Overall systematic approach to sepsis damages on urogenital tissues: protective power of lacosamide

• Published in: Archives of gynecology and obstetrics Vol. 300; no. 4; pp. 941 - 955
• Main Authors: Gunyeli, Ilker, Saygin, Mustafa, Ozmen, Ozlem
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-10-2019; Springer Nature B.V
• Subjects: Animals; Endocrinology; Female; General Gynecology; Gynecology; Human Genetics; Lacosamide - pharmacology; Lacosamide - therapeutic use; Male; Medicine; Medicine & Public Health; Obstetrics/Perinatology/Midwifery; Oxidative stress; Rats; Rats, Wistar; Sepsis; Sepsis - complications; Sepsis - drug therapy; Sepsis - pathology; Tumor necrosis factor-TNF; Urogenital System - drug effects; Urogenital System - pathology; Voltage-Gated Sodium Channel Blockers - pharmacology; Voltage-Gated Sodium Channel Blockers - therapeutic use; Immunohistochemistry; Lipopolysaccharide; Sepsis; Urogenital system; Lacosamide
• ISSN: 0932-0067; 1432-0711
• DOI: 10.1007/s00404-019-05262-1

Purpose
The aim of the study was to evaluate the harmful effects of sepsis on the urogynecological tissues and the ability of Lacosamide (LCM) on Lipopolysaccharide (LPS)-induced cytokine production, oxidative stress and apoptotic pathways, in the experimental rat sepsis model.
Methods
Twenty-four female Wistar albino rats (12 months old) were divided into 3 groups as follows: control group (Group I) (0.1 ml/oral and i.p. saline, single dose), sepsis group (Group II) (5 mg/kg LPS, i.p. single dose) and sepsis + LCM group (Group III) (5 mg/kg LPS, i.p. single dose and 40 mg/kg LCM). Six hours after the last LPS administration, the animals were sacrificed. Subsequently, the analyses of urogenital tissues total oxidant/antioxidant status, histopathological and immunohistochemical analyses were performed.
Results
Total oxidant capacity (TOC) and oxidative stress index (OSI) values in the urogenital tissues were increased in the urogenital tissues in Group II [Total antioxidant capacity (TAC) was decreased] compared to group I (
p
 < 0.05). LCM improved these values (
p
 < 0.05). The immunohistochemical markers (Tumor Necrosis Factor-alpha (TNF-α), interleukin-1 beta (IL-1β), heat shock protein 70 (HSP-70), C-reactive protein (CRP), Malondialdehyde (MDA) were significantly increased in Group II (
p
 < 0.001). With the administration of LCM (Group III), the expressions of above-mentioned markers were markedly decreased (
p
 < 0.001). Marked hyperemia and slight hemorrhages with neutrophil leukocyte infiltrations were seen histopathologically in Group II. LCM treatment ameliorated the pathological findings.
Conclusion
These findings demonstrated that sepsis caused oxidative stress, apoptosis and inflammation in the urogenital tissues. We revealed that LCM ameliorated the damage caused by sepsis in urogenital tissue.