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Protective Effects of Crocetin on Arsenic Trioxide-Induced Hepatic Injury: Involvement of Suppression in Oxidative Stress and Inflammation Through Activation of Nrf2 Signaling Pathway in Rats.
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-05-19 , DOI: 10.2147/dddt.s247947 Yanshuang Liu 1, 2 , Yingran Liang 3 , Bin Zheng 3 , Li Chu 3 , Donglai Ma 3 , Hongfang Wang 3 , Xi Chu 4 , Jianping Zhang 2, 5
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-05-19 , DOI: 10.2147/dddt.s247947 Yanshuang Liu 1, 2 , Yingran Liang 3 , Bin Zheng 3 , Li Chu 3 , Donglai Ma 3 , Hongfang Wang 3 , Xi Chu 4 , Jianping Zhang 2, 5
Affiliation
Purpose: Arsenic trioxide (ATO) has been shown to induce hepatic injury. Crocetin is a primary constituent of saffron, which has been verified to have antioxidant and anti-inflammatory effects. In the current experiment, we evaluated the efficacy of crocetin against ATO-induced hepatic injury and explored the potential molecular mechanisms in rats.
Methods: Rats were pretreated with 25 or 50 mg/kg crocetin 6 h prior to treating with 5 mg/kg ATO to induce hepatic injury daily for 7 days.
Results: Treatment with crocetin attenuated ATO-induced body weight loss, decreases in food and water consumption, and improved ATO-induced hepatic pathological damage. Crocetin significantly inhibited ATO-induced alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) increases. Crocetin prevented ATO-induced liver malondialdehyde (MDA) and reactive oxygen species (ROS) levels. Crocetin abrogated the ATO-induced decrease of catalase (CAT) and superoxide dismutase (SOD) activity. Crocetin was found to significantly restore the protein levels of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-alpha (TNF-α). Furthermore, crocetin promoted the expression of nuclear factor erythroid 2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NADP(H): quinone oxidoreductase 1 (NQO1).
Conclusion: These findings suggest that crocetin ameliorates ATO-induced hepatic injury in rats. In addition, the effect of crocetin might be related to its role in antioxidant stress, as an anti-inflammatory agent, and in regulating the Nrf2 signaling pathway.
Keywords: crocetin, arsenic trioxide, hepatotoxicity, oxidative stress, inflammation, Nrf2 signaling pathway
中文翻译：
藏红花素对三氧化二砷引起的肝损伤的保护作用：通过激活大鼠 Nrf2 信号通路参与抑制氧化应激和炎症。
目的：三氧化二砷 (ATO) 已被证明可诱发肝损伤。藏红花素是藏红花的主要成分，已被证实具有抗氧化和抗炎作用。在目前的实验中，我们评估了藏红花素对 ATO 诱导的肝损伤的疗效，并探索了大鼠潜在的分子机制。
方法：大鼠用 25 或 50 mg/kg 藏红花素预处理 6 小时，然后每天用 5 mg/kg ATO 诱导肝损伤，持续 7 天。
结果：藏红花素治疗可减轻 ATO 引起的体重减轻、食物和水消耗减少，并改善 ATO 引起的肝脏病理损伤。Crocetin 显着抑制 ATO 诱导的丙氨酸氨基转移酶 (ALT)、天冬氨酸氨基转移酶 (AST) 和碱性磷酸酶 (ALP) 增加。Crocetin 可防止 ATO 诱导的肝脏丙二醛 (MDA) 和活性氧 (ROS) 水平。Crocetin 消除了 ATO 诱导的过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 活性的降低。Crocetin 被发现可显着恢复白细胞介素 6 (IL-6)、白细胞介素 1β (IL-1β) 和肿瘤坏死因子-α (TNF-α) 的蛋白质水平。此外，藏红花素促进核因子红细胞2相关因子2（Nrf2）、血红素加氧酶1（HO-1）和NADP（H）：醌氧化还原酶1（NQO1）的表达。
结论：这些发现表明藏红花素可改善 ATO 诱导的大鼠肝损伤。此外，藏红花素的作用可能与其在抗氧化应激、抗炎剂和调节 Nrf2 信号通路中的作用有关。
关键词：藏红花素，三氧化二砷，肝毒性，氧化应激，炎症，Nrf2信号通路
更新日期：2020-05-19
Methods: Rats were pretreated with 25 or 50 mg/kg crocetin 6 h prior to treating with 5 mg/kg ATO to induce hepatic injury daily for 7 days.
Results: Treatment with crocetin attenuated ATO-induced body weight loss, decreases in food and water consumption, and improved ATO-induced hepatic pathological damage. Crocetin significantly inhibited ATO-induced alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) increases. Crocetin prevented ATO-induced liver malondialdehyde (MDA) and reactive oxygen species (ROS) levels. Crocetin abrogated the ATO-induced decrease of catalase (CAT) and superoxide dismutase (SOD) activity. Crocetin was found to significantly restore the protein levels of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-alpha (TNF-α). Furthermore, crocetin promoted the expression of nuclear factor erythroid 2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NADP(H): quinone oxidoreductase 1 (NQO1).
Conclusion: These findings suggest that crocetin ameliorates ATO-induced hepatic injury in rats. In addition, the effect of crocetin might be related to its role in antioxidant stress, as an anti-inflammatory agent, and in regulating the Nrf2 signaling pathway.
Keywords: crocetin, arsenic trioxide, hepatotoxicity, oxidative stress, inflammation, Nrf2 signaling pathway
中文翻译：
藏红花素对三氧化二砷引起的肝损伤的保护作用：通过激活大鼠 Nrf2 信号通路参与抑制氧化应激和炎症。
目的：三氧化二砷 (ATO) 已被证明可诱发肝损伤。藏红花素是藏红花的主要成分，已被证实具有抗氧化和抗炎作用。在目前的实验中，我们评估了藏红花素对 ATO 诱导的肝损伤的疗效，并探索了大鼠潜在的分子机制。
方法：大鼠用 25 或 50 mg/kg 藏红花素预处理 6 小时，然后每天用 5 mg/kg ATO 诱导肝损伤，持续 7 天。
结果：藏红花素治疗可减轻 ATO 引起的体重减轻、食物和水消耗减少，并改善 ATO 引起的肝脏病理损伤。Crocetin 显着抑制 ATO 诱导的丙氨酸氨基转移酶 (ALT)、天冬氨酸氨基转移酶 (AST) 和碱性磷酸酶 (ALP) 增加。Crocetin 可防止 ATO 诱导的肝脏丙二醛 (MDA) 和活性氧 (ROS) 水平。Crocetin 消除了 ATO 诱导的过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 活性的降低。Crocetin 被发现可显着恢复白细胞介素 6 (IL-6)、白细胞介素 1β (IL-1β) 和肿瘤坏死因子-α (TNF-α) 的蛋白质水平。此外，藏红花素促进核因子红细胞2相关因子2（Nrf2）、血红素加氧酶1（HO-1）和NADP（H）：醌氧化还原酶1（NQO1）的表达。
结论：这些发现表明藏红花素可改善 ATO 诱导的大鼠肝损伤。此外，藏红花素的作用可能与其在抗氧化应激、抗炎剂和调节 Nrf2 信号通路中的作用有关。
关键词：藏红花素，三氧化二砷，肝毒性，氧化应激，炎症，Nrf2信号通路
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