Objective To study the effects of Puerarin(Pue)on survival rate,expression of GAP-43 and NGF in spinal motoneurons following brachial roots avulsion. Methods From March, 2014 to December, 2015, 192 adult Sprague Dawley rats were divided into four groups: Avulsion, Pue 50 treatment, Pue 100 and Pue 200 groups. The right C5-C7nerve roots were avulsed through the methods of cervical dorsal approach. Puerarin or normal saline was given immediatedly once daily to the rats respectively by the intraperitoneal injection. The rats were killed at 1, 2, 4 and 6 weeks after injury. The paraffin sections of C7 segment were stained with neutral red. Expression of GAP-43 and NGF were detected by Western blot. Results Compared to the avuled group, the motoneuron survival rates of Pue 100 and Pue 200 dose treatment groups increased on the second week and the sixth week(P < 0.05 or P < 0.01), and the Pue 200 dose treatment group increased on the fourth week(P < 0.01).In the anterior horn of all three groups, expression of GAP-43 increased from the 1st week to the 6 week after the operation, and reached the peak at the 4th week, and decreased at the 6th week. Compared to the avuled group, expression of GAP-43 protein increased in the Pue 100 and Pue 200 dose treatment groups at the 1st week and 2nd week,the expression of NGF protein increased in the three Pue treatment groups at four time points(P < 0.05 or P < 0.01). Conclusion Puerarin can improve the survival rates of spinal motoneurons after the brachial plexus root avulsion, and the expression of GAP-43 and NGF increased, suggesting that Puerarin may play an role in the repair of brachial plexus avulsions by promoting the ex-pression of nerve growth factors.

AIM:To explore the promotion of ferroptosis by artesunate(Art)and its underlying mechanism in osteosarcoma.METHODS:Human osteosarcoma U-2 OS cells were divided into 4 groups:control,ferrostatin-1(Fer-1),Art,and Art+Fer-1 groups.Cell viability was measured by CCK-8 assay,while reactive oxygen species(ROS),Fe2+,and glutathione(GSH)levels were measured using biochemical assays.Mitochondrial morphology was evaluated by trans-mission electron microscopy.The mRNA and protein levels of p53,solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)were determined by RT-qPCR and Western blot,respectively.RESULTS:It was found that Art significantly reduced the growth of U-2 osteosarcoma cells,as well as inducing ferroptosis by promoting the accu-mulation of Fe2+and ROS and reducing GSH levels,while the ferroptosis inhibitor ferrostatin-1 inhibited ferroptosis.It was also observed that Art affected mitochondrial morphology,resulting in smaller mitochondria,higher mitochondrial mem-brane density,and reduced numbers of cristae.Treatment with Art also downregulated both the mRNA and protein expres-sion of the ferroptosis-associated genes SLC7A11 and GPX4,while upregulating expression of p53,an upstream regulator of ferroptosis,thus inducing ferroptosis.CONCLUSION:Artesunate induces ferroptosis in osteosarcoma cells through the p53/SLC7A11/GPX4 signaling pathway.