Using transgenic, conditional knockout mice, yeast two-hybrid, RNA interference, immunohistochemistry, in vivo imaging technology, electron microscope and other technologies, the molecular mechanism of nerve cell death in cerebral ischemia and Parkinson's disease was studied, and the mechanism of DNA oxidative damage and repair in ischemic brain injury was clarified. Using the concept of apoptosis regulation, a new type of intervention therapy was successfully designed in stroke model, and it was reported for the first time in the world that the anti-apoptosis protein Bcl-xL was successfully introduced into brain cells by protein introduction technology, and it showed remarkable anti-ischemic brain damage effect. Jun Chen Laboratory is one of the pioneers in the study of oxidative DNA damage and repair in ischemic brain injury, and it is the first time to show the evolution of oxidative DNA damage. It is suggested that single strand breaks and AP sites are early arbiters of neuron death or survival in brain injury caused by cerebral ischemia and epilepsy. The role of redox sensitive signal molecules in the apoptosis pathway in response to PD-related toxic stress was described for the first time. The results suggest that PRX2 and ASK 1 may be the intervention targets of PD treatment. It is proved for the first time that the mitochondria of neurons in the brain contain an active BER system to repair oxidative DNA damage, and the expression of APE or Beta-pol, the key enzyme of BER pathway, significantly affects the survival of neurons after ischemic injury. Published more than SCI papers 100 in PNAS, J Neurosci, Stroke, JCBFM and other journals, edited 2 monographs and summarized more than 30 articles.

research direction

Cell therapy and its rehabilitation mechanism after brain injury