Exogenous phosphatidic acid reduces acetaminophen-induced liver injury in mice by activating hepatic interleukin-6 signaling through inter-organ crosstalk.
10.1016/j.apsb.2021.08.024
- Author:
Melissa M CLEMENS
1
;
Stefanie KENNON-MCGILL
2
;
Joel H VAZQUEZ
1
;
Owen W STEPHENS
3
;
Erich A PETERSON
3
;
Donald J JOHANN
3
;
Felicia D ALLARD
4
;
Eric U YEE
4
;
Sandra S MCCULLOUGH
5
;
Laura P JAMES
5
;
Brian N FINCK
6
;
Mitchell R MCGILL
1
Author Information
1. Department of Pharmacology and Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
2. Department of Environmental and Occupational Health, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
3. Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
4. Department of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA.
5. Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
6. Division of Geriatrics and Nutritional Sciences, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
- Publication Type:Journal Article
- Keywords:
Acute liver failure;
Acute liver injury;
Adipokine;
Cytokine;
Dietary supplement;
Drug-induced liver injury;
Hepatotoxicity;
Lipid
- From:
Acta Pharmaceutica Sinica B
2021;11(12):3836-3846
- CountryChina
- Language:English
-
Abstract:
We previously demonstrated that endogenous phosphatidic acid (PA) promotes liver regeneration after acetaminophen (APAP) hepatotoxicity. Here, we hypothesized that exogenous PA is also beneficial. To test that, we treated mice with a toxic APAP dose at 0 h, followed by PA or vehicle (Veh) post-treatment. We then collected blood and liver at 6, 24, and 52 h. Post-treatment with PA 2 h after APAP protected against liver injury at 6 h, and the combination of PA and
