Objective Objective To explore the effects of Propofol on neuronal autophagy,memory function,and the classical protein kinase Cγ(cPKCγ)-related pathway in the offspring of rats during the second trimester of pregnancy.Methods Thirty-six SD rats at 14 d of gestation were randomly divided into the control group,the Propofol group and the Propofol+cPKCγ inhibitor group,with 12 rats in each group.Ten pregnant mice were randomly selected from each group.The pregnancy continued until the offspring mice were born.The Morris water maze test was performed on the offspring mice at 30-34 d after birth.Western blotting was used to detect microtubule-associated protein light chain 3Ⅱ/Ⅰ(LC3 Ⅱ/LC3 Ⅰ),Beclin-1,cPKCγ and growth-associated protein-43(GAP-43)expression levels in hippocampal tissue,and immunofluorescence was used to determine the expression of autophagy-related protein ATG7 in hippocampal tissue.Results Compared with the control group,the Propofol group and the propofol+cPKCγ inhibitor group showed increased escape latency at 31,32,33 and 34 d after birth(P<0.05),while there was significantly decreased escape latency in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the Propofol group and the Propofol+cPKCγ inhibitor group had significantly decreased number of platform crossings(P<0.05),while there was significantly increased number of platform crossings in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the Propofol group and the Propofol+cPKCγ inhibitor group had increased time spent in quadrant I and decreased time spent in quadrant Ⅱ(P<0.05),while there was decreased time spent in quadrant Ⅰ and increased time spent in quadrant Ⅱ in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the LC3 Ⅱ/LC3 Ⅰratio,and the expression of Beclin-1,cPKCγ,and GAP-43 protein in the hippocampal tissue of offspring rats in the Propofol group and the Propofol+cPKCγ inhibitor group were significantly increased(P<0.05).Compared with the Propofol group,the LC3Ⅱ/LC3Ⅰ ratio,and the expression of Beclin-1,cPKCγ,and GAP-43 protein in the hippocampal tissue of offspring rats in the Propofol+cPKCγ inhibitor group was significantly decreased(P<0.05).Compared with the control group,the expression of ATG7 in the hippocampal tissue of offspring rats in both the Propofol group and the Propofol+cPKCγ inhibitor group was significantly increased(P<0.05).Compared with the propofol group,the expression of ATG7 in the hippocampal tissue of offspring rats in the Propofol+cPKCγ inhibitor group was significantly decreased(P<0.05).Conclusion Propofol can cause cognitive impairment in the offspring of rats during the second trimester of pregnancy,promote neuronal autophagy,and inhibit activation of the cPKCγ/GAP-43 pathway in the hippocampus,which may improve cognitive impairment in the offspring rats.

Objective Objective To explore the effects of Propofol on neuronal autophagy,memory function,and the classical protein kinase Cγ(cPKCγ)-related pathway in the offspring of rats during the second trimester of pregnancy.Methods Thirty-six SD rats at 14 d of gestation were randomly divided into the control group,the Propofol group and the Propofol+cPKCγ inhibitor group,with 12 rats in each group.Ten pregnant mice were randomly selected from each group.The pregnancy continued until the offspring mice were born.The Morris water maze test was performed on the offspring mice at 30-34 d after birth.Western blotting was used to detect microtubule-associated protein light chain 3Ⅱ/Ⅰ(LC3 Ⅱ/LC3 Ⅰ),Beclin-1,cPKCγ and growth-associated protein-43(GAP-43)expression levels in hippocampal tissue,and immunofluorescence was used to determine the expression of autophagy-related protein ATG7 in hippocampal tissue.Results Compared with the control group,the Propofol group and the propofol+cPKCγ inhibitor group showed increased escape latency at 31,32,33 and 34 d after birth(P<0.05),while there was significantly decreased escape latency in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the Propofol group and the Propofol+cPKCγ inhibitor group had significantly decreased number of platform crossings(P<0.05),while there was significantly increased number of platform crossings in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the Propofol group and the Propofol+cPKCγ inhibitor group had increased time spent in quadrant I and decreased time spent in quadrant Ⅱ(P<0.05),while there was decreased time spent in quadrant Ⅰ and increased time spent in quadrant Ⅱ in the Propofol+cPKCγ inhibitor group,compared with the Propofol group(P<0.05).Compared with the control group,the LC3 Ⅱ/LC3 Ⅰratio,and the expression of Beclin-1,cPKCγ,and GAP-43 protein in the hippocampal tissue of offspring rats in the Propofol group and the Propofol+cPKCγ inhibitor group were significantly increased(P<0.05).Compared with the Propofol group,the LC3Ⅱ/LC3Ⅰ ratio,and the expression of Beclin-1,cPKCγ,and GAP-43 protein in the hippocampal tissue of offspring rats in the Propofol+cPKCγ inhibitor group was significantly decreased(P<0.05).Compared with the control group,the expression of ATG7 in the hippocampal tissue of offspring rats in both the Propofol group and the Propofol+cPKCγ inhibitor group was significantly increased(P<0.05).Compared with the propofol group,the expression of ATG7 in the hippocampal tissue of offspring rats in the Propofol+cPKCγ inhibitor group was significantly decreased(P<0.05).Conclusion Propofol can cause cognitive impairment in the offspring of rats during the second trimester of pregnancy,promote neuronal autophagy,and inhibit activation of the cPKCγ/GAP-43 pathway in the hippocampus,which may improve cognitive impairment in the offspring rats.

Objective To establish and evaluate the animal model induced by inhalation injury of airborne fine particulate matter (PM2?5). Methods We manufactured equipment for rats aerosol inhalation with PM2?5. The effects of several facters such as concentrations(100 ± 10 μg/m3、150 ± 10 μg/m3、200 ± 10 μg/m3 )、time(1w、2w、4w、8w、12w)、method (non?exposed intratracheal instillation method and aerosol inhalation) and animals (Wistar rats, BN rats and guinea pigs) were investigated to establish the model. The respiratory rate, forced vital capacity ratio of forced expiratory volume ( FEV1/FVC) and arterial partial pressure of oxygen ( PO2 ) were measured, the pathological changes of bronchial and lung tissues under light microscope were observed. The success animal model was builded as the pneumonia was observed from the pathological changes of lung tissue. Results The Wistar rats exposed to PM2?5 aerosol inhalation for 8 weeks, we can see that the weight growth rate of rat decreased, WBC count and mononuclear cells count increased, the macrophages ratio decreased in BALF, the respiratory rate of lung increased while arterial PO2 and FEV1/FVC decreased, inflammation and pulmonary fibrosis changes were observed by bronch and pulmonary pathology, inflammatory changes with a dose?response relationship were observed. Exposed to PM2?5 aerosol inhalation for different time(1 w、2 w、4 w、8 w、12 w)with same dose, the score issue lesions of lung and bronchus in Wistar rats increased and the 8w group is obvious. The Wistar rats exposed to PM2?5 with different method ( aerosol inhalation and non?exposed intratracheal instillation method) for 8w, the aerosol inhalation worked as effectively as perfusion while mortality rate of aerosol inhalation is lower. Different animals ( Wistar rats, BN rats and guinea pigs) exposed to PM2?5 aerosol inhalation for 8w, the same results were observed with three method respectively while mortality rate of Wistar rats lower. Conclusions The optional conditions that the Wistar rats were continuously inhaled for 8w PM2?5 with a dose of 150 ± 10 μg/m3 were established. The animal model could be used on a national scale, especially in Fujian province. The results would be useful for the development of the research of the prevention and countermeasures of PM2?5 pollution.

0.05).CONCLUSION:The mutagenesis of Leflunomide 3-methyl-isomer was not observed in these tests.