AI Summary & Key Takeaways
AI InsightOverall, 24 1-year-old female Wistar Albino rats were divided into three groups: Group I (control), Group II (LPS group: 5 mg/kg LPS intraperitoneally, single dose), and Group III (LCM group: 40 mg/kg LCM intraperitoneally once daily for 3 days plus 5 mg/kg LPS 30 min after the last LCM treatment).
📌 3 Key Takeaways
Abstract
Bacterial lipopolysaccharides (LPS) generally increase the pathogenicity of the agent. This study aimed to examine the hepatic pathology and possible prophylactic effects of lacosamide (LCM) in a LPS-induced sepsis rat model. Overall, 24 1-year-old female Wistar Albino rats were divided into three groups: Group I (control), Group II (LPS group: 5 mg/kg LPS intraperitoneally, single dose), and Group III (LCM group: 40 mg/kg LCM intraperitoneally once daily for 3 days plus 5 mg/kg LPS 30 min after the last LCM treatment). Animals were euthanized 6 hours after LPS administration. Blood and liver samples collected during necropsy were analyzed biochemically, pathologically, and immunohistochemically. LPS caused a significant increase in serum aspartate aminotransferase, alanine aminotransferase, total bilirubin, direct bilirubin, indirect bilirubin, and alkaline phosphatase levels. Histopathological analysis revealed numerous neutrophil leucocyte infiltrations, slight hemorrhages in the liver, and degenerative or necrotic changes in hepatocytes. Increased expressions of malondialdehyde, C-reactive protein, heat shock protein-70, interleukin-1β, and tumor necrosis factor-α were observed in the LPS administered group. LCM ameliorated the biochemical, histopathological, and immunohistochemical findings. The present study results revealed that LCM ameliorated the LPS-induced liver damage in the rat models as evidenced by the biochemical and pathological findings.