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树胶树脂减轻肾毒性:肿瘤坏死因子-α、白细胞介素、转化生长因子-β和脂质过氧化的作用。

Gum Resin Mitigates Renal Toxicity: Role of TNF-α, Interleukins, TGF-β, and Lipid Peroxidation.

作者信息

Eltahir Heba M, Shalkami Abdel-Gawad S, Shehata Ahmed M, Almikhlafi Mohannad, Aldhafiri Ahmed J, Alalawi Ali, Albadrani Muayad, Mahmoud Ahmad Bakur, Abouzied Mekky M

机构信息

Department of Pharmacology and Toxicology (Biochemistry Subdivision), College of Pharmacy, Taibah University, Madinah 41411, Saudi Arabia.

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Assiut 71524, Egypt.

出版信息

Life (Basel). 2024 Dec 17;14(12):1669. doi: 10.3390/life14121669.

DOI:10.3390/life14121669
PMID:39768376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11676428/
Abstract

Being a central organ in homeostasis and maintaining the health of the biological system, kidneys are exposed to variable toxicants. Long-term exposure to nephrotoxic molecules causes chronic renal damage that causes fibrosis and loss of function. Such damage can be initiated by oxidative stress which provokes inflammation. We aim at investigating the potential therapeutic effects of Boswellia serrata (BS) gum resin extract in managing CCl-induced renal toxicity. Male Wistar albino rats were assigned to groups: healthy control; CCl-treated (CCl, twice/week, for 6 weeks); CCl + BS-treated: CCl for 6 weeks followed by BS (150 mg/kg/day) for 2 weeks; and CCl + Silymarin-treated: CCl for 6 weeks followed by Silymarin (100 mg/kg/day) for 2 weeks. Blood and kidney tissue were utilized to assess oxidative stress status, inflammatory cytokines, and histopathological changes. BS treatment ameliorated signs of renal damage and fibrosis as it improved renal antioxidant status and renal function markers and significantly reduced the levels of inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-8 along with the fibrogenic marker TGF-β. Kidney tissues showed improved histological features after BS treatment. BS gum resin extract has significant therapeutic potential against CCl-induced renal damage and fibrosis. These effects could be mediated via its previously reported antioxidant, free radical scavenging, and anti-inflammatory effects.

摘要

作为体内平衡的中心器官并维持生物系统的健康,肾脏会接触到各种有毒物质。长期接触肾毒性分子会导致慢性肾脏损伤,进而引起纤维化和功能丧失。这种损伤可由引发炎症的氧化应激启动。我们旨在研究乳香(BS)树胶树脂提取物在处理四氯化碳(CCl)诱导的肾毒性方面的潜在治疗效果。将雄性Wistar白化大鼠分为几组:健康对照组;CCl处理组(每周两次CCl,共6周);CCl + BS处理组:先进行6周的CCl处理,随后进行2周的BS(150毫克/千克/天)处理;以及CCl + 水飞蓟素处理组:先进行6周的CCl处理,随后进行2周的水飞蓟素(100毫克/千克/天)处理。利用血液和肾脏组织评估氧化应激状态、炎性细胞因子和组织病理学变化。BS处理改善了肾损伤和纤维化的迹象,因为它改善了肾脏抗氧化状态和肾功能标志物,并显著降低了炎性细胞因子TNF-α、IL-1β、IL-6和IL-8以及纤维化标志物TGF-β的水平。BS处理后肾脏组织的组织学特征有所改善。乳香树胶树脂提取物对CCl诱导的肾损伤和纤维化具有显著的治疗潜力。这些作用可能是通过其先前报道的抗氧化、自由基清除和抗炎作用介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/d6e00c34a8d3/life-14-01669-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/d7db23402c64/life-14-01669-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/3819a2582fb3/life-14-01669-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/447fe50d5e92/life-14-01669-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/20094e20d5f8/life-14-01669-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/ceba6f4346ca/life-14-01669-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/d6e00c34a8d3/life-14-01669-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/d7db23402c64/life-14-01669-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/3819a2582fb3/life-14-01669-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/447fe50d5e92/life-14-01669-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/20094e20d5f8/life-14-01669-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/ceba6f4346ca/life-14-01669-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447c/11676428/d6e00c34a8d3/life-14-01669-g006.jpg

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本文引用的文献

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Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl via Attenuation of Oxidative Stress and Inflammation.肽Phe-Leu-Ala-Pro通过减轻氧化应激和炎症对四氯化碳所致急性肝肾损伤的改善作用
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Prostaglandin E2 receptors as therapeutic targets in renal fibrosis.
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