Key result
Capsaicin significantly reduced cardiac cell damage markers, inflammatory cytokines, and oxidative stress in male Wistar rats with cyclophosphamide-induced cardiotoxicity.
Why the study?
Cyclophosphamide causes cardiotoxicity, whereas capsaicin exhibits antioxidant and anti-inflammatory properties, prompting investigation into capsaicin's cardioprotective mechanisms against cyclophosphamide-induced cardiotoxicity.
Does capsaicin prevent cyclophosphamide-induced cardiotoxicity in male Wistar rats?
RCT
randomly assigned
Does capsaicin prevent cyclophosphamide-induced cardiotoxicity in male Wistar rats?
Capsaicin ameliorates cyclophosphamide-induced cardiotoxicity in a rat model by inhibiting oxidative stress, inflammation, and apoptosis.
Animal data on capsaicin do not support clinical cardioprotection strategies; leaves open translation to human trials.
Cyclophosphamide is an antineoplastic agent that has a broad range of therapeutic applications; however, it has numerous side effects, including cardiotoxicity. Furthermore, chili peppers contain a substance called capsaicin, having antioxidant and anti-inflammatory effects. Thus, this research paper focuses on the potential mechanism of capsaicin's cardioprotective activity against cyclophosphamide-induced cardiotoxicity by measuring the expression of oxidative and inflammatory marker such as interleukins and caspases. The following groups of rats were randomly assigned: only vehicle given for 6 days (control group); cyclophosphamide 200 mg/kg intraperitoneal on 4th day only (positive control group); capsaicin 10 mg/kg orally given for 6 days followed by cyclophosphamide 200 mg/kg on 4th day of treatment; capsaicin 20 mg/kg orally for six days followed by cyclophosphamide 200 mg/kg on 4th day of treatment; and maximum amount of capsaicin alone (20 mg/kg) orally for six days. Using ELISA kits, it was found that the cyclophosphamide administration significantly increased the levels of lactate dehydrogenase, troponin-I (cardiac cell damage marker), lipid peroxidation, triglyceride, interleukin-6, tumor necrosis factor-alpha, and caspase 3. However, it markedly reduced the antioxidant enzymes catalase and glutathione levels. Both doses of capsaicin could reverse cardiac cell damage markers, as shown by a significant decline in (lactate dehydrogenase and troponin-I). In addition, capsaicin significantly reduced the cytokine levels (interleukin-6 and tumor necrosis factor-alpha), caspase 3, lipid peroxidation, and triglycerides. However, capsaicin treatment significantly raised the antioxidant content of enzymes such as glutathione and catalase. The capsaicin-treated group restored the oxidative parameter's imbalance and generated considerable protection against cardiomyocyte harm from cyclophosphamide in male Wistar rats. These protective effects might be beneficial against the negative impacts of cyclophosphamide when used to treat cancer and immune-mediated diseases.
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Ahmed et al. (2023) conducted an RCT in Cyclophosphamide-induced cardiotoxicity. Capsaicin vs. Cyclophosphamide alone and vehicle control was evaluated on Cardiac cell damage markers (lactate dehydrogenase and troponin-I), oxidative and inflammatory markers. Capsaicin significantly reduced cardiac cell damage markers, inflammatory cytokines, and oxidative stress in male Wistar rats with cyclophosphamide-induced cardiotoxicity.
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