Protective effect of Salidroside on hypoxia-related liver oxidative stress and inflammation via Nrf2 and JAK2/STAT3 signaling pathways.
Protective effect of Salidroside on hypoxia-related liver oxidative stress and inflammation via Nrf2 and JAK2/STAT3 signaling pathways.
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DOI：
10.1002/fsn3.2459
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发表时间：
2021-09
影响因子：
3.9
通讯作者：
Teng L
中科院分区：
文献类型：
--
作者：
Xiong Y;Wang Y;Xiong Y;Teng L
高原缺氧诱导的氧化应激和炎症在肝损伤的发生和发展中发挥着重要作用。红景天苷（Salidroside，Sal）是一种从植物红景天中提取的苯丙素苷，最近被证明具有抗氧化、抗炎和抗缺氧的特性。在此，我们假设红景天苷可能通过抗氧化和抗氧化相关途径减轻缺氧诱导的肝损伤。采用低压舱建立高原低氧动物模型。雄性SD大鼠随机分为对照组、缺氧组、对照+Sal组、缺氧+Sal组。红景天苷处理显著抑制缺氧诱导的血清和肝脏促炎细胞因子释放、肝脏ROS产生和MDA含量的增加;减弱缺氧诱导的肝脏SOD、CAT和GSH-Px活性的降低。此外，红景天苷处理还增强了Nrf 2介导的抗氧化途径的激活，如通过上调n-Nrf 2及其下游HO-1和NQO-1所示。体外研究发现，使用特异性抑制剂ML 385阻断Nrf 2通路可显著逆转红景天苷对缺氧诱导的肝脏氧化应激的保护作用。此外，红景天苷治疗通过JAK 2/STAT 3介导的途径显著抑制肝脏促炎细胞因子释放。总之，我们的研究结果表明，红景天苷通过Nrf 2和JAK 2/STAT 3信号通路保护缺氧诱导的肝脏氧化应激和炎症。红景天苷对缺氧性肝损伤的保护机制红景天苷通过Nrf 2信号通路保护肝脏免受缺氧诱导的氧化应激。红景天苷的抗炎作用依赖于JAK 2/STAT 3通路的抑制和Nrf 2通路的激活。
High‐altitude hypoxia‐induced oxidative stress and inflammation played an essential role in the incidence and development of liver injury. Salidroside (Sal), a phenylpropanoid glycoside extracted from the plant Rhodiola rosea, has recently demonstrated antioxidant, anti‐inflammatory, and antihypoxia properties. Herein, we hypothesized that salidroside may alleviate hypoxia‐induced liver injury via antioxidant and antiinflammatory‐related pathways. A high‐altitude hypoxia animal model was established using hypobaric chamber. Male SD rats were randomly divided into the control group, hypoxia group, control +Sal group, and hypoxia +Sal group. Salidroside treatment significantly inhibited hypoxia‐induced increases of serum and hepatic pro‐inflammatory cytokines release, hepatic ROS production and MDA contents; attenuated hypoxia‐induced decrease of hepatic SOD, CAT, and GSH‐Px activities. Furthermore, salidroside treatment also potentiated the activation of Nrf2‐mediated anti‐oxidant pathway, as indicated by upregulation of n‐Nrf2 and its downstream HO‐1 and NQO‐1. In vitro study found that blocking the Nrf2 pathway using specific inhibitor ML385 significantly reversed the protective effect of salidroside on hypoxia‐induced liver oxidative stress. In addition, salidroside treatment significantly inhibited hepatic pro‐inflammatory cytokines release via JAK2/STAT3‐mediated pathway. Taken together, our findings suggested that salidroside protected against hypoxia‐induced hepatic oxidative stress and inflammation via Nrf2 and JAK2/STAT3 signaling pathways. Protective mechanisms of salidroside against hypoxia‐induced liver injury. Salidroside protected liver from hypoxia‐induced oxidative stress via the Nrf2 signaling pathway. The anti‐inflammatory effect of salidroside was dependent on the inhibition of the JAK2/STAT3 pathway combining with the activation of the Nrf2 pathway.
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影响因子：
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通讯作者：
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