BACKGROUND: The metabolism of acetylcholine in hippocampus reflects the function of cholinergic nervous system whose function is associated with learning and memory as well as intelligence.OBJECTIVE: To observe the changes of choline acetyltransferase activity in rat hippocampus after ischemia-reperfusion.DESIGN: Randomized controlled trial based on rats.SETTING: A Science and Research Department of Chengde Medical College.MATERIALS:The trial was conducted in the Central Laboratory of Chengde Medical College in 2002 and the subjects were 24 clean grade Wistar rats in equal number of the two sexes(weighting 260-280 g).METHODS:The 24 rats were randomly assigned into 3 groups: ① Model group:In this group the rats were made hyperlipemia and underwent bilateral carotid arteries blocking followed by reperfusion. ② Sham operation group:In this group the rats were made hyperlipemia and underwent only exposure of bilateral carotid arteries without ischemia-reperfusion. ③ Normal control group:In this group the rats received no intervention.The brains after the rats decapitated were harvested on the 1st 7th and 15th day respectively for colorimetric determination of the choline acetyltransferase activity in hippocampus.MAIN OUTCOME MEASURES:Determination of the choline acetyltransferase activity in the groups.RESULTS:None of the 24 rats was lost in the trial. ① The choline acetyltransferase activity in the model group on the 1st and 7th day was acetyltransferase activity in the model group on the 7th day was lower than that on the 1st and 7th day was lower than that in the normal controls[(0.037±0.006) μmol/g ·s, (0.017±0.006) μmol/g·s in model group vs (0.054±0.003) μ mol/g·s,(0.058±0.006) μmol/g·s in normal control group,P ＜ 0.01].② The choline acetyltransferase activity in the model group on the 7th day was lower than that on the 1st day. With repairing of ischemia-reperfusion injury,it recovered partially[(0.039±0.007) μnmol/g.s].③ Choline acetyltrans-ferase activity in sham operation group was not different from that in normal control(P ＞ 0.05).CONCLUSION:Simple exposure of carotid arteries does not change choline acetyltransferase activity.While ischemia-reperfusion can change the choline acetyltransferase activity and cause disorders of cholinergic nervous system function,which may be the reason for rat's intellectual disorders.

Apoptosis is important to the development of diseases. Research recently indicates that c-Jun N-terminal kinase (JNK) and cysteinyl aspartate-specific protease (caspase) play key roles in apoptosis and affect the development of diseases. This article is to introduce the function and relationship between JNK and caspase in apoptosis during the process of diseases.

ObjectiveTo observe the effect of nimodipine on hippocampal DNA-binding activity change of cAMP response element binding protein ( CREB )and CCAAT enhancer binding protein (C/EBP) in a rat model of vascular dementia(VD),and to explore the treatment mechanism of nimodipine.Methods66 healthy adult male SD rats were assigned to the following three groups of 22 each:VD model group,Sham-operated group,Nimodipine group.VD rat model was prepared by four-vessel occlusion.Physiological saline solution( 8 ml · kg-1 · d-1 )and Nimodipine (20 mg· kg-1 · d-1 )were administered by gavage respectively.The Morris maze was adopted to detect the changes of spatial learning and memorizing capacity,while HE straining was adopted to observe the changes of pathological characteristics in hippocampal CA1 area,and electrophoretic mobility shift assay(EMSA) were adopted to observe DNA-binding activity changes of CREB and C/EBP in hippocampus tissue.ResultsThe Morris maze showed:the learning and memory ability of nimodipine group rats ( escape latency period ( 26.63 ± 1.31 )s,the times of cross-platform(7.25 ±0.92) times) was higher than that of VD model group(escape latency period (41.25 ± 1.83 ) s,the times of cross-platform ( 5.33 ± 0.64 ) times ),with difference of statistical significance (P ＜0.05).HE results:in VD model group,neurons in CA1 were scaltered and boundaries were unclear,nuclei region was stained,coagulation necrosis appeared,obviously cells lost.The CA1 neurons of nimodipine group returned to be normal,nuclear membrane's profile and nudeolus were clear,regularly arranged; the number of hippocampal normal neurons in nimodipine group (43.19 ± 2.87 ) was more than that of VD model group( 16.33 ± 1.09 ),with difference of statistical significance(P＜0.05 ).EMSA:both CREB and C/EBP DNA-binding activity in rat hippocampus of nimodipine group ( ( 369.75 ± 13.22 ),( 428.25 ± 17.69 ) respectively ) were higher than those of VD model group ( ( 142.25 ± 27.86 ),(97.00 ± 5.88 ),respectively),with difference of statistical significance (P ＜0.01 )).ConclusionNimodipine can improve VD rats hippocampal neuronal injuries and their learning and memory impairment may be involved in the upregulating CREB and C/EBP DNA-binding activity.

BACKGROUND:During the progress of focal cerebral ischemia-reperfusion in rat with transient suture occlusion, bleeding combating and the line being plugged into the cerebral middle artery smoothly are important for successful modeling and research focus.
OBJECTIVE:To improve Longa suture occlusion method for focal cerebral ischemia reperfusion model in Sprague-Dawley rats in order to establish a simple surgical procedure with low rate of intraoperative bleeding and high rate of successful models.
METHODS:The two ends of the external carotid artery were clipped with electric knife, in addition to ligation of surgery lines intraoperatively;with the help of pincett, a fishing line was plugged into the carotid artery along the anteriomedialis artery wal (the direction of the internal carotid artery from the pterygopalatine arterial bifurcation). Postoperative behavior scores in rats, infarct volume calculation and histopathological evaluation under optical microscope were done.
RESULTS AND CONCLUSION:Transverse sections of the external carotid artery were changed from a“O”
shape to a“-”shape after being clipped with electric knife. Subsequently, line nodes were not easy to fal off any more, effectively preventing intraoperative bleeding. With the power of pincett, the rate of plugging the fishing line into artery was significantly increased. Rat’s neurological score and infarct volumes were significantly increased, and brain tissue pathological injury worsened. The modified suture occlusion method for focal cerebral ischemia reperfusion models effectively prevented line nodes off, successful y increased the rate of suture occlusion and models in Sprague-Dawley rats were developed successful y.

AIM To observe the effect of Yishenjiangzhuo decoction on the NE,5-HT contents of hippocampus in cerebral ischemia reperfusion rats. METHODS High pressure lipuid chromatography-electrochemical process was used to measure the NE and 5-HT contents on the d 1, d 7 and d 15 after cerebral ischemia reperfusion by common carotid artery occlusion. RESULTS The NE contents of hippocampus were respectively 364.25?66.47, 349.76?59.38, (344.59?70.31) ?g?g -1 and the 5-HT contents were respectively 646.72?83.33,629.11?90.64,(596.68?99.47) ?g?g -1 on the d 1, d 7 and d 15 in the model group, which significantly decreased compared with the control group( P

Objective To elucidates the effects of HPV18 E6 siRNA targeting at human papillomavirus(HPV)18 E6 gene on the proliferative activity of HeLa cells and chemotherapy sensitivity.Methods HPV18 E6 expression of HeLa cells was inhibited by siRNA interference,the change of P53 and P21 proteins expression level was measured by Western blot.MTT assay was used to detected proliferative activity and sensitivity to paclitaxel liposome of HeLa cells.Results After inhibition of E6 expression,P53 and P21 proteins increased and the growth of HeLa cells was decreased(P ＜0.01).The inhibition rate of HeLa was markedly increased after transfection of HPV18 E6 siRNA and paclitaxel liposome.Conclusion HPV18 E6 siRNA can effectively silence gene expression of E6 and inhibit proliferation of HeLa cells.HeLa cells are more sensitive to combine HPV18 E6 siRNA with paclitaxel liposome than that of control groups.

0.05).But PMA increased and SC-3088 decreased cAMP content and PKA activity in LPS-stimulated rat PIMs(P

0.05); but significantly increased cAMP content and PKA activity at high concentration [(10-9~10-5) mol?L-1] (compared with normal control group:P

Aim To investigate the effect of astragalus injection on the expression of JNK3(c-jun N terminal kinase)protein and JNK3 mRNA interrelated by apoptosis after hypoxia/hypoglycemia and reoxygenation in hippocampal neurons of rats.Methods The hippocampal neurons cultured for eight days were divided into four groups:normal control group,hypoxia/hypoglycemia and reoxygenation group,astragalus injection group and astragalus solution group.Hypoxia/hypoglycemia and reoxygenation group,astragalus injection group and astragalus solution group were treated with hypoglycemia and reoxygenation after being deprived of oxygen and glucose for 30 minutes.Methods of Western blot,ELISA and RT-PCR were used respectively to measure the expression of JNK3 mRNA after hypoxia/hypoglycemia and reoxygenation 0,0.5,2,6,24,72,120 h.Results Compared with normal control group,the mean optic density(MOD)of expression of JNK3 protein and activation of JNK3 protein in hippocampal neurons of rats every time points increased obviously in hypoxia/hypoglycemia and reoxygenation group except 120 h(P<0.05);compared with hypoxia/ hypoglycemia and reoxygenation group,MOD of expression of JNK3 mRNA and activation of JNK3 protein in hippocampal neurons of rats every time points decreased obviously except 120 h in astragalus injection group (P<0.05);compared with hypoxia/hypoglycemia and reoxygenation group,there was no difference in astragalus solution group.Compared with normal control group,MOD of expression of JNK3 mRNA in hippocampal neurons of rats every time points increased obviously in hypoxia/hypoglycemia and reoxygenation group(P<0.05);compared with hypoxia/ hypoglycemia and reoxygenation group,MOD of expression of JNK3 mRNA in hippocampal neurons of rats every time points decreased obviously in astragalus injection group except 120 h(P<0.05);compared with hypoxia/hypoglycemia and reoxygenation group,there was no difference in astragalus solution group.Conclusion Astragalus injection can inhibit the expression of JNK3 mRNA after hypoxia/hypoglycemia and reoxygenation,moreover,it can inhibit the expression of JNK3 protein and decrease the activation of JNK3 protein,accordingly it inhibits hippocampal neuronal apoptosis.

Aim To investigate the effects of astragalo-side IV on apoptosis of PC12 cells inducedby hypoxia/hypoglycemia and reoxygenation. Metheds PC12 cells were randomly divided into 4 groups: normal control group,hypoxia/hypoglycemia and reoxygenation group, astragaloside Ⅳ group and vehicle group. Hypoxia/hy-poglycemia and reoxygenation group, astragaloside Ⅳgroup and vehiclegroup were exposed to reoxygenation (12 h) after 3 h of oxygen and glucose deprivation, and astragaloside Ⅳ was added into cells at the same time. Inverted microscope was used to observe the morphological changes ofPC12 cells and MTT method to detect the activities of PC12 cells, and Annexin V-FITC/PI assay and TUNEL staining were used to meas-ure the apoptosis of PC12 cells. Results Compared with normal control group, cells became round or swol-len and its cellula processes were retracted or disap-peared in hypoxia/hypoglycemia and reoxygenation group;a large number of apoptotic cells could also be observed,whose nucleus were shrinkaged, fragmented or deep-stained. The activities of hypoxia/hypoglycemia and reoxygenation group were decreased markedly than those in normalcontrol group(P<0. 05),while the ap-optotic rates of hypoxia/hypoglycemia and reoxygen-ation group were increased obviously than those in nor-malcontrol group( P<0. 05 ) . Compared with hypoxia/hypoglycemia and reoxygenation group, a good cell growth state could be observed and cellula processes could also be observed significantly in astragaloside Ⅳgroup. The activities of astragaloside Ⅳ group were in-creased than those in hypoxia/hypoglycemia and reoxy-genation group(P<0. 05),while the apoptotic rates of astragalosideⅣgroup were decreased than those in hy-poxia/hypoglycemia and reoxygenation group ( P <0. 05 ) . There was no obvious difference between vehi-clegroup and hypoxia/hypoglycemia and reoxygenation group( P >0. 05 ) . Conclusion Astragaloside IV can reduce the damage of PC12 cells induced by hypoxia/hypoglycemia and reoxygenation, increase cell activity and inhibit cell apoptosis.