Objective Neuronal loss in the central nervous system is central to the occurrence of neurodegenerative diseases. Pharmaceutical companies have devoted much effort to developing new drugs against such diseases, since there are currently no effective drugs for neurodegenerative disease treatment. Promoting the capacity for nerve regeneration is an ideal treatment target. The present study aimed to investigate the neurotrophic effects of 7,8-dihydroxycoumarin (DHC) or daphnetin in primary cultured rat cortical neurons. Methods Cortical neurons were identified by microtubule-associated protein 2 (MAP2) immunostaining. Morphological observation was used to measure the average length of neurite outgrowth. MTT and lactate dehydrogenase assays were used to assess neuronal survival. The mRNA expression of MAP2 and brain-derived neurotrophic factor (BDNF) was measured by RT-PCR. Results MAP2 immunostaining showed that most of the cultured cells were neurons. Compared with the vehicle control group, DHC promoted neurite outgrowth and prolonged neuronal survival time at concentrations ranging from 2 to 8 μmol/L. Expression of both BDNF mRNA and MAP2 mRNAwas increased in the groups treated with 2, 4 and 8 μmol/L DHC. Conclusion DHC significantly increases neurite outgrowth and promotes neuronal survival in primary cultured rat cortical neurons. The neurotrophic effects of DHC are probably associated with increased BDNF expression. Objective Neuronal loss in the central nervous system is central to the occurrence of neurodegenerative diseases. an ideal treatment target. The present study aimed to investigate the neurotrophic effects of 7,8-dihydroxycoumarin (DHC) or daphnetin in primary cultured rat cortical neurons. Methods Cortical neurons were identified by microtubule-associated protein 2 (MAP2) immunostaining. Morphological observations was used to measure the average length of neurite outgrowth. MTT and lactate dehydrogenase assays were used to assess neuronal survival. The mRNA expression of MAP2 and brain-derived neurotrophic factor (BDNF) was measured by RT-PCR. Results MAP2 immunostaining showed that most of the cultured cells were neurons. Compared with the vehicle control gr oup, DHC promoted neurite outgrowth and prolonged neuronal survival time at concentrations ranging from 2 to 8 μmol / L. Expression of both BDNF mRNA and MAP2 mRNA was increased in the groups treated with 2, 4 and 8 μmol / L DHC. Conclusion DHC neurite outgrowth and promotes neuronal survival in primary cultured rat cortical neurons. The neurotrophic effects of DHC are probably associated with increased BDNF expression.