Wang, Xiaonan; Hu, Xuejun; Zhang, Li; Xu, Xi; Sakurai, Takashi published the artcile< Nicotinamide mononucleotide administration after sever hypoglycemia improves neuronal survival and cognitive function in rats>, Product Details of C7H7NO, the main research area is brain injury nicotinamide mononucleotide hypoglycemia neuron survival; Cognitive impairment; Hypoglycemia; Neuronal survival; Nicotinamide mononucleotide; PARP-1; ROS.
Here we investigated whether NMN could reduce brain injury after severe hypoglycemia. We used a rat model of insulin-induced severe hypoglycemia and injected NMN (500 mmg/kg, i.p., one week) following 30 min of severe hypoglycemia, at the time of glucose administration. ROS accumulation, PARP-1 activation, NAD+ and ATP levels in hippocampus were also measured. Cognitive function was assessed using the Morris water maze 6 wk after severe hypoglycemia. The addition of NMN reduced neuron death by 83 ± 3% (P < 0.05) after severe hypoglycemia. The hippocampal LTP was significantly reduced by severe hypoglycemia but showed recovery in the NMN addition group. NMN treatment also attenuated the severe hypoglycemia-induced spatial learning and memory impairment. Mech., we showed that NMN administration decreased ROS accumulation, suppressed PARP-1 activation, and restored levels of NAD+ and ATP in hippocampus. All these protective effects were reversed by 3-acetylpyridine (3-AP), which generates inactive NAD+. In summary, NMN administration following severe hypoglycemia could ameliorate neuronal damage and cognitive impairment caused by severe hypoglycemia. These results suggest that NMN may be a promising therapeutic drug to prevent hypoglycemia-induced brain injury. Brain Research Bulletin published new progress about Biological memory. 350-03-8 belongs to class pyridine-derivatives, and the molecular formula is C7H7NO, Product Details of C7H7NO.