Cardiovascular Toxicology and Its Evaluation

Gad, Shayne C.

doi:10.1002/9781118683484.ch19

Cited by 6 publications

(1 citation statement)

References 64 publications

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“…Cardiotoxicity is one of the most serious adverse effects of various chemotherapy medications, and it greatly increases morbidity and mortality rates [ 1 ]. The manifestations of cardiotoxicity are diverse, encompassing subtle alterations in blood pressure, the development of arrhythmias, and the onset of cardiomyopathy.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of nebivolol in doxorubicin-induced cardiotoxicity

Hadi,

Al-Amir,

Janabi

2023

JMedLife

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This study aimed to investigate the potential of nebivolol in preventing doxorubicin-induced cardiotoxicity by targeting the inflammatory, oxidative, and apoptotic pathways. Twenty-eight male rats were randomly divided into four groups, each consisting of seven rats. The control group received standard diets and unrestricted access to water. The rats in the normal saline (N/S) group were administered a 0.9% normal saline solution for two weeks. The doxorubicin group (the “induced group”) received doxorubicin at a dosage of 2.5 mg/kg three times per week for two weeks. The nebivolol group received an oral dose of 4 mg/kg of nebivolol for the same duration. The cardiac tissues of rats treated with doxorubicin exhibited increased levels of tumor necrosis factor, interleukin-1, malondialdehyde, and caspase-3 compared to the normal saline control group (p<0.05), along with decreased levels of total antioxidant capacity and Bcl-2. These results show that doxorubicin is harmful to the heart. The administration of nebivolol significantly reduced the cardiotoxic effects induced by doxorubicin, as indicated by a statistically significant decrease in the levels of inflammatory markers, specifically tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) (p<0.05). The nebivolol group exhibited a significant decrease in malondialdehyde levels, which serves as a signal of oxidation, in cardiac tissue compared to the doxorubicin-only group (p<0.05). Additionally, the nebivolol group showed a significant increase in overall antioxidant capacity. Nebivolol dramatically attenuated doxorubicin-induced cardiotoxicity in rats, likely by interfering with oxidative stress, the inflammatory response, and the apoptotic pathway.

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Section: Introductionmentioning

confidence: 99%