Anti-inflammatory effect of omega-7 against doxorubicin-induced cardiotoxicity in male rats: An observational study

Background : Doxorubicin is a crucial anticancer medication, however, cardiotoxicity is a severe adverse effect of doxorubicin therapy. Various mechanisms, including inflammation, have been postulated to account for this negative effect. The omega-7 fatty acid is a polyunsaturated fatty acid with anti-inflammatory and antioxidant properties. Therefore, the study's objective was to see whether omega-7 had any possible protective benefits against doxorubicin-induced cardiotoxicity in male rats. Methods: 28 male Wister rats were split into four groups (seven per group). Group 1 (negative control): healthy animals received normal saline orally as the vehicle for eight successive days and were sacrificed on day nine. Group 2 (positive control): animals that received a single dose of doxorubicin hydrochloride (IP 15mg/kg) were sacrificed the next day. Group 3: the animals were administered omega-7 orally at a 100 mg/kg/day dose for eight days. A single injection of doxorubicin IP (15 mg/kg) was given on day nine. The animals were sacrificed on day 10. Group 4: the animal was administered omega-7 orally at a 300 mg/kg/day dose for eight days. A single injection of doxorubicin IP (15 mg/kg) was given on day nine. The animals were sacrificed on day 10. Serum was collected and used to measure lactate dehydrogenase, creatinine kinase-MB, tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta. Results: Lactate dehydrogenase and creatinine kinase-MB levels in group 3 (100mg/kg) were significantly lower than in group 2 (p>0.05) and significantly lower in group 4 (300mg/kg) than in group 2. Tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta levels were considerably lower in the omega-7-treated groups (100 and 300mg/kg) than in the positive control group (p<0.05). Conclusion: Through a mechanism involving the reduction of inflammation, omega-7 may preserve the cardiac tissue against doxorubicin-induced damage.