Necrostatin-1 prolongs latency to convulsion in mice exposed to high oxygen partial pressure.

Autor:	Guan ZB; Department of Respiratory and Critical Illness, Changhai Hospital, the Naval Military Medical University, People's Liberation Army, Shanghai, 200433, China., Zhou YY; Department of Orthopedic Surgery, Changzheng Hospital, the Naval Military Medical University, People's Liberation Army, Shanghai, 200003, China., Cen Y; Department of Anesthesiology and Perioperative Medicine, Shanghai Fourth People's Hospital, Tongji University School of Medicine, Shanghai, China., Feng HD; Department of Anesthesiology and Perioperative Medicine, Shanghai Fourth People's Hospital, Tongji University School of Medicine, Shanghai, China., Liu WW; Department of Diving and Hyperbaric Medicine, the Naval Military Medical University, People's Liberation Army, Shanghai, 200433, China., Yi HJ; Department of Hyperbaric Oxygen, Changhai Hospital, the Naval Military Medical University, People's Liberation Army, Shanghai, 200433, China., Chen H; Department of Hyperbaric Oxygen, Changhai Hospital, the Naval Military Medical University, People's Liberation Army, Shanghai, 200433, China.; Corresponding author: Dr Hui Chen, Department of Anesthesiology and Perioperative Medicine, Shanghai Fourth People's Hospital, Tongji University School of Medicine, No 1279, Sanmen Road, 200434, Shanghai, China, chenhui_md@163.com.
Jazyk:	angličtina
Zdroj:	Diving and hyperbaric medicine [Diving Hyperb Med] 2021 Jun 30; Vol. 51 (2), pp. 134-139.
DOI:	10.28920/dhm51.2.134-139
Abstrakt:	Introduction: Exposure to very high oxygen partial pressure may cause central nervous system oxygen toxicity (CNS-OT). The role of necroptosis in the pathogenesis of CNS-OT is still unclear. Methods: In experiment one, male C57BL/6 mice in the oxygen toxicity (OT) group (n = 5) and necrostatin-1 (Nec-1; a necroptosis inhibitor) (1.5 mg·kg-1, intraperitoneal) group (n = 5) were exposed to pure oxygen at 600 kPa, and the latency to tonic-clonic seizure was recorded. In experiment two, mice were divided into three groups: control group (n = 11), OT group (n = 12) and Nec-1 group (n = 12). Nec-1 was intraperitoneally administered 30 min before oxygen exposure. Mice in the OT group and Nec-1 group were exposed to pure oxygen at 400 kPa for 30 min, and then sacrificed; the brain was harvested for the assessment of inflammation, oxidative stress and necroptosis. Results: Experiment one. Nec-1 pre-treatment significantly prolonged the latency to seizure (245 [SD 18] seconds in the OT group versus 336 (34) seconds in the Nec-1 group). Experiment two. Nec-1 pre-treatment markedly reduced inflammatory cytokines and inhibited cerebral necroptosis, but failed to significantly suppress cerebral oxidative stress. Conclusions: These findings indicate necroptosis is involved in the pathogenesis of CNS-OT, and inhibition of necroptosis may prolong seizure latency, but the specific mechanisms should be investigated further. (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)
Databáze:	MEDLINE
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