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类黄酮补充剂对纳米材料诱导毒性的影响:临床前动物研究的荟萃分析

Effects of Flavonoid Supplementation on Nanomaterial-Induced Toxicity: A Meta-Analysis of Preclinical Animal Studies.

作者信息

Xie Dongli, Hu Jianchen, Wu Tong, Xu Wei, Meng Qingyang, Cao Kangli, Luo Xiaogang

机构信息

College of Textile and Clothing Engineering, Soochow University, Suzhou, China.

Shanghai Jing Rui Yang Industrial Co., Ltd, Shanghai, China.

出版信息

Front Nutr. 2022 Jun 14;9:929343. doi: 10.3389/fnut.2022.929343. eCollection 2022.

DOI:10.3389/fnut.2022.929343
PMID:35774549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9237539/
Abstract

BACKGROUND

Nanomaterials, widely applied in various fields, are reported to have toxic effects on human beings; thus, preventive or therapeutic measures are urgently needed. Given the anti-inflammatory and antioxidant activities, supplementation with flavonoids that are abundant in the human diet has been suggested as a potential strategy to protect against nanomaterial-induced toxicities. However, the beneficial effects of flavonoids remain inconclusive. In the present study, we performed a meta-analysis to comprehensively explore the roles and mechanisms of flavonoids for animals intoxicated with nanomaterials.

METHODS

A systematic literature search in PubMed, EMBASE, and Cochrane Library databases was performed up to April 2022. STATA 15.0 software was used for meta-analyses.

RESULTS

A total of 26 studies were identified. The results showed that flavonoid supplementation could significantly increase the levels of antioxidative enzymes (superoxide dismutase, catalase, glutathione, glutathione peroxidase, and glutathione-S-transferase), reduce the production of oxidative agents (malonaldehyde) and pro-inflammatory mediators (tumor necrosis factor-α, interleukin-6, IL-1β, C-reactive protein, immunoglobulin G, nitric oxide, vascular endothelial growth factor, and myeloperoxidase), and alleviate cell apoptosis (manifested by decreases in the mRNA expression levels of pro-apoptotic factors, such as caspase-3, Fas cell surface death receptor, and Bax, and increases in the mRNA expression levels of Bcl2), DNA damage (reductions in tail length and tail DNA%), and nanomaterial-induced injuries of the liver (reduced alanine aminotransferase and aspartate aminotransferase activities), kidney (reduced urea, blood urea nitrogen, creatinine, and uric acid concentration), testis (increased testosterone, sperm motility, 17β-hydroxysteroid dehydrogenase type, and reduced sperm abnormalities), and brain (enhanced acetylcholinesterase activities). Most of the results were not changed by subgroup analyses.

CONCLUSION

Our findings suggest that appropriate supplementation of flavonoids may be effective to prevent the occupational detriments resulting from nanomaterial exposure.

摘要

背景

纳米材料广泛应用于各个领域,据报道对人类具有毒性作用;因此,迫切需要预防或治疗措施。鉴于其抗炎和抗氧化活性,补充人类饮食中丰富的黄酮类化合物被认为是预防纳米材料诱导毒性的一种潜在策略。然而,黄酮类化合物的有益作用仍不明确。在本研究中,我们进行了一项荟萃分析,以全面探讨黄酮类化合物对纳米材料中毒动物的作用及其机制。

方法

截至2022年4月,在PubMed、EMBASE和Cochrane图书馆数据库中进行了系统的文献检索。使用STATA 15.0软件进行荟萃分析。

结果

共纳入26项研究。结果表明,补充黄酮类化合物可显著提高抗氧化酶(超氧化物歧化酶、过氧化氢酶、谷胱甘肽、谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶)水平,减少氧化剂(丙二醛)和促炎介质(肿瘤坏死因子-α、白细胞介素-6、IL-1β、C反应蛋白、免疫球蛋白G、一氧化氮、血管内皮生长因子和髓过氧化物酶)的产生,并减轻细胞凋亡(表现为促凋亡因子如半胱天冬酶-3、Fas细胞表面死亡受体和Bax的mRNA表达水平降低,以及Bcl2的mRNA表达水平升高)、DNA损伤(尾长和尾DNA%降低),以及纳米材料引起的肝脏损伤(丙氨酸转氨酶和天冬氨酸转氨酶活性降低)、肾脏损伤(尿素、血尿素氮、肌酐和尿酸浓度降低)、睾丸损伤(睾酮、精子活力、17β-羟类固醇脱氢酶升高,精子异常率降低)和脑损伤(乙酰胆碱酯酶活性增强)。大多数结果在亚组分析中未发生变化。

结论

我们的研究结果表明,适当补充黄酮类化合物可能有效地预防纳米材料暴露导致的职业危害。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/0bcbe7de1210/fnut-09-929343-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/35db016e8bc3/fnut-09-929343-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/c484afaadff0/fnut-09-929343-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/5f226697e461/fnut-09-929343-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/635c80b5e1ad/fnut-09-929343-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/243785e5bb26/fnut-09-929343-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/0efc9d105f1d/fnut-09-929343-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/d9c65aef6b12/fnut-09-929343-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/e230ee53e281/fnut-09-929343-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/0bcbe7de1210/fnut-09-929343-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/35db016e8bc3/fnut-09-929343-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/c484afaadff0/fnut-09-929343-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/5f226697e461/fnut-09-929343-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/635c80b5e1ad/fnut-09-929343-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/243785e5bb26/fnut-09-929343-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/0efc9d105f1d/fnut-09-929343-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/d9c65aef6b12/fnut-09-929343-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/e230ee53e281/fnut-09-929343-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b48/9237539/0bcbe7de1210/fnut-09-929343-g009.jpg

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