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姜黄素对动物模型中肥胖诱导的多器官生化和组织病理学异常的抗毒作用。

Antitoxic Effects of Curcumin against Obesity-Induced Multi-Organs' Biochemical and Histopathological Abnormalities in an Animal Model.

作者信息

Hassan Mohammed H, Awadalla Eatemad A, Abd El-Kader Abd El-Kader M, Seifeldin Esraa A, Mahmoud Marwa Ahmed, Muddathir Abdel Rahim Mahmoud, Abdelsadik Ahmed

机构信息

Department of Medical Biochemistry, Faculty of Medicine, South Valley University, Qena 83523, Egypt.

Department of Zoology, Faculty of Science, Aswan University, Aswan 81528, Egypt.

出版信息

Evid Based Complement Alternat Med. 2022 Oct 6;2022:9707278. doi: 10.1155/2022/9707278. eCollection 2022.

DOI:10.1155/2022/9707278
PMID:36248416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9560822/
Abstract

BACKGROUND

Obesity is a significant public health problem that is characterized by an increase in oxidative stress and enhanced inflammatory responses associated with immune cell invasion of adipose tissues. This study assessed several biochemical abnormalities, apoptosis, oxidative stress status, and associated histological changes in the liver, duodenum, and heart brought on by high-fat diet-induced obesity in rats. It also assessed the mechanistic benefits of curcumin in reversing these inflammatory, metabolic, and histological impairments.

METHODS

Rats were assigned into three groups each including ten rats: the control group (CD), the high-fat diet group (HFD), and the high-fat diet + curcumin (HFDC) group. Serum glucose, insulin, and triglycerides (TAGs) were observed. In addition, apoptosis (indicated by hepatic DNA fragmentation) and oxidative stress status (indicated by hepatic MPO, GSH, and SOD) were assessed. Histopathological examinations included the GIT (liver and duodenum) and heart in addition to quantitative real-time polymerase chain reaction (qRT-PCR) assays of the adipose tissue genetic expressions for inflammatory signaling pathways (TLR4, IL-6, and TNF-).

RESULTS

The overall findings showed that the HFD group exhibited significantly higher levels of glucose, TAGs, and insulin than the control group ( < 0.01). The histological abnormalities of the studied organs in the HFD group were paralleled by these biochemical abnormalities, which were strongly associated with increased apoptosis, increased oxidative stress, and increased expression of the inflammatory signaling markers. There were significant improvements in the HFDC group in terms of biochemical, inflammatory, and histological investigations.

CONCLUSIONS

This study's findings concluded that obesity is significantly associated with biochemical and microscopic alterations in many organs. Curcumin exerted potent antitoxic, antioxidant, tissue-protective, and antiobesity effects. Curcumin is recommended to be added to various dietary regimens to prevent or delay the organs' dysfunction among obese people.

摘要

背景

肥胖是一个重大的公共卫生问题,其特征是氧化应激增加以及与脂肪组织免疫细胞浸润相关的炎症反应增强。本研究评估了高脂饮食诱导的大鼠肥胖所导致的肝脏、十二指肠和心脏的几种生化异常、细胞凋亡、氧化应激状态以及相关的组织学变化。它还评估了姜黄素在逆转这些炎症、代谢和组织学损伤方面的机制性益处。

方法

将大鼠分为三组,每组十只:对照组(CD)、高脂饮食组(HFD)和高脂饮食+姜黄素组(HFDC)。观察血清葡萄糖、胰岛素和甘油三酯(TAGs)。此外,评估细胞凋亡(以肝脏DNA片段化表示)和氧化应激状态(以肝脏MPO、GSH和SOD表示)。组织病理学检查包括胃肠道(肝脏和十二指肠)和心脏,以及对脂肪组织炎症信号通路(TLR4、IL-6和TNF-)基因表达的定量实时聚合酶链反应(qRT-PCR)检测。

结果

总体研究结果表明,HFD组的葡萄糖、TAGs和胰岛素水平显著高于对照组(<0.01)。HFD组所研究器官的组织学异常与这些生化异常并行,这些生化异常与细胞凋亡增加、氧化应激增加以及炎症信号标志物表达增加密切相关。HFDC组在生化、炎症和组织学研究方面有显著改善。

结论

本研究结果得出结论,肥胖与许多器官的生化和微观改变显著相关。姜黄素具有强大的抗毒、抗氧化、组织保护和抗肥胖作用。建议在各种饮食方案中添加姜黄素,以预防或延缓肥胖人群器官功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/96e682a7bdab/ECAM2022-9707278.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/e6bd76e9ef74/ECAM2022-9707278.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/2c5850a01351/ECAM2022-9707278.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/12ecc8af64de/ECAM2022-9707278.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/03d49bbc806b/ECAM2022-9707278.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/96e682a7bdab/ECAM2022-9707278.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/e6bd76e9ef74/ECAM2022-9707278.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/2c5850a01351/ECAM2022-9707278.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/12ecc8af64de/ECAM2022-9707278.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/03d49bbc806b/ECAM2022-9707278.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76e5/9560822/96e682a7bdab/ECAM2022-9707278.005.jpg

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