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一项实验研究:地高辛对甲氨蝶呤治疗所致肝毒性的益处。

An Experimental Study: Benefits of Digoxin on Hepatotoxicity Induced by Methotrexate Treatment.

作者信息

Taskin Banu, Erdoğan Mümin Alper, Yiğittürk Gürkan, Alper Sibel, Erbaş Oytun

机构信息

Department of Dermatology, Koc University Hospital, Istanbul, Turkey.

Department of Physiology, Faculty of Medicine, Izmir Katip Celebi University, Izmir, Turkey.

出版信息

Gastroenterol Res Pract. 2021 Nov 10;2021:6619844. doi: 10.1155/2021/6619844. eCollection 2021.

Abstract

PURPOSE

The aim of the study is to examine the possible therapeutic effects of a known cardiac glycoside, digoxin, on a rat model of MTX-induced hepatotoxicity.

METHODS

The study was conducted on twenty-four male rats. While eighteen rats received a single dose of 20 mg/kg MTX to obtain an injured liver model, six rats constituted the control group. Also, the eighteen liver toxicity model created rats were equally divided into two groups, one of which received digoxin 0.1 mg/kg/day digoxin (Group 1) and the other group (Group 2) was given saline (% 0.9NaCl) with a dose of 1 ml/kg/day for ten days. Following the trial, the rats were sacrificed to harvest blood and liver tissue samples to determine blood and tissue MDA, serum ALT, plasma TNF-, TGF-, IL-6, IL-1-Beta, and PTX3 levels.

RESULTS

MTX's structural and functional hepatotoxicity was observable and evidenced by relatively worse histopathological scores and increased biochemical marker levels. Digoxin treatment significantly reduced the liver enzyme ALT, plasma TNF-, TGF-, PTX3, and MDA levels and decreased histological changes in the liver tissue with MTX-induced hepatotoxicity in the rat model.

CONCLUSION

We suggest that digoxin has an anti-inflammatory and antihepatotoxic effect on the MTX-induced liver injury model.

摘要

目的

本研究旨在探讨一种已知的强心苷地高辛对甲氨蝶呤(MTX)诱导的肝毒性大鼠模型的可能治疗作用。

方法

对24只雄性大鼠进行研究。18只大鼠接受单剂量20mg/kg的MTX以建立肝损伤模型,6只大鼠作为对照组。此外,将18只建立肝毒性模型的大鼠平均分为两组,其中一组接受0.1mg/kg/天地高辛治疗(第1组),另一组(第2组)给予剂量为1ml/kg/天的生理盐水(0.9%NaCl),持续10天。试验结束后,处死大鼠以采集血液和肝组织样本,测定血液和组织中的丙二醛(MDA)、血清谷丙转氨酶(ALT)、血浆肿瘤坏死因子-α(TNF-α)、转化生长因子-β(TGF-β)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和五聚体蛋白3(PTX3)水平。

结果

MTX的结构和功能肝毒性是可观察到的,组织病理学评分相对较差以及生化标志物水平升高证明了这一点。地高辛治疗显著降低了肝酶ALT、血浆TNF-α、TGF-β、PTX3和MDA水平,并减少了大鼠模型中MTX诱导的肝毒性所致肝组织的组织学变化。

结论

我们认为地高辛对MTX诱导的肝损伤模型具有抗炎和抗肝毒性作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1a/8598353/128eb0d0d55d/GRP2021-6619844.001.jpg

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