The Effects of Lipoic Acid on Markers of Oxidative Stress and Inflammation in the Lungs of Valproic Acid-Treated Rats

In this experimental study, the effect of lipoic acid (LA) on lung damage caused by valproic acid (VPA) was investigated. The antioxidant, oxidative stress, and inflammation indicators such as glutathione (GSH), lipid peroxidation (LPO), catalase (CAT), superoxide dismutase (SOD), glutathione-S-tran...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of the Turkish Chemical Society, Section A, Chemistry Section A, Chemistry, 2024-08
Hauptverfasser: Alev, Burcin, Türkyılmaz, İsmet Burcu, İpekçi, Hazal, Üstündağ, Ünsal Veli, Tunalı-akbay, Tuğba, Emekli Alturfan, Ebru, Yanardağ, Refiye, Yarat, Ayşen
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:In this experimental study, the effect of lipoic acid (LA) on lung damage caused by valproic acid (VPA) was investigated. The antioxidant, oxidative stress, and inflammation indicators such as glutathione (GSH), lipid peroxidation (LPO), catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), nitric oxide (NO), sialic acid (SA), myeloperoxidase (MPO), and tissue factor (TF) were examined. Sprague Dawley rats were used, and they were randomly divided into four groups as follows: Control group, LA group received 50 mg LA/kg/day for 15 days, VPA group received 500 mg VPA/kg/day for 15 days, and VPA+LA group received the same doses of VPA and LA for 15 days. On day 16, lung tissues were taken. VPA caused the decreases in GSH, SA and SOD values and the increases LPO, NO, and TF values. LA reversed the changes in GSH, SOD, and TF values. GST and CAT activities did not change significantly by the effect of VPA or LA. On the other hand, the inhibitory effect of VPA on MPO, which is an inflammatory marker, and the pro-oxidant effects of LA causing the increases in both LPO and MPO values were observed in lung tissue. These regulations may help LA to overcome oxidative stress caused by VPA in the lung. Further studies are needed to confirm the mechanism underlying VPA-induced MPO inhibition in the lung.
ISSN:2149-0120
2149-0120
DOI:10.18596/jotcsa.1520611