Why the study?
Myocardial injury induced by cisplatin necessitated identifying a treatment modality to address cardiotoxicity in cisplatin-treated patients.
Do breast milk mesenchymal stem cells abate cisplatin-induced cardiotoxicity in adult male albino rats?
Do breast milk mesenchymal stem cells abate cisplatin-induced cardiotoxicity in adult male albino rats?
Breast milk mesenchymal stem cells demonstrate a protective role against cisplatin-induced cardiac injury in a rat model, an effect that is enhanced by the addition of metformin.
Br-MSCs may attenuate cisplatin cardiotoxicity in rats; hypothesis-generating for stem cell cardioprotection, with clinical translation unproven.
Myocardial injury influenced by cisplatin (Cis) is a compelling reason to hunt out a treatment modality to overcome such a threat in cisplatin-treated patients. Breast Milk mesenchymal stem cells (Br-MSCs) are a non-invasive, highly reproducible source of stem cells. Herein, we investigate Br-MSCs' role in cardiotoxicity induced by cisplatin. Rats were divided into; control, Cis-treated (received 12 mg/kg single intraperitoneal injection), BrMSCs-treated (received single intraperitoneal injection of 0.5 ml sterilized phosphate-buffered saline containing 2 × 10 7 cells of Br-MSCs); metformin-treated (received 250 mg/kg/day orally) and BrMSCs + metformin + Cis treated groups. At the experiment end, serum creatine kinase (CK-MB) and cardiac troponin T (cTnT) activates were estimated, cardiac malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α) levels were measured, cardiac expression of Bax and Bcl-2 and AMP-activated protein kinase (AMPK), as well as heart histopathology, were evaluated. Study results showed that Cis explored acute cardiotoxicity evidenced by deteriorated cardiac indices, induction of oxidative stress, and inflammation with myocardium histological alterations. Treatment with Br-MSCs restored heart function and structure deteriorated by Cis injection. The antioxidant/anti-inflammatory/anti-apoptotic results of Br-MSCs were supported by AMPK activation denoting their protective role against cisplatin-induced cardiac injury. These results were superior when metformin was added to the treatment protocol.
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Nageeb et al. (2022) studied this question.
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