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森氏短猛蚁(Brachyponera sennaarensis)毒液对四氯化碳体内毒性中TNF-α/NF-κB介导的炎症的潜在影响。

Potential effects of samsum ant, Brachyponera sennaarensis, venom on TNF-α/NF-κB mediated inflammation in CCL4-toxicity in vivo.

作者信息

Al-Tamimi Jameel, Alhazza Ibrahim M, Al-Khalifa Mohamed, Metwalli Ali, Rady Ahmed, Ebaid Hossam

机构信息

Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.

Department of Food Science, College of Agriculture and Food Science, King Saud University, Riyadh, Saudi Arabia.

出版信息

Lipids Health Dis. 2016 Nov 18;15(1):198. doi: 10.1186/s12944-016-0364-7.

DOI:10.1186/s12944-016-0364-7
PMID:27863485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5116174/
Abstract

BACKGROUND

Ant venom shows antimicrobial, anti-parasitic and anti-inflammatory activities, both in vitro and in vivo. Our recent studies have confirmed the role of samsum ant venom (SAV) as a powerful antioxidant. This study aimed to investigate whether SAV as a potential treatment for CCl4-induced acute liver toxicity in an animal (rat) model.

METHODS

Thirty-two rats were assigned into four groups; the first one served as the control. The second group received a single dose of 1 ml/kg CCl in a 1:1 ratio with olive oil through an intraperitoneal injection. The third group received a single dose of 1 ml/kg CCl and then treated with SAV at a dose of 100 μg SAV twice a week for three weeks. The fourth group received a dose of 100 μg SAV only twice a week for three weeks. ELISA, RT-PCR and histopathological examinations were applied.

RESULTS

Results showed that antioxidant enzymes were significantly reduced in the diseased animals. SAV was found to significantly restore the oxidative stability in diseased animals. ELISA estimation and RT-PCR analysis also showed significant upregulation of both nuclear factor (κB) NF-κB and inhibitor (κB) IκB, respectively, in the diseased animals compared to the normal ones. The expression of tumour necrosis factor alpha (TNF-α) and pro-apoptotic receptor (Fas) were also significantly up-regulated in the diseased rats. Interestingly, SAV was found to significantly restore NF-κB, IκB and TNF-α in the diseased rats to the normal values. As a result, liver enzymes, serum proteins and lipid concentrations were significantly improved by SAV in CCl4-animals in comparison with the control ones. Moreover, SAV obviously improved the hepatic tissues of the same group was.

CONCLUSION

SAV treatment restores the normal biochemical and oxidative stability by improving the TNF-α/NF-κB mediated inflammation in CCL4-treated rats.

摘要

背景

蚂蚁毒液在体外和体内均表现出抗菌、抗寄生虫和抗炎活性。我们最近的研究证实了萨姆森蚁毒液(SAV)作为一种强大抗氧化剂的作用。本研究旨在探讨SAV在动物(大鼠)模型中作为四氯化碳诱导的急性肝毒性潜在治疗方法的可能性。

方法

将32只大鼠分为四组;第一组作为对照组。第二组通过腹腔注射以1:1的比例接受单剂量1 ml/kg四氯化碳与橄榄油的混合液。第三组接受单剂量1 ml/kg四氯化碳,然后以每周两次、每次100 μg SAV的剂量治疗三周。第四组仅每周两次、每次接受100 μg SAV的剂量,持续三周。采用酶联免疫吸附测定(ELISA)、逆转录-聚合酶链反应(RT-PCR)和组织病理学检查。

结果

结果显示,患病动物体内的抗氧化酶显著减少。发现SAV能显著恢复患病动物的氧化稳定性。ELISA评估和RT-PCR分析还显示,与正常动物相比,患病动物体内的核因子(κB)NF-κB和抑制剂(κB)IκB分别显著上调。患病大鼠体内肿瘤坏死因子α(TNF-α)和促凋亡受体(Fas)的表达也显著上调。有趣的是,发现SAV能将患病大鼠体内的NF-κB、IκB和TNF-α显著恢复至正常值。结果,与对照组相比,SAV使四氯化碳处理动物的肝酶、血清蛋白和脂质浓度显著改善。此外,SAV明显改善了同一组的肝组织。

结论

SAV治疗通过改善四氯化碳处理大鼠中TNF-α/NF-κB介导的炎症,恢复正常的生化和氧化稳定性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/31c5d4c71863/12944_2016_364_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/e6fb5ae3b5b4/12944_2016_364_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/121ccd88dbcc/12944_2016_364_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/69c74c15051e/12944_2016_364_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/22e2298881a3/12944_2016_364_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/4b5afa5c3963/12944_2016_364_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/48587fca5c96/12944_2016_364_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/31c5d4c71863/12944_2016_364_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/e6fb5ae3b5b4/12944_2016_364_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/121ccd88dbcc/12944_2016_364_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/69c74c15051e/12944_2016_364_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/22e2298881a3/12944_2016_364_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/4b5afa5c3963/12944_2016_364_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/48587fca5c96/12944_2016_364_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5116174/31c5d4c71863/12944_2016_364_Fig7_HTML.jpg

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