Objective:To explore the role of P2Y1Receptor(P2Y1R)-activated astrocytes in delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods:SD rats were randomly divided into Control,DEACMP,DEACMP+DMSO,and DEACMP+MRS2179 groups.The latter three groups were exposed to static CO inhalation to establish the DEACMP model,while the Control group inhaled air.The rats in DEACMP+MRS2179 group were injec-ted with 3 μl of P2Y1R antagonist MRS2179 with concentration of 1 mmol/L via lateral ventricle,while the DEACMP+DMSO group an equal volume of DMSO.At 14 and 21 day after DEACMP model establishment,the spatial learning and memory ability of rats were observed by Morris water maze,the injury of pyramidal cells in the CA1 area of the hippo-campus was observed by HE staining.The protein levels of glial fibrillary acidic protein(GFAP)and P2Y1receptor(P2Y1R)in the hippocampal tissues of rats were detected by immunohistochemistry and Western blot.The expressions of interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in the hippocampal tissues of rats were detected by ELISA.Results:In comparison with the Control group,the escape latency was found to be signifi-cantly prolonged in the DEACMP group and the DEACMP+DMSO group.Furthermore,the expression levels of GFAP,P2Y1R,IL-1β,IL-6,and TNF-α were significantly increased in the pyramidal cells of the CA1 region of the hippocam-pal tissue(P<0.05).In contrast,the escape latency was significantly reduced and the expression levels of GFAP,P2Y1R,IL-1β,IL-6,and TNF-α were significantly decreased in the DEACMP+MRS2179 group when compared with the DEACMP+DMSO group(P<0.05).Conclusion:P2Y1R activates astrocytes to release inflammatory factors lead-ing to the onset of cognitive impairment in DEACMP,and inhibition of P2Y1R reduces the expression of inflammatory factors and thus improves cognitive function in DEACMP.

Objective:To explore the role of P2Y1Receptor(P2Y1R)-activated astrocytes in delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods:SD rats were randomly divided into Control,DEACMP,DEACMP+DMSO,and DEACMP+MRS2179 groups.The latter three groups were exposed to static CO inhalation to establish the DEACMP model,while the Control group inhaled air.The rats in DEACMP+MRS2179 group were injec-ted with 3 μl of P2Y1R antagonist MRS2179 with concentration of 1 mmol/L via lateral ventricle,while the DEACMP+DMSO group an equal volume of DMSO.At 14 and 21 day after DEACMP model establishment,the spatial learning and memory ability of rats were observed by Morris water maze,the injury of pyramidal cells in the CA1 area of the hippo-campus was observed by HE staining.The protein levels of glial fibrillary acidic protein(GFAP)and P2Y1receptor(P2Y1R)in the hippocampal tissues of rats were detected by immunohistochemistry and Western blot.The expressions of interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in the hippocampal tissues of rats were detected by ELISA.Results:In comparison with the Control group,the escape latency was found to be signifi-cantly prolonged in the DEACMP group and the DEACMP+DMSO group.Furthermore,the expression levels of GFAP,P2Y1R,IL-1β,IL-6,and TNF-α were significantly increased in the pyramidal cells of the CA1 region of the hippocam-pal tissue(P<0.05).In contrast,the escape latency was significantly reduced and the expression levels of GFAP,P2Y1R,IL-1β,IL-6,and TNF-α were significantly decreased in the DEACMP+MRS2179 group when compared with the DEACMP+DMSO group(P<0.05).Conclusion:P2Y1R activates astrocytes to release inflammatory factors lead-ing to the onset of cognitive impairment in DEACMP,and inhibition of P2Y1R reduces the expression of inflammatory factors and thus improves cognitive function in DEACMP.

OBJECTIVETo investigate the protective effects of oxysophoridine (OSR) on primary cultured hippocampus neurons subjected to anoxia injury in neonatal rats and its mechanism.

METHODThe model of anoxia injury of hippocampus neurons in neonatal rats were primarily cultured in vitro by physical oxygen deficiency using glucose-free culture fluid. The survival rate of neurons, the leaking rate of lactate dehydrogenase (LDH), the intracellular contents of malondialdehyde (MDA) and nitric oxide (NO), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. The intracellular free calcium concentration ([Ca2+]i) in hippocampus neurons were detected with Ca(2+)-sensitive dual wavelength fluorescence spectrophotometer.

RESULTNeuron death occurred in the anoxia injury model group with increase of LDH leaking rate, the contents of NO, MDA, intracellular [Ca2+] and the elevated activity of NOS while decreased activities of SOD and GSH-PX. The hippocampus neurons subjected to anoxia injury were alleviated in OSR (0.625, 5, 10 microg x L(-1)) group.

CONCLUSIONOSR has significant protective effects on hippocampus neurons subjected to anoxic injury. The mechanism of its protective effect may relate to its reduction of calcium overload and against oxidation injury.

Alkaloids ; administration & dosage ; Animals ; Cells, Cultured ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Glutathione Peroxidase ; metabolism ; Hippocampus ; cytology ; drug effects ; enzymology ; metabolism ; Humans ; Hypoxia ; drug therapy ; enzymology ; metabolism ; prevention & control ; Malondialdehyde ; metabolism ; Neurons ; cytology ; drug effects ; enzymology ; metabolism ; Nitric Oxide Synthase ; metabolism ; Protective Agents ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Sophora ; chemistry ; Superoxide Dismutase ; metabolism

Objective To investigate the expression of galectin-3 in pancreatic cancer cell and its effect on the proliferation and invasion of SW1990.Methods Immunocytochemistry and semi-quantitative RT-PCR was used to detect the expression of galectin-3 protein and mRNA in SW1990,PANC1 and ASPC-1 cell lines.Galectin-3 mono-antibody of different concentrations ( 1,2,3,5 μg/ml) was used to treat SW1990 cells for 24,48,72 h,CCK-8 kits were used to detect the proliferation in SW1990 cells; Transwell chamber was used to study the invasion in SW1990.Results Expression of galectin-3 protein and mRNA was present in SW1990,PANC1,and ASPC-1.Galectin 3 mono-antibody inhibited the proliferation and number of invasive cells in a dose and time dependant manner.The inhibitory rates at 72 h were 19.8％,29.9％ and 42.7％ in 2,3,5 μg/ml galectin 3 mono-antibody groups,the difference among them and control group was statistically significant ( P ＜ 0.05 ).The inhibite rate of permeating membrane cells in 3 μg/ml galectin-3 mono antibody was 37.1％,the difference between this group and control group was statistically significant (P ＜0.05 ).ConcLusions Galectin-3 is highly expressed in pancreatic cancer cells.Galectin-3 antibody can inhibit the proliferation and migration capability of SW1990 cells.