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Necrosis

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...

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Propofol Suppresses Ferroptosis via Modulating eNOS/NO Signaling Pathway to Improve Traumatic Brain Injury.

Zi-Lei Zheng^1,2, Xu-Peng Wang¹, Yu-Fei Hu¹

¹Department of Anesthesiology, The Third Hospital of Hebei Medical University, Shijiazhuang, China.

Brain and Behavior

|December 27, 2024

Summary

Propofol, an anesthetic, protects the brain after traumatic brain injury (TBI) by reducing iron-induced cell death (ferroptosis) via the endothelial nitric oxide synthase (eNOS)/NO pathway, improving cognitive function.

Keywords:

eNOS ferroptosis nitric oxide propofol traumatic brain injury

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

Traumatic brain injury (TBI) is a significant cause of mortality and disability.
Ferroptosis, a form of regulated cell death, plays a critical role in TBI pathogenesis.
The endothelial nitric oxide synthase (eNOS)/NO signaling pathway is implicated in neuroprotection.

Purpose of the Study:

To investigate the neuroprotective effects of propofol in TBI.
To determine if propofol inhibits ferroptosis by modulating the eNOS/NO signaling pathway.

Main Methods:

Bioinformatic analysis of the GSE173975 dataset for TBI-related gene expression.
Establishment of a mouse TBI model with propofol or saline treatment.
Assessment of neuronal function, iron deposition, ferroptosis, neuroinflammation, and cognitive deficits using histological staining, Western blot, immunofluorescence, Morris water maze, and novel object recognition tests.

Main Results:

TBI induced significant iron deposition, ferroptosis, neuronal apoptosis, neuroinflammation, and cognitive dysfunction.
Propofol treatment markedly reduced these TBI-induced pathologies.
Propofol increased eNOS protein expression and NO content, with effects reversed by L-NAME, an eNOS inhibitor.

Conclusions:

Propofol demonstrates significant neuroprotective effects in TBI by inhibiting ferroptosis via the eNOS/NO pathway.
These findings support the clinical use of propofol for TBI and suggest new therapeutic strategies.