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تأثیر پیش درمانی با تروگزروتین بر فیبروز میوکارد در رتهای مبتلا به سمیت قلبی ناشی از دوکسوروبیسین.

Background. Doxorubicin (DOX) is a highly effective anthracycline drug widely used in cancer treatment. Myocardial fibrosis, a key pathological consequence of DOX-induced cardiotoxicity, impairs cardiac function and increases the risk of heart failure. Troxerutin (TXR), a natural bioflavonoid, has s...

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Published in:Medical Journal of Tabriz University of Medical Sciences Vol. 47; no. 3; pp. 287 - 298
Main Authors: سارا بابائی کوچک, رضا بدل زاده, وهاب باباپور, نگار پناهی, احمد جامعی خسروش
Format: pictorial research tables/charts Journal Article
Published: Tabriz University of Medical Sciences Aug2025
Online Access:View this record in EBSCOhost
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      dt: Aug2025
      vid: 47
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      pid: 69573
      pub: Tabriz University of Medical Sciences
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      tig:
        atl: تأثیر پیش درمانی با تروگزروتین بر فیبروز میوکارد در رتهای مبتلا به سمیت قلبی ناشی از دوکسوروبیسین.
      aug:
        au:
          سارا بابائی کوچک
          رضا بدل زاده
          وهاب باباپور
          نگار پناهی
          احمد جامعی خسروش
        affil: گروه علوم پایه دانشکده دامپزشکی دانشگاه آزاد اسلامی واحد علوم و تحقیقات، تهران، ایران.
      sug:
        subj:
          Rutin Pharmacodynamics
          Flavonoids Pharmacodynamics
          Myocardial Diseases Prevention and Control
          Gene Expression Drug Effects
          Oxidative Stress Drug Effects
          Mitochondria Metabolism
          Models, Biological
          Animal Studies
          Iran
          Rats
          Transforming Growth Factor beta Drug Effects
          Random Assignment
          Flavonoids Administration and Dosage
          Lactate Dehydrogenase Blood
          Enzyme-Linked Immunosorbent Assay
          Paraffin
          Staining and Labeling
          Microscopy Methods
          Reverse Transcriptase Polymerase Chain Reaction
          One-Way Analysis of Variance
          Post Hoc Analysis
          Histological Techniques
          Mitochondria
          Biological Phenomena
      ab: Background. Doxorubicin (DOX) is a highly effective anthracycline drug widely used in cancer treatment. Myocardial fibrosis, a key pathological consequence of DOX-induced cardiotoxicity, impairs cardiac function and increases the risk of heart failure. Troxerutin (TXR), a natural bioflavonoid, has shown promise in mitigating myocardial injury. This study evaluated the protective effects of TXR against DOX-induced myocardial fibrosis and expression of fibrosis markers, TGFβ and Smad3. Methods. Twenty-four male Wistar rats were randomly divided into four groups: control, TXR, DOX, and DOX+TXR. TXR was administered orally at 150 mg/kg daily for 4 weeks before treatment with DOX. DOX was injected intraperitoneally at 20 mg/kg. One week after the administration of DOX, serum lactate dehydrogenase (LDH) activity was measured to assess myocardial damage, and myocardial fibrosis was evaluated histologically using Masson's trichrome staining. Gene expression of TGF-β and Smad3 was analyzed by real-time PCR. Results. DOX significantly increased serum LDH activity and myocardial fibrosis compared to controls (P<0.01). Pre-treatment with TXR significantly reduced LDH activity and myocardial fibrosis in the DOX+TXR group compared to the DOX group (P<0.05). Additionally, TXR decreased the expression of TGF-β (and Smad3 (P<0.01) genes, indicating a reduction in fibrotic signaling. Conclusion. TXR shows significant potential as a preventive treatment for DOXinduced myocardial toxicity. Its ability to reduce myocardial damage and fibrosis while modulating key fibrotic signaling molecules offers a promising approach for improving cardiac outcomes following DOX therapy. Practical Implications. Troxerutin could be used as an effective preventative treatment for improving cardiovascular health in cancer patients undergoing chemotherapy with DOX.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: Persian
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