Profile of Molecular Markers of Cardiac Fibrosis in Rats Exposed to Different Doxorubicin Doses

Podyacheva, Ekaterina; Шмакова, Т. В.; Andreeva, Daria; Toropov, Roman; Cheburkin, Yuri; Danilchuk, Maria; Martynov, M. O.; Toropova, Yana

doi:10.1134/s0022093023020059

Cited by 4 publications

(1 citation statement)

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“…Increased expression of type I and II collagen, endothelin-1 (ET1), broblast growth factor 4 (FGF4), and tumor necrosis factor-alpha (TNFα) could be involved in the in ammatory processes. This dual manifestation suggests a dynamic interplay between brosis and in ammation against the backdrop of DOX's pronounced cardiotoxic effects, as elucidated by Podyacheva et al 52 Unexpectedly, pretreatment with CAR exhibited a slight increase in red color staining, indicating a minor degree of collagen deposition. Furthermore, a pivotal and promising outcome emerged as a signi cant decrease in brosis area was discerned in the CAR-pretreated group compared to the DOX-alone group.…”

Section: Discussionmentioning

confidence: 73%

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

Retnosari,

Ghani,

Alkharji

et al. 2024

Preprint

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Doxorubicin (DOX), a widely used chemotherapy, extends its impact beyond cancer cells, notably affecting the heart, leading to substantial concerns about DOX-induced cardiotoxicity (DIC). However, subclinical DIC remains unresolved, necessitating advanced cardio-protection strategies in cancer therapy. Recent research explores carvacrol (CAR), a natural substance with antioxidant and anti-inflammatory properties, as a potential shield against DIC. However, further exploration is warranted, particularly concerning hypertrophy and cardiac fibrosis. This study investigated CAR’s potential cardioprotective properties against DIC in H9c2 cardiomyocytes and rats. Induction with DOX reduced cardiomyocyte viability, while pretreatment with 0.01 µg/mL CAR enhanced the viability of DOX-induced cardiomyocytes. Meanwhile, administration of DOX induced adverse effects in rats, causing decreased total heart weight and left ventricular mass, and lowered blood pressure. DOX also caused cardiac dysfunction, lipid peroxidation, hypertrophy, and fibrosis. In rat models, CAR pretreatment effectively mitigated DOX-induced reductions in blood pressure, hypertrophy, and cardiac fibrosis. However, the pretreatment kept the heart function, oxidative stress, and antioxidant enzymes unaltered. In conclusion, the results show that CAR could be an adjuvant to reduce DIC by ameliorating cardiac fibrosis and hypertrophy.

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Section: Discussionmentioning

confidence: 73%