis, and autophagy in the mouse liver.