Objective:To observe the effects of zinc supplementation on the function of brain after sleep deprivation(SD).Methods:Rats SD model was made by the “Flower Pot" technique.Three days later,the rats received Y-labyrinth test to test the function of learning and memory.NADPH-d histochemistry and ABC immunohistochemistry were applied to exam the activity of NOS and the levels of protein expression of nNOS in hippocampus of rats.Results:Compared with the normal group,Learning times of rats in Y-labyrinth test of the SD group increased(89.3?25.3 /67.1?29.3,t=1.81,P0.05).Compared with the SD group,in TZC supplementation group,the levels of NOS in sub-area of hippocampus(CA_1:27.2?2.8;CA_3:15.3?1.6;DG:21.8?1.9,P0.05).Conclusions:TZC supplementation can improve learning and memory function of rats,and the mechanisms might be related to increased level of NOS and the protein expression of nNOS in hippocampus of animals.

AIM:To investigate the effect of Sonic Hedgehog ( Shh) signaling blockade on the growth of hema-tocarcinoma cells and underlying mechanisms.METHODS: The expression of Shh signaling molecules in hematocarci-noma cell lines BEL-7402, Huh7 and HepG2 was detected by RT-PCR.The cell viability was detected by MTT assay.The cell cycle and apoptosis were analyzed by flow cytometry.The expression of apoptosis-related proteins was determined by Western blot.RESULTS:Shh signaling molecules were all expressed in BEL-7402, Huh7 and HepG2 cells.The mRNA expression of Patched ( Ptch) , Gli1 and Gli2 was down-regulated by anti-Shh antibody.Blockade of Shh signaling pathway inhibited the proliferation of hepatocarcinoma cells with increasing cells in G0/G1 phase and induced the apoptosis of hepa-tocarcinoma cells.Treatment with anti-Shh antibody down-regulated the protein expression of pro-caspase-3, pro-caspase-8 and pro-caspase-9, while up-regulated the protein levels of cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 in BEL-7402 cells.CONCLUSION:Blockade of Shh signaling pathway inhibits the growth of hepatocarcinoma at different levels by cell cycle arrest and inducing apoptosis of hematocarcinoma cells.