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Article

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

1
Laboratory for Critical Care Physiology, Feinstein Institutes for Medical Research, Manhasset, NY 11030, USA
2
Department of Emergency Medicine, North Shore University Hospital, Manhasset, NY 11030, USA
3
Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY 11549, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2023, 24(24), 17451; https://doi.org/10.3390/ijms242417451
Submission received: 30 October 2023 / Revised: 7 December 2023 / Accepted: 9 December 2023 / Published: 14 December 2023
(This article belongs to the Special Issue Lysophosphatidic Acid Signaling in Health and Disease)

Abstract

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 (n = 10) and vehicle-treated (n = 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, p = 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, p < 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.
Keywords: biomarkers; lysophospholipids; cardiac arrest; brain function; neurological outcomes biomarkers; lysophospholipids; cardiac arrest; brain function; neurological outcomes

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MDPI and ACS Style

Nishikimi, M.; Choudhary, R.C.; Shoaib, M.; Yagi, T.; Becker, L.B.; Kim, J. Neurological Improvement via Lysophosphatidic Acid Administration in a Rodent Model of Cardiac Arrest-Induced Brain Injury. Int. J. Mol. Sci. 2023, 24, 17451. https://doi.org/10.3390/ijms242417451

AMA Style

Nishikimi M, Choudhary RC, Shoaib M, Yagi T, Becker LB, Kim J. Neurological Improvement via Lysophosphatidic Acid Administration in a Rodent Model of Cardiac Arrest-Induced Brain Injury. International Journal of Molecular Sciences. 2023; 24(24):17451. https://doi.org/10.3390/ijms242417451

Chicago/Turabian Style

Nishikimi, Mitsuaki, Rishabh C. Choudhary, Muhammad Shoaib, Tsukasa Yagi, Lance B. Becker, and Junhwan Kim. 2023. "Neurological Improvement via Lysophosphatidic Acid Administration in a Rodent Model of Cardiac Arrest-Induced Brain Injury" International Journal of Molecular Sciences 24, no. 24: 17451. https://doi.org/10.3390/ijms242417451

APA Style

Nishikimi, M., Choudhary, R. C., Shoaib, M., Yagi, T., Becker, L. B., & Kim, J. (2023). Neurological Improvement via Lysophosphatidic Acid Administration in a Rodent Model of Cardiac Arrest-Induced Brain Injury. International Journal of Molecular Sciences, 24(24), 17451. https://doi.org/10.3390/ijms242417451

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