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丁香油通过抗氧化、抗炎和抗凋亡机制减轻镉诱导的肝肾毒性的治疗潜力

Therapeutic Potential of Clove Oil in Mitigating Cadmium-Induced Hepatorenal Toxicity Through Antioxidant, Anti-Inflammatory, and Antiapoptotic Mechanisms.

作者信息

Elgharib Inas M, Abdelhamid Fatma M, Elshopakey Gehad E, Sembawa Hatem, Albukhari Talat A, Filimban Waheed A, Bagadood Rehab M, El-Boshy Mohamed E, Risha Engy F

机构信息

Department of Clinical Pathology, Faculty of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt.

Department of Veterinary Diseases, Faculty of Veterinary Medicine, Delta University for Science and Technology, Gamasa 35712, Egypt.

出版信息

Pharmaceuticals (Basel). 2025 Jan 14;18(1):94. doi: 10.3390/ph18010094.

DOI:10.3390/ph18010094
PMID:39861156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11768416/
Abstract

UNLABELLED

Hazardous heavy metals, particularly cadmium (Cd), are widely distributed in the environment and cause oxidative stress in various animal and human organs. Clove oil (CLO), a common aromatic spice, has been used as a traditional medication as it has potent anti-inflammatory, antioxidant, and hepatoprotective properties.

BACKGROUND/OBJECTIVES: This study aimed to investigate the antioxidant, antiapoptotic, and anti-inflammatory effects of clove oil (CLO) against hepatorenal toxicity induced by cadmium (Cd).

METHODS

Twenty rats were equally divided into four groups: a control group, a Cd group treated with 15 mg/kg b.wt CdCl, a CLO group administered 200 mg/kg b.wt CLO, and a Cd+CLO group. All groups were orally treated for 4 weeks.

RESULTS

Cadmium (Cd) exposure caused anemia and hepatorenal damage, as evidenced by increased serum levels of urea, creatinine, uric acid, total bilirubin (including its direct and indirect fractions), and elevated activities of liver enzymes such as alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). However, total protein and albumin levels decreased. Furthermore, there was a decrease in the levels of glutathione, glutathione transferase, and catalase in the liver antioxidant profiles. Meanwhile, malondialdehyde levels increased. Cadmium toxicity caused elevated expression of liver apoptosis markers, such as tumor necrosis factor-alpha (TNF-α) and caspase-3, and inflammation. CLO ameliorated the oxidative effects of Cd through decreasing urea (27.4%), creatinine (41.6%), liver enzymes, and hepatic apoptotic markers while increasing levels of total protein, albumin, and hepatic values of SOD (60.37%), CAT (64.49%), GSH (50.41%), and GST (9.16%).

CONCLUSIONS

Hematological and biochemical parameters, as well as the antioxidant system, improved following clove oil treatment, leading to a reduction in hepatorenal damage. Therefore, it is possible to conclude that CLO protects rats from inflammation, apoptosis, and hepatorenal oxidative damage caused by Cd poisoning. Comprehensive translational research is required to validate CLO's efficacy and safety of use in humans. Future studies should focus on elucidating the precise molecular mechanisms, optimal dosing strategies, and potential synergistic effects of CLO with other therapeutic agents.

摘要

未标记

有害重金属,尤其是镉(Cd),广泛分布于环境中,并在各种动物和人体器官中引起氧化应激。丁香油(CLO)是一种常见的芳香香料,因其具有强大的抗炎、抗氧化和肝脏保护特性,已被用作传统药物。

背景/目的:本研究旨在探讨丁香油(CLO)对镉(Cd)诱导的肝肾毒性的抗氧化、抗凋亡和抗炎作用。

方法

将20只大鼠平均分为四组:对照组、用15mg/kg体重CdCl处理的Cd组、给予200mg/kg体重CLO的CLO组和Cd + CLO组。所有组均口服给药4周。

结果

镉(Cd)暴露导致贫血和肝肾损伤,血清尿素、肌酐、尿酸、总胆红素(包括其直接和间接组分)水平升高以及丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和碱性磷酸酶(ALP)等肝酶活性升高证明了这一点。然而,总蛋白和白蛋白水平下降。此外,肝脏抗氧化谱中的谷胱甘肽、谷胱甘肽转移酶和过氧化氢酶水平降低。同时,丙二醛水平升高。镉毒性导致肝脏凋亡标志物如肿瘤坏死因子-α(TNF-α)和半胱天冬酶-3的表达升高以及炎症。CLO通过降低尿素(27.4%)、肌酐(41.6%)、肝酶和肝脏凋亡标志物,同时提高总蛋白、白蛋白水平以及肝脏超氧化物歧化酶(SOD,60.37%)、过氧化氢酶(CAT,64.49%)、谷胱甘肽(GSH,50.41%)和谷胱甘肽转移酶(GST,9.16%)的值,改善了Cd的氧化作用。

结论

丁香油治疗后血液学和生化参数以及抗氧化系统得到改善,导致肝肾损伤减轻。因此,可以得出结论,CLO可保护大鼠免受Cd中毒引起的炎症、凋亡和肝肾氧化损伤。需要进行全面的转化研究以验证CLO在人体中的疗效和使用安全性。未来的研究应侧重于阐明CLO的确切分子机制、最佳给药策略以及CLO与其他治疗药物的潜在协同作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba94/11768416/82068dd1e723/pharmaceuticals-18-00094-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba94/11768416/69945e0648c9/pharmaceuticals-18-00094-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba94/11768416/82068dd1e723/pharmaceuticals-18-00094-g007.jpg

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