Protective effect of misoprostol against paclitaxel-induced cardiac damage in rats

IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Prostaglandins & other lipid mediators Pub Date : 2024-01-20 DOI:10.1016/j.prostaglandins.2024.106813
İbrahim Aktaş , Fatih Mehmet Gur , Sedat BİLGİÇ
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Abstract

Objective

One of the most critical reasons for limiting cancer treatment is the toxic effects of anti-cancer drugs on healthy tissues and organs. This study aims to investigate the possible protective effects of misoprostol (MS) against the damage that arises from paclitaxel (PT), an anti-cancer pharmacological agent, in the rat heart using histopathological and biochemical analyses.

Methods

In this study, four groups, each containing seven animals, were formed by random selection from 28 Sprague Dawley female rats. Control group rats were administered 1 ml of normal saline orally and intraperitoneally (i.p.) for six days. While the PT group rats were administered PT at a dose of 2 mg/kg intraperitoneally (i.p.) on days 0, 2, 4, and 6, the MS group was administered MS at a dose of 0.2 mg/kg in 1 ml normal saline by oral gavage for six days. PT and MS were administered to the PT + MS group rats in the same dose and route as the previous groups.

Results

Administration of PT increased serum lactate dehydrogenase (LDH), cardiac troponin I (cTn-I), creatine kinase isoenzyme MB (CK-MB), and brain natriuretic peptide (BNP) levels. PT administration also decreased the levels of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) in the heart tissue while increasing the level of malondialdehyde (MDA) (p < 0.05). In histopathological examinations, pathological changes, such as edema, congestion, hemorrhage, apoptosis, and degeneration, occurred in the heart tissue of PT-treated rats. The negative changes in histopathological and biochemical parameters that occurred in the PT group were almost not observed in the PT + MS group (p < 0.005).

Conclusion

When the findings were evaluated, it was concluded that MS protects the heart tissue from the harmful effects of PT, probably due to its antioxidant, anti-apoptotic and TNF-alpha suppressive effects.

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米索前列醇对紫杉醇诱导的大鼠心脏损伤的保护作用
目的限制癌症治疗的最关键原因之一是抗癌药物对健康组织和器官的毒性作用。本研究旨在通过组织病理学和生化分析,探讨米索前列醇(MS)对抗癌药紫杉醇(PT)对大鼠心脏造成的损伤可能具有的保护作用。对照组大鼠口服和腹腔注射 1 毫升生理盐水,连续六天。PT 组大鼠在第 0、2、4 和 6 天腹腔注射 PT,剂量为 2 毫克/千克;MS 组大鼠口服 MS,剂量为 0.2 毫克/千克,溶于 1 毫升生理盐水中,连续六天。结果 PT 会增加血清乳酸脱氢酶(LDH)、心肌肌钙蛋白 I(cTn-I)、肌酸激酶同工酶 MB(CK-MB)和脑钠肽(BNP)的水平。服用 PT 还会降低心脏组织中谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的水平,同时增加丙二醛(MDA)的水平(p<0.05)。在组织病理学检查中,PT 处理大鼠的心脏组织出现了水肿、充血、出血、细胞凋亡和变性等病理变化。在 PT 组中出现的组织病理学和生化指标的负向变化在 PT + MS 组中几乎没有观察到(p<0.005)。
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来源期刊
Prostaglandins & other lipid mediators
Prostaglandins & other lipid mediators 生物-生化与分子生物学
CiteScore
5.80
自引率
3.40%
发文量
49
审稿时长
2 months
期刊介绍: Prostaglandins & Other Lipid Mediators is the original and foremost journal dealing with prostaglandins and related lipid mediator substances. It includes basic and clinical studies related to the pharmacology, physiology, pathology and biochemistry of lipid mediators. Prostaglandins & Other Lipid Mediators invites reports of original research, mini-reviews, reviews, and methods articles in the basic and clinical aspects of all areas of lipid mediator research: cell biology, developmental biology, genetics, molecular biology, chemistry, biochemistry, physiology, pharmacology, endocrinology, biology, the medical sciences, and epidemiology. Prostaglandins & Other Lipid Mediators also accepts proposals for special issue topics. The Editors will make every effort to advise authors of the decision on the submitted manuscript within 3-4 weeks of receipt.
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