Neurological Improvement via Lysophosphatidic Acid Administration in a Rodent Model of Cardiac Arrest-Induced Brain Injury

• Published in: International journal of molecular sciences Vol. 24; no. 24; p. 17451
• Main Authors: Nishikimi, Mitsuaki, Choudhary, Rishabh C, Shoaib, Muhammad, Yagi, Tsukasa, Becker, Lance B, Kim, Junhwan
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 14.12.2023
• Subjects: biomarkers; Brain damage; brain function; Brain research; Cardiac arrest; Cardiac arrhythmia; Fatty acids; Heart rate; Hemodynamics; Ischemia; Lipids; lysophospholipids; Metabolism; Metabolites; neurological outcomes; Physiology; Traumatic brain injury; brain function; neurological outcomes; lysophospholipids; cardiac arrest; biomarkers
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms242417451

Lysophosphatidic acid (LPA) serves as a fundamental constituent of phospholipids. While prior studies have shown detrimental effects of LPA in a range of pathological conditions, including brain ischemia, no studies have explored the impact of LPA in the context of cardiac arrest (CA). The aim of this study is to evaluate the effects of the intravenous administration of an LPA species containing oleic acid, LPA (18:1) on the neurological function of rats (male, Sprague Dawley) following 8 min of asphyxial CA. Baseline characteristics, including body weight, surgical procedure time, and vital signs before cardiac arrest, were similar between LPA (18:1)-treated ( = 10) and vehicle-treated ( = 10) groups. There was no statistically significant difference in 24 h survival between the two groups. However, LPA (18:1)-treated rats exhibited significantly improved neurological function at 24 h examination (LPA (18:1), 85.4% ± 3.1 vs. vehicle, 74.0% ± 3.3, = 0.045). This difference was most apparent in the retention of coordination ability in the LPA (18:1) group (LPA (18:1), 71.9% ± 7.4 vs. vehicle, 25.0% ± 9.1, < 0.001). Overall, LPA (18:1) administration in post-cardiac arrest rats significantly improved neurological function, especially coordination ability at 24 h after cardiac arrest. LPA (18:1) has the potential to serve as a novel therapeutic in cardiac arrest.