Objective To investigate the protective effects and mechanisms of soybean phospholipid powder on nerve cells in vitro and rats neural tissues.Methods In the cell experiments, the cytotoxicity of soybean phospho-lipid powder with different concentrations on mouse microglia cells (BV2) and rat adrenal pheochromocytoma (PC12) cells was observed by cell counting kit-8(CCK-8) assay.The effect of soybean phospholipid powder on the NO level of BV2 cells was analyzed by NO determination experiment, and the synaptic growth of PC12 cells was observed under the microscope.In the animal experiment, the cognitive dysfunction of rat was simulated by scopol-amine rat model.Then the learning and memory abilities of rat were tested by Morris water maze experiment;hipp-ocampal tissue morphology and nerve cell density of scopolamine model mice were observed by hematoxylin-eosin staining (HE) staining.Results Soybean phospholipid powder had no obvious cytotoxicity on BV2 cells and PC12 cells within the concentration of 1000μg/ml.Compared with the control group, the NO secretion of BV2 cells pre-treated with soybean phospholipid powder significantly decreased (P<0.01) , and the neuronal synapse growth of PC12 cells significantly increased (P <0.01) .In comparison to the model group, soybean phospholipid powder significantly improved the learning and memory ability of scopolamine model rats (P<0.05) , reduced the neuronal damage in dentate gyrus (DG), cornu ammonis3 (CA3), cornu ammonis1 (CA1) areas of hippocampus, and in-creased the density of nerve cells (P<0.001).Conclusion Soybean phospholipid powder can play a neuropro-tective role by reducing neuroinflammation and promoting neuronal synapse growth at the cellular level, and im-prove the learning and memory ability of rats with cognitive impairment, reduce hippocampal tissue damage.

Objective : To investigate the protective effect and mechanism of Hudi Enteric capsules in ionizing radiation injury to small intestinal crypt cells (IEC⁃6 cells) in rats. Methods : IEC⁃6 cells were irradiated with 6 mega electron volt X ⁃rays (2 , 4 , 6 , 8 and 10 Gy) , cell clone formation assay was used to detect cell proliferation , and the 6 Gy ionizing radiation was selected to establish a cellular radiation damage model according to the cell survival rate. The effect of each concentration ( 12. 5 , 25 , 50 , 100 and 200 μg/ml) of Hudi enteric extract on the viability of IEC⁃6 cells was examined by cell counting kit⁃8(CCK⁃8) method , and the effect on the viability of IEC⁃6 cells after irradiation at ( 10 , 20 , 40 and 80 μg/ml) concentrations was examined according to the results. After obtaining the optimal irradiation dose and extract concentration , the cells were divided into control group , model group and Hudi extract group (80 μg/ml) , the control group was pseudo⁃irradiated and the other two groups received 6 Gy of ionizing radiation , and the Hudi enteric extract group was pre⁃treated with drugs 2 h before irradiation. Apoptosis was detected by Annexin V ⁃PI double staining; cell senescence was detected by β ⁃galactosidase (β⁃Gal) staining; reactive oxygen species was detected by DCFH⁃DA fluorescent probe ; the corresponding protein expression of p16 , p21 , Catalase (CAT) and Superoxide dismutase ( SOD2) was detected by Western blot. Results : The proliferation of IEC⁃6 cells was inhibited by radiation doses ranging from 4 Gy to 10 Gy(P < 0. 001) ; (P < 0. 001) , and the apoptosis rate , β ⁃Gal positivity rate and DCFH⁃DA fluorescence intensity in the Hudi enteric extract group were lower than those in the model group (P < 0. 05) . The protein expressions of CAT and SOD2 in the Hudi extract group were higher than those in the model group ( P < 0. 05) , and the protein expressions of p16 and p21 were lower than those in the model group (P < 0. 05) . Conclusion The mechanism of action of Hudi enteric capsules that attenuate radiation damage in IEC⁃6 cells may be related to the inhibition of reactive oxygen species production , reduction of oxidative stress , and attenuation of cellular senescence and apoptosis.