Qianfeng Chen, Yuxia Zhong, Bohan Li, Yucong Feng, Yuandie Zhang, Tao Wei, Margaret Zaitoun, Shuang Rong, Hua Wan, Qing Feng
{"title":"丙烯醛通过 AMPK/SIRT1-CLOCK/BMAL1 通路诱发动脉粥样硬化以及间歇性禁食的保护作用","authors":"Qianfeng Chen, Yuxia Zhong, Bohan Li, Yucong Feng, Yuandie Zhang, Tao Wei, Margaret Zaitoun, Shuang Rong, Hua Wan, Qing Feng","doi":"10.7555/JBR.38.20240025","DOIUrl":null,"url":null,"abstract":"<p><p>Circadian clock plays a vital role in the pathological progression of cardiovascular disease (CVD). Our previous studies showed that acrolein, an environmental pollutant, promoted atherosclerosis by reducing CLOCK/BMAL1 and disturbing circadian rhythm. Whereas, intermittent fasting (IF), a diet pattern, was able to ameliorate acrolein-induced atherosclerosis. <i>In vivo</i>, mice were fed acrolein 3 mg/kg/day <i>via</i> drinking water and IF for 18h (0:00-18:00). We observed that IF decreased acrolein-accelerated the formation of aortic lesion in <i>ApoE</i> <sup>-/-</sup> mice. Up-regulation of <i>NF-κB, IL-1β</i> and <i>TNF-α</i> levels were found in liver and heart tissue upon acrolein exposure, while was down-regulated by IF. Interestingly, IF treatment exhibited higher AMPK, p-AMPK and SIRT1and lower MAPK expression which was caused by acrolein. Besides, circadian genes <i>Clock/ Bmal1</i> expression were suppressed and disturbed treated with acrolein, while were reversed by IF. Furthermore, consistent with that <i>in vivo</i>, short-term starvation as a fasting cell model <i>in vitro</i> could improve the disorders of CLOCK/BMAL1 and raised SIRT1 <i>via</i> regulating AMPK, as well as ROS-MAPK induced by acrolein. In conclusion, we demonstrated that IF repressed ROS-MAPK while activated AMPK to elevate the expression of circadian clock genes to ameliorate acrolein-induced atherogenesis, which shed a novel light to prevent cardiovascular diseases.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-15"},"PeriodicalIF":2.2000,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Acrolein-triggered atherosclerosis <i>via</i> AMPK/SIRT1-CLOCK/BMAL1 pathway and a protection from intermittent fasting.\",\"authors\":\"Qianfeng Chen, Yuxia Zhong, Bohan Li, Yucong Feng, Yuandie Zhang, Tao Wei, Margaret Zaitoun, Shuang Rong, Hua Wan, Qing Feng\",\"doi\":\"10.7555/JBR.38.20240025\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Circadian clock plays a vital role in the pathological progression of cardiovascular disease (CVD). Our previous studies showed that acrolein, an environmental pollutant, promoted atherosclerosis by reducing CLOCK/BMAL1 and disturbing circadian rhythm. Whereas, intermittent fasting (IF), a diet pattern, was able to ameliorate acrolein-induced atherosclerosis. <i>In vivo</i>, mice were fed acrolein 3 mg/kg/day <i>via</i> drinking water and IF for 18h (0:00-18:00). We observed that IF decreased acrolein-accelerated the formation of aortic lesion in <i>ApoE</i> <sup>-/-</sup> mice. Up-regulation of <i>NF-κB, IL-1β</i> and <i>TNF-α</i> levels were found in liver and heart tissue upon acrolein exposure, while was down-regulated by IF. Interestingly, IF treatment exhibited higher AMPK, p-AMPK and SIRT1and lower MAPK expression which was caused by acrolein. Besides, circadian genes <i>Clock/ Bmal1</i> expression were suppressed and disturbed treated with acrolein, while were reversed by IF. Furthermore, consistent with that <i>in vivo</i>, short-term starvation as a fasting cell model <i>in vitro</i> could improve the disorders of CLOCK/BMAL1 and raised SIRT1 <i>via</i> regulating AMPK, as well as ROS-MAPK induced by acrolein. In conclusion, we demonstrated that IF repressed ROS-MAPK while activated AMPK to elevate the expression of circadian clock genes to ameliorate acrolein-induced atherogenesis, which shed a novel light to prevent cardiovascular diseases.</p>\",\"PeriodicalId\":15061,\"journal\":{\"name\":\"Journal of Biomedical Research\",\"volume\":\" \",\"pages\":\"1-15\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2024-05-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biomedical Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.7555/JBR.38.20240025\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomedical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.7555/JBR.38.20240025","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Acrolein-triggered atherosclerosis via AMPK/SIRT1-CLOCK/BMAL1 pathway and a protection from intermittent fasting.
Circadian clock plays a vital role in the pathological progression of cardiovascular disease (CVD). Our previous studies showed that acrolein, an environmental pollutant, promoted atherosclerosis by reducing CLOCK/BMAL1 and disturbing circadian rhythm. Whereas, intermittent fasting (IF), a diet pattern, was able to ameliorate acrolein-induced atherosclerosis. In vivo, mice were fed acrolein 3 mg/kg/day via drinking water and IF for 18h (0:00-18:00). We observed that IF decreased acrolein-accelerated the formation of aortic lesion in ApoE-/- mice. Up-regulation of NF-κB, IL-1β and TNF-α levels were found in liver and heart tissue upon acrolein exposure, while was down-regulated by IF. Interestingly, IF treatment exhibited higher AMPK, p-AMPK and SIRT1and lower MAPK expression which was caused by acrolein. Besides, circadian genes Clock/ Bmal1 expression were suppressed and disturbed treated with acrolein, while were reversed by IF. Furthermore, consistent with that in vivo, short-term starvation as a fasting cell model in vitro could improve the disorders of CLOCK/BMAL1 and raised SIRT1 via regulating AMPK, as well as ROS-MAPK induced by acrolein. In conclusion, we demonstrated that IF repressed ROS-MAPK while activated AMPK to elevate the expression of circadian clock genes to ameliorate acrolein-induced atherogenesis, which shed a novel light to prevent cardiovascular diseases.