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牛磺酸通过其对大鼠的膜稳定作用保护阿霉素诱导的肝毒性。

Taurine Protects Doxorubicin-Induced Hepatotoxicity via Its Membrane-Stabilizing Effect in Rats.

作者信息

Gedikli Esra, Barış Veysel Özgür, Yersal Nilgün, Dinçsoy Adnan Berk, Müftüoğlu Sevda Fatma, Erdem Ayşen

机构信息

Department of Physiology, Hacettepe University Faculty of Medicine, 06230 Ankara, Turkey.

Department of Cardiology, Dr Ersin Arslan Research and Education Hospital, 27010 Gaziantep, Turkey.

出版信息

Life (Basel). 2023 Oct 9;13(10):2031. doi: 10.3390/life13102031.

DOI:10.3390/life13102031
PMID:37895413
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10608465/
Abstract

BACKGROUND

Doxorubicin (dox) is a chemotherapeutic agent widely used against various tumors. However, the clinical use of this agent is limited due to various organ toxicities. Taurine is an intracellular free β-amino acid with antioxidant properties. The present study investigated the protective mechanism of taurine on dox-induced hepatotoxicity.

METHODS

In total, 31 male Sprague-Dawley rats were used in the study. The control group received intraperitoneal (i.p.) 0.9% NaCl alone for 14 days; the taurine (Tau) group received i.p. taurine 150 mg/kg body weight/day for 14 days; the dox group received dox on days 12, 13, and 14 at a cumulative dose of 25 mg/kg body weight/3 days; and the tau+dox group received taurine and dox together at the same dose and through the same route. On day 15, biochemical evaluations were performed on blood samples taken from the left ventricle followed by histological examinations on liver samples.

RESULTS

Dox was found to increase liver function enzymes and tissue protein carbonyl levels, causing congestion and tissue damage, thereby leading to dysfunction. Tau was found to histologically preserve the liver morphology without showing any corrective effect on oxidative stress parameters. These findings suggest that the membrane-stabilizing effect of taurine may be more effective than its radical scavenging activity in preventing dox-induced toxicity.

CONCLUSION

Taurine can prevent doxorubicin-induced hepatotoxicity through non-antioxidant pathways.

摘要

背景

阿霉素(多柔比星)是一种广泛用于治疗各种肿瘤的化疗药物。然而,由于其对各种器官的毒性,该药物的临床应用受到限制。牛磺酸是一种具有抗氧化特性的细胞内游离β-氨基酸。本研究探讨了牛磺酸对阿霉素诱导的肝毒性的保护机制。

方法

本研究共使用了31只雄性Sprague-Dawley大鼠。对照组腹腔注射0.9%氯化钠溶液,持续14天;牛磺酸(Tau)组腹腔注射150mg/kg体重/天的牛磺酸,持续14天;阿霉素组在第12、13和14天注射阿霉素,累积剂量为25mg/kg体重/3天;牛磺酸+阿霉素组以相同剂量和途径同时给予牛磺酸和阿霉素。在第15天,对从左心室采集的血液样本进行生化评估,随后对肝脏样本进行组织学检查。

结果

发现阿霉素会增加肝功能酶和组织蛋白羰基水平,导致充血和组织损伤,从而引起功能障碍。发现牛磺酸在组织学上可保持肝脏形态,但对氧化应激参数没有任何纠正作用。这些发现表明,在预防阿霉素诱导的毒性方面,牛磺酸的膜稳定作用可能比其自由基清除活性更有效。

结论

牛磺酸可通过非抗氧化途径预防阿霉素诱导的肝毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22a5/10608465/6320bc7f6104/life-13-02031-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22a5/10608465/1df30a0b42a7/life-13-02031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22a5/10608465/6320bc7f6104/life-13-02031-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22a5/10608465/1df30a0b42a7/life-13-02031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22a5/10608465/6320bc7f6104/life-13-02031-g002a.jpg

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