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Updated: Jan 12, 2026
LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
Published on: April 4, 2016
Exogenous carbon monoxide prevents a decrease of mitochondrial membrane potential in lipopolysaccharide-stimulated
Tomiko Yakura1, Eri Nanizawa2, Yutaro Natsuyama1
1Department of Anatomy, Tokyo Medical University.
Background:
Acute inflammation is induced by lipopolysaccharide (LPS), accompanied by activation of platelets. Carbon monoxide (CO), an endogenous bioactive gas, has been shown to bind to mitochondria and exert anti-inflammatory effects. In this study, we investigated the effect of CO on the mitochondrial membrane potential of platelets activated by LPS.
Methods:
To elucidate the mechanism of the LPS-induced platelet response, human platelets were stimulated with LPS (10 μg/mL). Human platelet concentrates were divided into four groups: Untreated (Control), LPS-treated (LPS), LPS and CO-dissolved solution-treated (LPS + CO), and LPS and exogenous carbon monoxide releasing molecule-2-treated (LPS + CORM-2) groups. After 30 minutes, lactate levels and mitochondrial membrane potential (ΔΨm) in the platelets were measured. Morphological changes of the platelets were also observed using transmission electron microscopy.
Results:
In the LPS group, the proportion of platelets with depolarized ΔΨm increased, accompanied by elevated lactate levels compared with the control group. On the other hand, in the LPS+CO and LPS+CORM-2 groups, the proportion of depolarized platelets did not significantly increase, and lactate levels were not significantly elevated. Morphologically, elongating pseudopods and cell condensation were observed in the LPS group, however, these changes were not induced in the LPS+CO and LPS+CORM-2 groups.
Conclusion:
These results suggest that CO prevents a decrease in the platelet ΔΨm and thereby inhibits platelet activation by LPS treatment.
