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首页> 外文期刊>The Journal of Nutritional Biochemistry >Ursolic acid alleviates heat stress-induced lung injury by regulating endoplasmic reticulum stress signaling in mice
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Ursolic acid alleviates heat stress-induced lung injury by regulating endoplasmic reticulum stress signaling in mice

机译：熊糖酸通过调节小鼠中的内质网胁迫信号传导来减轻热应激诱导的肺损伤

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Acute lung injury has been reported to be associated with heat stress in various animals. Ursolic acid is a natural pentacyclic triterpenoid compound with multiple bioactivities. However, it remains unknown whether ursolic acid supplementation alleviates heat stress-induced lung injury. In the present study, male Institute of Cancer Research mice were left untreated under a normal temperature condition (23 +/- 1 degrees C), receiving orally administrated with vehicle (phosphate buffered saline) or ursolic acid (40 mg/kg BW -1.d -1 for 2 d), and then were subjected to high temperature (41 +/- 1 degrees C) for 2 h. Histological alterations, activities of antioxidative enzymes, apoptosis, generation of reactive oxygen species, abundance of inflammatory cytokines, and endoplasmic reticulum stress-related proteins were analyzed. Compared with the controls, heat stress treatment led to enhanced apoptosis, increased H2O2 production, and upregulated protein levels of inflammatory cytokines in the serum, including tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta. Activities of malondialdehyde, lactate dehydrogenase, and myeloperoxidase were increased, while the activities for superoxide dismutase and catalase were reduced in lung tissues of mice. All these alterations were significantly prevented by ursolic acid administration. Further study showed that heat stress led to activation of protein kinase-like ER kinase eukaryotic initiation factor 2 alpha-the transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP) signaling, which was attenuated by ursolic acid supplementation. These findings indicated that ursolic acid pretreatment protected lung tissues against heat stress-induced injury by regulating inflammatory cytokines and unfolded protein response in mice. Ursolic acid supplementation might be a therapeutic strategy to alleviate high temperature-induced lung injury in humans and animals. (c) 2020 Elsevier Inc. All rights reserved.
机译：据报道，急性肺损伤与各种动物的热应激有关。熊果酸是一种具有多种生物活性的天然五环三萜化合物。然而，补充熊果酸是否能减轻热应激诱导的肺损伤尚不清楚。在本研究中，雄性癌症研究所小鼠在常温（23+/-1摄氏度）条件下未经治疗，口服溶媒（磷酸盐缓冲盐水）或熊果酸（40毫克/千克体重-1.d-1，持续2天），然后在高温（41+/-1摄氏度）下2小时。组织学变化、抗氧化酶活性，分析细胞凋亡、活性氧生成、炎性细胞因子和内质网应激相关蛋白。与对照组相比，热应激治疗导致细胞凋亡增强，H2O2生成增加，血清中炎性细胞因子（包括肿瘤坏死因子α、白细胞介素-6和白细胞介素-1β）的蛋白水平上调。小鼠肺组织丙二醛、乳酸脱氢酶和髓过氧化物酶活性升高，而超氧化物歧化酶和过氧化氢酶活性降低。所有这些改变都被熊果酸给药显著阻止。进一步的研究表明，热应激导致蛋白激酶样内质网激酶真核启动因子2α（转录因子CCAAT增强子结合蛋白同源蛋白（CHOP）信号传导）的激活，补充熊果酸可使其减弱。这些结果表明，熊果酸预处理通过调节炎症细胞因子和未折叠蛋白反应保护小鼠肺组织免受热应激诱导的损伤。补充熊果酸可能是缓解人类和动物高温诱导的肺损伤的一种治疗策略。（c） 2020爱思唯尔公司版权所有。

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