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Objective To investigate the synergetic effect of combined astaxanthin ( AST) and lith-ium chloride ( LiCl) treatment on cognitive dysfunction of chronic omethoate poisoned mice. Methods 8 mice were selected randomly as control group from 55 healthy adult male Kunming mice,and the rest were used to establish chronic organophosphate poisoning cognitive impairment models by injecting omethoate 5 mg/kg subcutaneously every day for 4 weeks. Totally 40 successfully established models were randomly divid-ed into model group,AST group,edaravone group,LiCl group and AST+LiCl group with 8 in each. Morris wa-ter maze test was used to examine the learning and memory ability of mice. Contents of reactive oxygen spe-cies (ROS) in hippocampus were measured by enzyme-linked immunosorbent assay (ELISA). Activity of superoxide dismutase ( SOD) in hippocampus was measured by colorimetric assay. Morphology of hippocam-pus area was observed by HE staining. The distribution and expression of p-PI3K,p-Akt,p-GSK3β and p-CREB were determined by immunohistochemical staining ( IHC staining) and Western blot. Results The average escape latency of 5 days in each group was statistically significant (F=1662.147, P<0.05) . The av-erage escape latency of 5 days in AST+LiCl group was significantly lower than that in model group ( all P<0.05) and was lower than other treatment groups. Compared with the control group (0.087±0.007,0.084± 0.009,0.097±0.002,0.076±0.012),the hippocampal neuronal injury in model group was serious,the expres-sions of p-PI3K (0.032±0.008),p-Akt (0.03±0.006),p-GSK3β (0.028±0.007) and p-CREB (0.020± 0.008) was significantly lower ( all P<0.05) . The injuries of hippocampal neurons in AST+LiCl group were slightly lighter than that in model group,and the expression of p-PI3K (0.067±0.008),p-Akt (0.065± 0.005),p-GSK3β (0.068±0.009) and p-CREB (0.062±0.008) in hippocampus was significantly higher than that in model group ( all P<0.05) . Conclusion Combined AST and LiCL treatment exerts neuroprotec-tive effect on cognitive dysfunction induced by chronic organophosphate poisoning via up-regulating the ex-pression of Akt/GSK3β/CREB.
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Objective To optimize the therapeutic dose and time window of picroside Ⅱ in treating cerebral ischemic injury in rats by orthogonal test. Methods The forebrain ischemia models were established by bilateral common carotid artery occlusion (BCCAO) method. The successful models were randomly grouped according to orthogonal experimental design and treated by injecting picroside Ⅱintraperitoneally at different ischemic time with different doses. The concentrations of MDA, NO and H2O2 in serum and brain tissue were respectively determined by thiobarbituric acid assay, nitratase reductase assay and chemiluminescence immunoassay. Results The optimized composition of the therapeutic dose and time window of picroside Ⅱ in cerebral ischemic injury were ischemia 1.5 h with 10 mg/kg, 1.5 h with 20 mg/kg and 1.5 h with 10 mg/kg body weight according to the expressions of MDA, NO and H2O2 in serum, and ischemia 1.5 h with 10 mg/kg, 1.5 h with 20 mg/kg and 1.5 h with 20 mg/kg body weight according to the expressions of MDA, NO and H2O2 in brain tissue. Conclusion On the basis of the principle of lowest therapeutic dose with longest time window, the optimized composition of the therapeutic dose and time window in cerebral ischemic injury is injecting picroside Ⅱ intraperitoneally with 10-20 mg/kg body weight at ischemia 1.5 h.
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To establish a quantitative estimate model for diagnosing traditional Chinese medicine (TCM) syndromes of patients with osteoporosis.
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ObjectiveTo investigate the effect of neuregulin1β (NRG1β) on the learning memory abilities and the neuronal apoptosis and the expressions of nuclear factor kappa B (NFκB) in experimental Alzheimer's disease model in rats induced with beta-amyloid protein1-40 (Aβ1-40) injection.To explore the mechanisms of NRG in improving the capabilities of learning and memory.MethodsThirty adult healthy male wistar rats were randomly divided into control group (n =10),model group (n =10) and treated group (n =10).Alzheimer's disease models were established by stereotactically injecting Aβ1-40 into the left lateral ventricle,and treated by injecting NRG1β(0.3 μg · kg-1 ) into the right lateral ventricle.The learning and memory abilities of rats were evaluated with Y-electric maze before the experiment and 7 days after making Alzheimer's disease models and 14 days after treatment.HE staining was used to observe the structure of hippocampal neurons.The neuronal apoptosis of hippocampus was investigated by TUNEL assay.The expressions of NFκB in hippocampal neurons were determined with immunohistochemistry technique.ResultsCompared with control group (57.50 ± 1.58,7.20 ±1.03 ),the model group rats ( 59.50 ± 2.79,7.50 ± 1.08 ) showed low cognitive ability ( t =20.36,5.28,P ＜0.05 ),the hippocampal pyramidal cells of rats in the model group were sparse and disturbed pyramidal cells,noticeable neuron loss.The number of neuronal apoptosis and the expressions of NFκB increased significantly than those in control group (P＜0.05).Compared with model group (79.10 ±4.12,4.40 ±0.69),NRG1β strikingly improved cognitive ability ( 67.70 ± 4.90,5.80 ± 0.63 ) and normal cell structure ( t =5.63,4.69,P ＜ 0.05 ).The expressions of NFκB (25.90 ± 6.67 ) reduced while the number of neuronal apoptosis ( 23.50 ± 3.89 ) decreased markablely than those ( 41.10 ±7.95,29.30 ± 7.24) in model group(t =4.63,2.23,P ＜ 0.05).ConclusionNRG1β might decrease the neuronal apoptosis by inhibiting NFκB expressions,so that to improve the learning and memory abilities of experimental dementia rats.
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To establish diagnostic criteria for common traditional Chinese medicine (TCM) syndromes in osteoporosis.
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Objective: To establish a quantitative model for evaluating the degree of traditional Chinese medicine (TCM) syndromes often seen in patients with coronary heart disease (CHD). Methods: Medical literature concerning clinical investigation of TCM syndromes of CHD was collected and organized, and the "Hall for Workshop of Metasynthetic Engineering" expert symposium method was applied. First, the 100 millimeter scaling was used for combining with scoring on degree of symptoms to establish a quantitative criterion for classification of symptom degree in CHD patients, and the model was established by using comprehensive analytic hierarchy process as the mathematical tool to estimate the weight of the criterion for evaluating qualitative syndromes in various layers by specialists. Then the model was verified in clinical practice and the outcomes were compared with fuzzy evaluation from the specialists. Results: A total of 287 clinical observation forms on CHD cases were collected, and 167 forms were available after excluding any irregular forms. The results showed that basic coincidence rate between the outcomes derived from specialists and those from the model was 68.26% (114/167), and part coincidence rate was 88.62%(148/167). Conclusion: This model, with good rationality and feasibility, has a high coincidence rate with fuzzy evaluation from specialists, and can be promoted in clinical practice. It is a good quantitative model for evaluating the degree of TCM syndromes of CHD.
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Objective To observe the effects of expressions of neurocyte adhesion molecule (NCAM) and growth associated protein-43 (GAP-43) in neurological function recovery following cerebral ischemia-reperfusion in rats. Methods The model of focal ischemia-reperfusion in SD rat was induced by intraluminal middle cerebral artery (MCA) occlusion with a nylon monofilament suture. In situ hybridization (ISH) was performed to examine the expression of NCAM mRNA and GAP-43 mRNA at 2,12 h and 1,2,3,7,14 d after reperfusion and in sham-operated controls. Results There was no functional deficit and little expression of NCAM mRNA and GAP-43 mRNA in brain cells in rats of the sham-operated group. In the experimental group, NCAM mRNA expression was observed after reperfusion for 2 h in cortex and striatum and peaked at 12 h and was still higher at 7 d. The neurological function improved at reperfusion of 3 d~14 d compared to reperfusion 2 h. In the ischemic cortex and striatum, GAP-43 mRNA expression demonstrated "double-peak" at 12 h and 2 d after reperfusion, then decreased gradually to the level of sham-operated group at 14 d. Conclusion The increasing NCAM expression might be an important factor of the neural reparation and GAP-43 might enhance the neurological functional recovery with ischemic brain injury in rat.