Researchers show that supplementing rats with an extract from a plant called Boesenbergia rotunda (BrE) protects against chemotherapy-induced cardiac toxicity.
Highlights:
Curtailing the destructive effects of cancer often requires patients to undergo chemotherapy, a standard treatment for extinguishing cancerous cells. And although chemotherapy’s protective effects are well-established, it’s important to highlight the treatment’s potentially harmful side effects, particularly multiorgan toxicity, which can severely compromise a patient’s recovery and even worsen their health. In efforts to address this arduous challenge, scientists have turned to medicinal plants with potent antioxidative and anti-inflammatory properties, as inflammation and oxidative stress are critical drivers of organ damage.
In a new study published in Scientific Reports, Zhang and colleagues explored the protective effects of the medicinal plant Boesenbergia rotunda (BrE) on cardiac toxicity in rats receiving doxorubicin (DOX). The investigators found that treating DOX rats with BrE extract mitigated structural abnormalities in the heart and significantly reduced markers of cardiac damage. Furthermore, the findings showed that BrE treatment enhanced antioxidant defenses while lowering both inflammation and oxidative stress.
Despite DOX exhibiting powerful antitumor properties, its use remains limited due to the possibility of severe cardiotoxicity. Following DOX treatment, individuals are susceptible to heart shrinking and tissue degeneration, which drive cardiac decline. Accordingly, Zhang and colleagues measured heart size and analyzed cardiac tissue integrity in mice to determine whether BrE treatment could ameliorate common features of DOX-induced cardiotoxicity.
The investigators supplemented rats with a low dose (100 mg/kg) or high dose (400 mg/kg) of BrE daily for five weeks. As expected, untreated DOX rats presented with notably smaller hearts than healthy control rats. Conversely, those treated with a low or high dose of BrE had hearts similar in size to healthy control rats, demonstrating that BrE blunts cardiac shrinking.
Further analysis of cardiac tissue revealed that untreated rats displayed degenerated heart tissue and necrotic (dead) cells, reaffirming that DOX compromises the structural integrity of the heart. Additionally, untreated rats exhibited drastically higher levels of markers (MPO, AST, ALP) indicative of damaged tissue, supporting the tissue analysis findings.
When the investigators examined BrE-treated rats, they found that BrE dose-dependently mitigated the observed cardiac structural abnormalities, with high-dose-treated rats exhibiting minimal tissue degeneration, fewer necrotic cells, and lower levels of MPO, AST, and ALP. Collectively, the findings suggest that BrE successfully hinders DOX-induced heart damage.
Inflammation and oxidative stress are two hallmarks of aging, and researchers have confirmed that DOX triggers heightened levels of inflammation and oxidative stress, both of which have been found to exacerbate cardiotoxicity and organ deterioration in patients. With this in mind, Zhang and colleagues sought to determine whether BrE could ameliorate these parameters, as BrE is known to lower inflammation and increase antioxidant defenses.
Zhang and colleagues proceeded to measure inflammation in cardiac tissue and found that BrE dose-dependently reduced markers of inflammation, demonstrating BrE’s anti-inflammatory properties. The investigators then measured the levels of glutathione (GSH), a highly abundant natural antioxidant in the body whose depletion is associated with cellular damage. The results showed that BrE-treated rats, especially those in the high-dose group, had significantly higher levels of GSH than untreated DOX rats. Furthermore, the cardiac tissue of treated rats exhibited much lower levels of oxidative stress, highlighting BrE’s ability to quench oxidative stress by increasing antioxidant defenses.
Overall, the study’s findings suggest that BrE effectively protects the heart against chemotherapy-induced cardiotoxicity by restoring antioxidant defense mechanisms and regulating inflammation and oxidative stress. As a promising therapeutic, it’s important to highlight BrE’s composition to better understand why it works. Accordingly, BrE is comprised of compounds known as flavonoids – plant-based polyphenols – which have well-established anti-inflammatory and antioxidative properties. Many of these compounds have been shown to promote healthy aging, with some even extending the lifespan and healthspan of multiple model organisms. For those interested in taking BrE, it can either be consumed directly from fingerroot or through supplementation. Remember, always consult with a physician before starting any new supplements.
Model: Sprague-Dawley Rats
Dosage: low dose (100 mg/kg) or high dose (400 mg/kg) of BrE daily for five weeks; oral gavage