Ameliorative effects of sinapic acid against vancomycin-induced testicular oxidative damage, apoptosis, inflammation, testicular histopathologic disorders and decreased epididymal sperm quality

Akarsu, Serkan Ali; İleritürk, Mustafa; Küçükler, Sefa; Akaras, Nurhan; Gür, Cihan; Kandemir, Fatih Mehmet

doi:10.1016/j.reprotox.2024.108666

Reproductive Toxicology

2024

DOI: 10.1016/j.reprotox.2024.108666

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Ameliorative effects of sinapic acid against vancomycin-induced testicular oxidative damage, apoptosis, inflammation, testicular histopathologic disorders and decreased epididymal sperm quality

Serkan Ali Akarsu,

Mustafa İleritürk,

Sefa Küçükler

et al.

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Cited by 2 publications

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Assessment of sinapic acid’s protective effects against ethanol-induced gastric ulcers in rats

Akdemir,

Güler,

Eraslan

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Assessment of sinapic acid’s protective effects against ethanol-induced gastric ulcers in rats

Akdemir,

Güler,

Eraslan

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Carvacrol Ameliorates Cisplatin-Induced Cardiotoxicity By Regulating Notch/Hes1 Signaling Pathway, Oxidative Stress and Cell Death In Rat Cardiac Tissue

Akaras,

Kandemir,

Şimşek

2024

Türk Doğa Ve Fen Dergisi

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Cisplatin is one of the most active cytotoxic agents used mainly in the treatment of solid tumors. High doses and long-term use of Cisplatin are known to cause cardiotoxicity. In recent years, the antiapoptotic and antioxidant effects of Carvacrol in cardiovascular diseases have attracted attention. In this study, the effects of Carvacrol on Cisplatin-induced cardiotoxicity in a rat model were investigated using biochemical and histological methods. Twenty-eight rats were divided into 4 groups: 1. Control group, 2. Carvacrol group, 3. Cisplatin group, 4. Cisplatin + Carvacrol group. The expression of antioxidant enzymes, proinflammatory cytokines, apoptotic, and autophagic proteins was examined in heart tissue obtained from rats sacrificed after the last drug administration. Additionally, heart tissue was evaluated histopathologically. Cisplatin has been observed to cause oxidative stress and inflammatory damage in animal heart tissue. Carvacrol administration significantly increased antioxidant enzyme (superoxide dismutase and glutathione peroxidase) activities while suppressing inflammatory markers (NF-κB, TNF-α, IL-1β). Additionally, Cisplatin induced apoptotic (caspase-3, Bax, Bcl-2) and autophagic (Beclin-1, LC3A, LC3B) markers. It has been determined that carvacrol can protect heart tissues from the destructive effects of cisplatin by exerting anti-apoptotic and anti-autophagic effects. The expression levels of Notch1 and Hes1, which were decreased by cisplatin administration, were upregulated after administration of Carvacrol. H&E staining results showed that Carvacrol preserved myocardial tissue integrity. In conclusion, Carvacrol showed a cardioprotective effect against cisplatin-induced cardiotoxicity.

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Ameliorative effects of sinapic acid against vancomycin-induced testicular oxidative damage, apoptosis, inflammation, testicular histopathologic disorders and decreased epididymal sperm quality

Cited by 2 publications

References 53 publications

Assessment of sinapic acid’s protective effects against ethanol-induced gastric ulcers in rats

Assessment of sinapic acid’s protective effects against ethanol-induced gastric ulcers in rats

Carvacrol Ameliorates Cisplatin-Induced Cardiotoxicity By Regulating Notch/Hes1 Signaling Pathway, Oxidative Stress and Cell Death In Rat Cardiac Tissue

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