Effects of omega 3 on doxorubicin-induced cardiotoxicity in an experimental rabbit model

To evaluate the effects of the use of omega 3 at different doses, following the response through stereological and morphometric evaluations in doxorubicin-induced acute cardiotoxicity in an experimental rabbit model. Thirty healthy adult New Zealand rabbits were divided into six groups with different doses of omega 3 treatment, GT125, GT500 and GT 2000, receiving doses of 125mg / kg, 500mg / kg and 2000mg / kg, respectively. The induction of acute cardiotoxicity with doxorubicin was treated for six days prior to intravenous administration of 10mg / kg single dose. Then, the animals were euthanized and myocardial samples were collected for stereological and morphometric evaluations. The stereological evaluation showed an increase in the transverse area of ​​cardiomocytes between the SHAM and GT2000 groups and an increase in the interstitial collagen volume density between the SHAM and GT500 and SHAM and GT2000 groups. The omega 3 500mg/kg dose has the potential to attenuate the fibrotic effects of doxorubicin use and the use of a single dose of 10mg/kg doxorubicin can be used as an acute dilated cardiomyopathy induction protocol in an experimental model using rabbits.

Protection against Doxorubicin-Related Cardiotoxicity by Jaceosidin Involves the Sirt1 Signaling Pathway

The clinical use of doxorubicin (DOX) is largely limited by its cardiotoxicity. Previous studies have shown that jaceosidin has many biological activities. However, little is known about whether jaceosidin can attenuate DOX-related acute cardiotoxicity. Here, we investigated the therapeutic effects of jaceosidin on DOX-induced acute cardiotoxicity. Mice were intraperitoneally injected with a single dose of DOX to establish an acute cardiac injury model. To explore the protective effects, mice were orally administered jaceosidin daily for 7 days, with dosing beginning 2 days before DOX injection. The results demonstrated that jaceosidin dose-dependently reduced free radical generation, inflammation accumulation, and cell loss induced by DOX in cardiomyocytes. Further studies showed that jaceosidin treatment inhibited myocardial oxidative damage and the inflammatory response and attenuated myocardial apoptotic death, thus improving cardiac function in mice injected with DOX. The inhibitory effects of jaceosidin on DOX-related acute cardiotoxicity were mediated by activation of the sirtuin1 (Sirt1) signaling pathway. Jaceosidin lost its protective effect against DOX-related injury in Sirt1-deficient cardiomyocytes and mice. In conclusion, jaceosidin has protective potential in treating DOX-related cardiac injury through activation of the Sirt1 signaling pathway.

Nerolidol Attenuates Oxidative Stress, Inflammation, and Apoptosis by Modulating Nrf2/MAPK Signaling Pathways in Doxorubicin-Induced Acute Cardiotoxicity in Rats

The clinical usage of doxorubicin (DOX), a potent anthracycline antineoplastic drug, is often limited by its cardiotoxic effects. Thus, for improving usage of DOX, the aim of this study was to assess the cardioprotective effects of nerolidol (NERO) in a rat model of DOX-induced acute cardiotoxicity and examine underlying molecular mechanisms that contribute to these effects. To induce acute cardiotoxicity male albino Wistar rats were injected with single dose intraperitoneal DOX (12.5 mg/kg). The rats were treated with NERO (50 mg/kg, orally) for five days. DOX-injected rats showed elevated levels of cardiac marker enzymes and enhanced oxidative stress markers along with altered Nrf2/Keap1/HO-1 signaling pathways. DOX administration also induced the activation of NF-κB/MAPK signaling and increased the levels and expression of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) as well as expression of inflammatory mediators (iNOS and COX-2) in the heart. DOX also triggered DNA damage and apoptotic cell death in the myocardium. Additionally, histological studies revealed structural alterations of the myocardium. NERO treatment exhibited protection against the deleterious results of DOX on myocardium, as evidenced by the restoration of altered biochemical parameters, mitigated oxidative stress, inflammation, and apoptosis. The findings of the present study demonstrate that NERO provides cardioprotective effects against DOX-induced acute cardiotoxicity attributed to its potent antioxidant, anti-inflammatory, and antiapoptotic activities through modulating cellular signaling pathways.

Cardioprotective effect of the aqueous extract of seeds of Datura metel (Solanaceae) on acute cardiotoxicity induced with doxorubicin in Wistar rats

The current study evaluated the cardioprotective effect of the aqueous extract of seeds of Datura metel (AESDM) on the acute cardiotoxicity induced with doxorubicin in the Wistar rats. Indeed, 30 rats have been randomized then, divided into 6 groups of 5 animals each: 3 control groups (normal, negative and positive) and 3 test groups (AESDM 100, 200 and 300 mg/kg). These animals received orally, six consecutive days, 1 mL/200 g distilled water (normal and negative control), 100 mg/kg Vitamin-E (positive control), AESDM at 100, 200 and 300 mg/kg (test groups). On the seventh day of treatment, animals in the different groups excepted the normal control received a single intraperitoneal injection of 15 mg/kg doxorubicin followed respective treatments up to the tenth day of the trial period. Serum parameters (ASAT/ALAT), biochemical markers of oxidative stress (MDA, SOD, CAT, GSH) and lipid parameters (total cholesterol, triglycerides, HDL and LDL) were evaluated. Histological sections of animal hearts were prepared. The results of this study showed that treatment with AESDM resulted in a significant decrease (P ˂ 0.001) in MDA, triglycerides and LDL-cholesterol levels, ASAT/ALAT activity and a significant increase (P ˂ 0.001) in HDL-cholesterol concentration and SOD, CAT and GSH activities, compared to the negative control. Histological observation revealed that AESDM protected the heart from doxorubicin-induced damage. In conclusion, AESDM would have a cardioprotective effect that could be attributed to its antioxidant potential.

Anthracycline-related acute cardiotoxicity in a very young Omani patient with acute myeloid leukaemia

Anthracycline-related cardiomyopathy is of concern in children treated for acute myeloid leukemia (AML). Risk is dose-dependent, increasing with higher doses. We aim to highlight the risk of early-onset cardiotoxicity with low-cumulative anthracycline dose in a young Omani boy with AML. We conclude in the presence of other known risk factors for cardiac dysfunction, there is probably no risk-free anthracycline dose.