Lady’s Bedstraw as a Powerful Antioxidant for Attenuation of Doxorubicin-Induced Cardiotoxicity

Abstract

This study aimed to examine the effects of a 14-day treatment with lady’s bedstraw methanol extract on doxorubicin-induced cardiotoxicity through functional, biochemical and histological examinations. We used 24 male Wistar albino rats divided into the following groups: control (CTRL), doxorubicin (DOX), and DOX + GVE (Galium verum extract). GVE was administered orally at a dose of 50 mg/kg per day for 14 days, while a single dose of doxorubicin was injected into the DOX groups. After accomplishing treatment with GVE, cardiac function was assessed, which determined the redox state. During the autoregulation protocol on the Langendorff apparatus, ex vivo cardiodynamic parameters were measured. Our results demonstrated that the consumption of GVE effectively suppressed the disturbed response of the heart to changes in perfusion pressures caused by administration of DOX. Intake of GVE was associated with a reduction in most of the measured prooxidants in comparison to the DOX group. Moreover, this extract was capable of increasing the activity of the antioxidant defense system. Morphometric analyses showed that rat hearts treated with DOX showed more pronounced degenerative changes and necrosis compared to the CTRL group. However, GVE pretreatment seems to be able to prevent the pathological injuries caused by DOX injection via decrease in oxidative stress and apoptosis.

Deciphering the Protective Effects of Carvacrol Against Doxorubicin-Induced Cardiotoxicity In Vitro and In Vivo

“…This study also showed cardiac dysfunction in Langendorff-perfused rat hearts isolated from DOXadministered rats. LVDP, EDP, LV + dP/dt, and LV -dP/dt as markers for LV contractile markers were impaired in the DOX group, indicating contractile dysfunction, in line with previous results 22 . The study identi ed several mechanisms underlying cardiac dysfunction triggered by DOX, including heightened generation of reactive oxygen species (ROS) resulting in oxidative stress damage, disturbed calcium ion (Ca 2+ ) homeostasis, and compromised expression of genes associated with the apoptosis and necrosis of cardiomyocytes 34 .…”

“…In extending our exploration to rat models, the in uence of CAR on DIC was evaluated by performing functional, biochemical, and histological examinations. The induction of cardiomyopathy in rats was achieved by administering a single cumulative intraperitoneal dose of DOX at 15 mg/kg to create a DOXinduced acute cardiotoxicity model, a well-established method documented in previous studies 22,23 . In addition, the risk of cardiotoxicity with DOX becomes signi cant when cumulative doses exceed 200 mg/m 2 , equivalent to 5 mg/kg in humans 24 .…”

Artemisia annua Extract Attenuate Doxorubicin-Induced Hepatic Injury via PI-3K/Akt/Nrf-2-Mediated Signaling Pathway in Rats

“…The DOX has been shown to cause an imbalance of redox status and attenuation of the antioxidants that led to the oxidization of macromolecules, leading to liver injuries [10,[39][40][41]. Allied with previous results, the study showed a significant increase in the MDA levels with a reduction in GSH levels herein in DOX-injected rats; this could be assigned to the impaired hepatic tissue under the damaging effects of DOX.…”

Sophocarpine alleviates doxorubicin-induced heart injury by suppressing oxidative stress and apoptosis

“…The pathological changes of DOX-induced heart injury are complex, such as oxidative stress, inflammatory response, endoplasmic reticulum stress, DNA damage, apoptosis, autophagy, mitochondrial dysfunction, disturbed calcium homeostasis, and fibrosis 4 – 9 . Among them, oxidative stress and apoptosis have been demonstrated to be important factors for the development of DOX-induced heart injury 10 , 11 . Therefore, alleviating oxidative stress and apoptosis may be a promising strategy for the treatment of DOX-induced heart injury.…”