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肉桂醛对脂多糖诱导的小鼠肝炎症反应、氧化应激和细胞凋亡的保护作用。

Protective Effects of Cinnamaldehyde on the Inflammatory Response, Oxidative Stress, and Apoptosis in Liver of -Challenged Mice.

机构信息

State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing 100193, China.

DadHank Biotechnology Corporation, Chengdu 611130, China.

出版信息

Molecules. 2021 Apr 16;26(8):2309. doi: 10.3390/molecules26082309.

Abstract

infection is associated with gastrointestinal disorder and cellular injury in the liver of both humans and animals. Cinnamaldehyde, the main component of essential oil from cinnamon, has been reported to have anti-inflammatory, anti-oxidative, and anti-apoptotic effects. However, it remains unknown whether cinnamaldehyde can alleviate infection-induced liver injury in mice. In the present study, we found that cinnamaldehyde attenuated -induced body weight loss, the increase of organ (liver and spleen) indexes, hepatocyte apoptosis, and the mortality rate in mice. Further study showed that cinnamaldehyde significantly alleviated -induced liver injury as shown by activities of alanine transaminase, aspartate transaminase, and myeloperoxidase, as well as malondialdehyde. The increased mRNA level of pro-inflammatory cytokines (, , , and ) and chemokines ( and ) induced by were significantly abolished by cinnamaldehyde supplementation. These alterations were associated with a regulatory effect of cinnamaldehyde on , , and . 16S rDNA sequence analysis showed that infection led to upregulation of the abundances of genera , , , , and , and downregulation of the abundances of genera , , and (unclassified). These alterations were reversed by cinnamaldehyde supplementation. In conclusion, cinnamaldehyde attenuated the inflammatory response, oxidative stress, and apoptosis in the liver of -infected mice. Supplementation of cinnamaldehyde might be a preventive strategy to alleviate liver injury caused by infection in humans and animals.

摘要

感染与人类和动物的胃肠道紊乱和肝损伤有关。肉桂醛是肉桂精油的主要成分,已被报道具有抗炎、抗氧化和抗细胞凋亡作用。然而,肉桂醛是否能减轻感染诱导的小鼠肝损伤仍不清楚。在本研究中,我们发现肉桂醛可减轻感染引起的体重减轻、器官(肝和脾)指数增加、肝细胞凋亡和死亡率。进一步的研究表明,肉桂醛可显著减轻感染引起的肝损伤,如丙氨酸转氨酶、天冬氨酸转氨酶和髓过氧化物酶活性以及丙二醛水平升高。肉桂醛可显著抑制 诱导的促炎细胞因子(、、、和)和趋化因子(和)的 mRNA 水平升高。这些变化与肉桂醛对、和的调节作用有关。16S rDNA 序列分析显示,感染导致属的丰度上调,属的丰度下调,包括 、 、 、 、 和 (未分类)。这些变化可通过肉桂醛补充来逆转。总之,肉桂醛可减轻感染小鼠肝脏的炎症反应、氧化应激和细胞凋亡。肉桂醛的补充可能是预防人类和动物感染引起肝损伤的一种策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a75/8073330/b95660f6a477/molecules-26-02309-g001.jpg

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