Potential Roles of NIX/BNIP3L Pathway in Rat Traumatic Brain Injury

Jialing Ma  ¹ , Haibo Ni  ² , Qin Rui  ³ , Huixiang Liu  ² , Feng Jiang  ² , Rong Gao  ² , Yanping Gao  ¹ , Di Li  ⁴ , Gang Chen  ⁵

• ¹ 1 Department of Anesthesia, The First People’s Hospital of Zhangjiagang, Soochow University, Suzhou, China.
• ² 2 Department of Neurosurgery, The First People’s Hospital of Zhangjiagang, Soochow University, Suzhou, China.
• ³ 3 Department of Laboratory, The First People’s Hospital of Zhangjiagang, Soochow University, Suzhou, China.
• ⁴ 4 Department of Neurosurgery and Translational Medicine Center, The First People’s Hospital of Zhangjiagang, Soochow University, Suzhou, China.
• ⁵ 5 Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of 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.

Keywords: NIX/BNIP3L; apoptosis; autophagy; traumatic brain injury.