Abstract
Sepsis is a systemic inflammatory consequence resulting from microbial infection, assessed as a worldwide healthcare issue. Sepsis can result in multiorgan dysfunction, including cardiac, renal, hepatic, and cerebral dysfunction. Cardiotoxicity can occur in humans and rodents during sepsis, leading to increased mortality. The current study aims to explore the possible cardioprotective effects of octreotide during sepsis-induced cardiotoxicity. This study was done with a total of forty male albino Swiss mice, aged 8-12 weeks and weighing 25-30 gm. These animals had free access to food and water. After two weeks of adaptation, mice were divided into four groups (n=10): 1) Normal group: healthy mice; 2) CLP group: mice underwent CLP operation; 3) Vehicle group: mice received DMSO. 4) Octreotide group: mice received octreotide (10 mg/kg) subcutaneously in 2 divided doses for 5 consecutive days. All groups underwent CLP operation on the 4th day, then sacrificed on the 5th day then blood, and tissue sampling was done. The Octreotide group demonstrated a significant (P<0.05) decrease in the myocardial levels of cardiac troponin-I as compared to the CLP group. Furthermore, the octreotide group demonstrated a significant (P<0.05) decrease in the serum level of inflammatory cytokines (TNF-α, IL-6, & IL-1β) as compared to the CLP group. Additionally, the octreotide group showed a significant (P<0.05) elevation in the myocardial activity of SOD and a reduction in MDA level compared to the CLP group. Histologically, all mice in the CLP group showed a significant (P<0.05) cardiac tissue injury, while the octreotide groups showed a significant (P<0.05) reduced level of cardiac tissue injury. The results of the present study revealed that octreotide attenuates sepsis-induced cardiotoxicity through different protective effects; they include the anti-inflammatory effect through their ability to decrease serum levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6). Also, the anti-oxidant effect through their ability to decrease myocardial levels of MDA and increase the myocardial activity of SOD. Additionally, the direct cardiac protective effect through the lower level of cardiac troponin- I and the reduction of histopathological changes during sepsis-induced cardiotoxicity.