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利用负载于层状双氢氧化物上的橙皮苷纳米颗粒减轻大鼠扑热息痛所致肝毒性:生物转化、氧化应激、炎症和细胞凋亡的调控

Utilizing Nanoparticles of Hesperidin Loaded on Layered Double Hydroxide to Reduce Hepatotoxicity Caused by Paracetamol in Rats: Controlling of Biotransformation, Oxidative Stress, Inflammation, and Apoptosis.

作者信息

Shaban Deyaa A, El-Shahawy Ahmed A G, Zanaty Mohamed I, Eldin Zienab E, Abd-Elbaset Mohamed, Shams Anwar, Tamur Shadi, Ahmed Osama M

机构信息

Department of Biotechnology and Life Sciences, Faculty of Postgraduate Studies for Advanced Sciences (PSAS), Beni-Suef University, Beni-Suef 62511, Egypt.

Materials Science and Nanotechnology Department, Faculty of Postgraduate Studies for Advanced Sciences (PSAS), Beni-Suef University, Beni-Suef 62511, Egypt.

出版信息

Pharmaceutics. 2025 Mar 27;17(4):429. doi: 10.3390/pharmaceutics17040429.

DOI:10.3390/pharmaceutics17040429
PMID:40284423
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12030007/
Abstract

: The most used antipyretic and pain relief treatment is paracetamol (acetaminophen), also known as N-acetyl-para-aminophenol (APAP). However, it is considered potentially hazardous if consumed repeatedly in large doses or over prolonged periods. This investigation explores the effectiveness of hesperidin (Hesp) and Hesp loaded on layered double hydroxide nanoparticles (Hesp-NPs) in inhibiting the progression of acute hepatotoxicity in rats induced by APAP. : LDH-Hesp-NPs were prepared and characterized. Male Wistar rats were orally treated with Hesp and Hesp-NPs at the same adjusted dose (100 mg/kg) every other day for six weeks. After 2 h of the first doses of Hesp and Hesp-NPs, the rats received one oral dose of APAP (750 mg/kg). : Administering of Hesp and Hesp-NPs to APAP-treated rats significantly reduced oxidant parameter (malondialdehyde) and serum enzymes (ALT, AST, LDH, and ALP) associated with liver function. Antioxidant markers in the liver, such as catalase and glutathione, also increased notably. Moreover, Hesp and Hesp-NPs enhanced the mRNA expression of liver , , and . Conversely, the mRNA expressions of liver , , , , and decreased. These improvements in biochemical and molecular markers were corroborated by liver histopathology. : Hesp and Hesp-NPs protect significantly against APAP-induced hepatotoxicity in male Wistar rats. Hesp-NPs treatment was more potent. The protective effects may be mediated modulation of APAP biotransformation, oxidative stress, inflammation and apoptosis.

摘要

最常用的解热镇痛治疗药物是对乙酰氨基酚(扑热息痛),也称为N - 乙酰 - 对氨基苯酚(APAP)。然而,如果大剂量反复服用或长期服用,它被认为具有潜在危险性。本研究探讨了橙皮苷(Hesp)和负载于层状双氢氧化物纳米颗粒上的橙皮苷(Hesp - NPs)在抑制APAP诱导的大鼠急性肝毒性进展方面的有效性。:制备并表征了LDH - Hesp - NPs。雄性Wistar大鼠每隔一天以相同调整剂量(100 mg/kg)口服Hesp和Hesp - NPs,持续六周。在首次给予Hesp和Hesp - NPs 2小时后,大鼠口服一剂APAP(750 mg/kg)。:给APAP处理的大鼠施用Hesp和Hesp - NPs显著降低了与肝功能相关的氧化参数(丙二醛)和血清酶(ALT、AST、LDH和ALP)。肝脏中的抗氧化标志物,如过氧化氢酶和谷胱甘肽,也显著增加。此外,Hesp和Hesp - NPs增强了肝脏、和的mRNA表达。相反,肝脏、、、和的mRNA表达下降。肝脏组织病理学证实了这些生化和分子标志物的改善。:Hesp和Hesp - NPs对雄性Wistar大鼠中APAP诱导的肝毒性具有显著的保护作用。Hesp - NPs治疗效果更强。其保护作用可能通过调节APAP生物转化、氧化应激、炎症和细胞凋亡来介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/1cb65f9e9752/pharmaceutics-17-00429-g012.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/3cad1de648d4/pharmaceutics-17-00429-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/63c4831cf640/pharmaceutics-17-00429-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/9773de715133/pharmaceutics-17-00429-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/ab1ef03ce9ee/pharmaceutics-17-00429-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/a8e422d8791b/pharmaceutics-17-00429-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/5c96935abd15/pharmaceutics-17-00429-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/9cf65e58e646/pharmaceutics-17-00429-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/1cb65f9e9752/pharmaceutics-17-00429-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/4bb79b0b5e75/pharmaceutics-17-00429-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/c5775f070d55/pharmaceutics-17-00429-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/d077c1d5decc/pharmaceutics-17-00429-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/fb1bdd6b7663/pharmaceutics-17-00429-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/b39ca7062416/pharmaceutics-17-00429-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/3cad1de648d4/pharmaceutics-17-00429-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/63c4831cf640/pharmaceutics-17-00429-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/9773de715133/pharmaceutics-17-00429-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/ab1ef03ce9ee/pharmaceutics-17-00429-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/a8e422d8791b/pharmaceutics-17-00429-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/5c96935abd15/pharmaceutics-17-00429-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/9cf65e58e646/pharmaceutics-17-00429-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7541/12030007/1cb65f9e9752/pharmaceutics-17-00429-g012.jpg

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