Objective To investigate the significance of Tafazzin(TAZ) regulating mitophagy in traumatic brain injury(TBI).

Methods The controlled cortical impingement(CCI) model of rat brain was established. The mitochondrial autophagy after CCI and role of TAZ in TBI were examined by western blotting, electron microscopy, immunofluorescence, TUNEL, HE and FJC. The mechanical stretching model of neuron cells was established in vitro, and the effects of TAZ knockdown on mitochondrial autophagy was investigated by western blot and double immunofluorescence staining.

Results Within 24h after CCI injury, the levels of general autophagy and mitophagy increased significantly, and at the same time, the expression of TAZ protein increased with time increasing. In vivo and in vitro results showed that TAZ knockdown blocked mitophagy without affecting general autophagy. In addition, TAZ knockdown led to a significant increase in the number of FJC-positive cells in the damaged cortex after 1 week of CCI (P < 0.01), and the lesion volume in both cortical and hippocampal tissues was larger (P < 0.05).

Conclusions The activation of TAZ dependent mitophagy is an important part of endogenous repair induced by experimental TBI. Inhibition of TBI-induced mitochondrial autophagy may worsen cognitive function by increasing apoptosis.