A Rat Model of Surgical Brain Injury

Inhibition of the NKCC1/NF-κB Signaling Pathway Decreases Inflammation and Improves Brain Edema and Nerve Cell Apoptosis in an SBI Rat Model

“…At the same time, due to incision, electrocoagulation, bleeding, and other invasive operations in the process of brain surgery, there will be some damage to the brain tissue around the operation site, which is called surgical brain injury (SBI) (Akyol et al, 2018). Studies have shown that nearly one-fifth of patients experience serious complications after craniocerebral operation (Sherchan et al, 2016). After brain injury caused by various reasons, immune cells are activated, triggering the release of pro-inflammatory cytokines, thus resulting in the formation of an inflammatory environment in the brain, which is a feature of many brain pathologies.…”

“…After brain injury, inflammatory cytokines such as IL-1β, IL-6, TNF-α, as well as oxidative stress mediators are upregulated, which then may result in apoptosis of large neurons and incur blood-brain barrier (BBB) damage, thereby exacerbating brain edema and nerve cell damage (Chen et al, 2014;Zhang et al, 2020b). Inflammation can increase cell permeability, disrupt the BBB, and lead to vasogenic brain edema; it also causes cell degeneration and apoptosis, and if necrotic and apoptotic cells are not immediately consumed by phagocytes, then these could release toxic signals to surrounding cells, leading to cytotoxic brain edema (Sherchan et al, 2017;Xiao et al, 2018).…”