The Cardioprotective Effects of Atorvastatin in Experimental Endotoxemia

Abstract

Sepsis, a potentially fatal illness caused by infection, frequently leads to the failure of multiple organs, including the heart. This study aimed to investigate the potential mechanism by which atorvastatin improves heart function following sepsis. A total of 35 male Swiss albino mice, weighing between 30 and 38 grams and aged 8 to 12 weeks, were randomly allocated into five groups. Each group consisted of seven animals. The control group maintained their regular diet until the designated sampling time. The sham group underwent laparotomy and anesthesia. The sepsis group underwent the cecal ligation and puncture procedure. The vehicle group received intraperitoneal injections of an equivalent volume of dimethyl sulfoxide (DMSO) for five days, followed by the cecal ligation and puncture procedure. The Atorvastatin group received intraperitoneal injections of 20 mg/kg of Atorvastatin for five days after the cecal ligation and puncture procedure. Twenty hours following the cecal ligation and puncture procedure, the mice were humanely killed and samples of serum and heart tissue were obtained. The serum levels of NF-KB, FOXO3A, CASPASE3, and NT-PROPNB were evaluated. The data, which followed a normal distribution, was examined using t-tests and ANOVA tests with a significance level of p<0.05. The group of sepsis exhibited considerably elevated levels of NF-KB, FOXO3A, CASPASE3, and NT-PROPNB compared to the sham group. However, the pre-treated group with Atorvastatin demonstrated significantly reduced levels (p<0.05) of these markers compared to the sepsis group. The histological characteristics of mice treated with Atorvastatin showed slight variations in comparison to control and sham groups. Our inquiry findings suggest that Atorvastatin exhibits anti-apoptotic and cardioprotective properties in cases of polymicrobial sepsis; this is supported by a significant reduction in levels of NF-KB, FOXO3A, CASPASE3, and NT-PROPNB in the bloodstream.