Duration of lipid peroxidation after acute spinal cord injury in rats and the effect of methylprednisolone

Abstract

<jats:sec> <jats:title>Object</jats:title> <jats:p>Oxidative stress leading to lipid peroxidation is a major cause of secondary injury following spinal cord injury (SCI). The objectives of this study were to determine the duration of lipid peroxidation following acute SCI and the efficacy of short-and long-term administration of methylprednisolone on decreasing lipid peroxidation.</jats:p></jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>A total of 226 female Wistar rats underwent clip-compression induced SCI. In the first part of the study, spinal cords of untreated rats were assayed colorimetrically for malondialdehyde (MDA) to determine lipid peroxidation levels at various time points between 0 and 10 days. In the second part of the study, animals were treated with methylprednisolone for either 24 hours or 7 days. Control animals received equal volumes of normal saline. Treated and control rats were killed at various time points between 0 and 7 days.</jats:p></jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>The MDA levels initially peaked 4 hours postinjury. By 12 hours, the MDA levels returned to baseline. A second increase was observed from 24 hours to 5 days. Both peak values differed statistically from the trough values (p &lt; 0.008). The methylprednisolone reduced MDA levels (p &lt; 0.04) within 12 hours of injury. No effect was seen at 24 hours or later.</jats:p></jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>The results of this study indicate that oxidative stress persists for 5 days following SCI in rats, and although methylprednisolone reduces MDA levels within the first 12 hours, it has no effect on the second lipid peroxidation peak.</jats:p></jats:sec>

The biochemical, histopathological and clinical comparison of the neuroprotective effects of subcutaneous adalimumab and intravenous methylprednisolone in an experimental compressive spinal cord trauma model

“…However, many clinics are now abandoning the use of methylprednisolone in clinical spinal cord trauma. Plasma MDA levels increase in spinal cord injury (11,45,48,49). A significant decrease in MDA levels has been shown to be present following the administration of methylprednisolone for the treatment of spinal cord compression injury (46).…”

Antioxidant effects of curcumin in spinal cord injury in rats

“…Spinal cord trauma results in a rapid and extensive oxidative stress. It has long been established that oxidative stress plays a critical role in the pathophysiology of SCI [27][28][29] Oxidative stress can result from increased reactive oxygen species (ROS) production, and/or from decreased ROS scavenging capability. The cells' natural protective system against the devastating actions of ROS includes the protective enzymes including SOD and other antioxidants.…”

Therapeutic effects of vitamin D3 on motor functions following experimental spinal cord injury

“…Çalışmamızda klinik olarak iyileşme saptanmış olsada histolojik olarak bulguların desteklenmemesinin sebebi olarak yaralanma sonrası ortaya çıkan sekonder hasarlanmanın yıkıcı etkisinin net süresinin bilinmemesine bağlandı. Hasar sonrası etki 3-6 haftaya kadar uzayabilmektedir ve çalışmamızda histolojik inceleme için örnek alınan dönemde bu etkilerin devam ettiği varsayılmıştır (60,61 Resim 6. Travma uygulanan ve cerrahi işlem sonrası 1., 3., 5. ve 7.…”