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Updated: Jan 26, 2026

Detecting Behavioral Deficits in Rats After Traumatic Brain Injury
Published on: January 30, 2018
Potential Roles of NIX/BNIP3L Pathway in Rat Traumatic Brain Injury
Jialing Ma1, Haibo Ni2, Qin Rui3
11 Department of Anesthesia, The First People's Hospital of Zhangjiagang, Soochow University, Suzhou, China.
Abstract:
NIX/BNIP3L is known as a proapoptotic protein that is also related to mitophagy. Previous reports have shown that NIX could be involved in neuronal apoptosis after intracerebral hemorrhage, but it also plays a protective role in mitophagy in ischemic brain injury. How NIX works in traumatic brain injury (TBI) is unclear. Thus, this study was designed to observe the expression of NIX and perform a preliminary exploration of the possible effects of NIX in a rat TBI model. The results showed that NIX expression decreased after damage, and colocalized with neuronal cells in cortical areas. Moreover, when we induced upregulation of NIX, autophagy was increased, while neuronal apoptosis and brain water content decreased along with neurological deficits. These findings remind us that NIX probably plays a neuroprotective role in TBI through autophagy and apoptosis pathways.
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