Effects of rolipram on learning and memory and the activity of PDE4 in hippocampus following the focal brain injury induced by ischemia- reperfusion in rats

AIM: To investigate the effects of rolipram on the ability of learning and memory and the activity of PDE4 in hippocampus following the focal brain injury induced by ischemia- reperfusion in rats. METHODS: The cerebral ischemia-reperfusion injury model was made by middle cerebral artery occlusion (MCAO) in rats. The rats were randomly divided into sham-operated group, model group, and rolipram group. Rolipram was administered once a day (1 mg/kg, ip) from 6 h after the onset of the operation for 2 weeks. Then the learning and memory abilities were tested after Morris water maze and step-though training. The activity of PDE4 in hippocampus was evaluated by HPLC. RESULTS: In the Morris water maze test, compared to sham-operated group, the platform-finding time and swimming distance in model group were significantly longer (P<0.05). Compared to model group, the platform-finding time and swimming distance in rolipram group were significantly shorter (P<0.05). In the step-through test, compared to sham-operated group, the lantent period in model group was significantly shorter (P<0.01) and the error times were statistically increased(P<0.05). Compared with model group, the lantent period in rolipram group were significantly longer (P<0.05), and the error times were markedly decreased. The assay of the HPLC demonstrated that the activities of PDE4 in hippocampus in model group were higher than those in the sham-operated group and rolipram group. CONCLUSION: Rolipram reduces the activity of PDE4 in hippocampus and enhances the ability of learning and memory after the injury induced by ischemia-reperfusion.     

Effect of crystallin βB2 on the aging of lens

AIM: To study the effect of crystallin βB₂ on the aging of lens. METHODS: SD rats were maintained routinely and killed at 6 different ages (1 d, 8 d, 2 weeks, 8 weeks, 8 months and 1.5 years). Water-soluble crystallins were extracted and separated by two-dimensional polyacrylamide gel electrophoresis (IEF/SDS-PAGE). After Comassize blue staining, the crystallin patterns were screened and analyzed. βB₂ crystallin and the main chaperone proteins (αA₂, αB₂) were identified and the relative quantity was measured. RESULTS: (1) The quantity of water-soluble crystalline βB₂ increased in close relation to the aging of the rat. (2) αA₂, αB₂ chaperone proteins increased with the aging of the rat too. (3) The change of the quantity of water-soluble crystalline βB₂ was closely related to the changes of αA₂ , αB₂ chaperone proteins. (4) Degraded and modified crystallins began to appear clearly in the lens after 8 months old. CONCLUSION: Based on our results, we infer that water-soluble crystalline βB₂ increases with the aging dof the rat, which is helpful to maintain the structure and transparency of the lens.     

Mitochondrial DNA deletion of the brain tissue of aged rats with learning and memory deficit

AIM and METHODS: The ratio of mitochondrial DNA (mtDNA) deletion was measured to find the relationship between mtDNA deletion and aged learning and memory deficit. The aged rats were divided into two groups, aged learning and memory deficit group and aged learning and memory normal group. The ratio of mtDNA deletion was measured by dilution polymerase chain reaction. RESULTS: There are deleted mtDNA (about 4834 bp) in the cerebral cortex, hippocampus and cerebellum of both young and aged rats. The ratios of deleted mtDNA were similar in the cerebral cortex,hippocampus and cerebellum of young rats (about 0.00018%). The ratio mtDNA of aged learning and memory normal rats had increased by five-fold in the cerebral cortex and hippocampus, or one-fold in the cerebellum over young rats. The ratio of aged learning and memory dificit rats had increased by one-fold in the cerebral cortex or 0.8-fold in the hippocampus or two-fold in the cerebellum over aged learning and memory normal rats.CONCLUSIONS: There was really the increase of mtDNA in aging rat brain. And this increase was double in amount in aged learning and memory deficit rats compared to the normal learning and memory aged rats. It is suggested that the mtDNA deletions in the brain regions associated with learning and memory may be contributed to the cellular and molecular mechanism of learning and memory deicit with aged rats.     

Inhibitory effect of basic fibroblast growth factor on apoptosis induced by β-amyloid in PC12 cells

AIM:To clarify the effect of bFGF on the neurotoxity of Aβ_25-35 in PC12 cells and its potential application in the treatment of Alzheimer's disease. METHODS:Giema's, PI stainning, DNA agarose gel electrophoresis, Western blot and FCM were used to detect the morphological and biochemical changes of cultured PC12 cells treated with Aβ_25-35 and bFGF+ Aβ_25-35, and the expression of apoptosis-related gene bcl-2, bax. RESULTS:Morphological and biochemical characteristics of apoptosis, such as internuclear DNA fragmentation, compaction of nuclear chromatin, membrane blobbing, formation of apoptotic bodies, were observed in PC12 cells treated with Aβ_25-35. However, in PC12 cells treated with bFGF+ Aβ_25-35 , the above changes were significantly reversed, the expression of Bcl-2 was up-regulated while that of Bax was down-regulated. CONCLUSION:bFGF can inhibit the neurotoxity of Aβ_25-35 to neurons by regulating the expression of the apoptosis-related gene Bcl-2 and Bax.     

Therapeutic effect of neuregulin-1β on pressure overload-induced myocardial hypertrophy in rats

AIM：To investigate the therapeutic effect and the mechanism of neuregulin-1β (NRG-1β) on the rat model of myocardial hypertrophy induced by pressure overload．METHODS：Eight weeks after coarctation of abdominal aorta, the Wistar rats were randomly divided into 4 groups: myocardial hypertrophy (model) group, sham operation (sham) group, NRG-1β treatment group (intravenous injection of NRG-1β at dose of 10 μg/kg daily for 7 d) and NRG-1β+Herceptin (HERCE) treatment group ［intravenous injection of NRG-1β (10 μg/kg) plus HERCE (10 μg/kg) daily for 7 d］. The characteristics of heart functions were evaluated by the methods of hemodynamics and echocardiography. Masson staining was employed to observe the pathological changes of myocardial tissues. The concentration of angiotensin II (Ang II) in myocardial tissues was measured by radioimmunoassay. The level of tumor necrosis factor α (TNF-α) in myocardial tissues was detected by ELISA. The mRNA expression of B-cell lymphoma/leukemia-2 (bcl-2) and bcl-2-associated X protein (bax) in the myocardium was determined by RT-PCR. RESULTS：The left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were higher, while the left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) were smaller in NRG-1β group than those in model group. The left ventricular end-systolic pressure (LVESP) and maximal rate of increase/decrease in left ventricular pressure (±dp/dtmax) were higher, and left ventricular end-diastolic pressure (LVEDP) was significantly lower in NRG-1β group than those in model group. Compared with model group, treatment with NRG-1β decreased collagen volume fraction (CVF), reduced the Ang II and TNF-α, increased bcl-2 mRNA expression, and decreased bax mRNA expression in myocardial tissues. No difference of the above parameters between model group and NRG-1β+HERCE treatment group was observed. CONCLUSION：NRG-1 reduces the expression of Ang II and TNF-α in myocardial tissues in pressure-overload rats, thus reducing Ang II and TNF-α mediated myocardial interstitial remodeling. Increase in the mRNA expression of bcl-2 and decrease in the mRNA expression of bax by NRG-1 inhibit myocardial cell apoptosis, which is responsible for its role of improving cardiac function of myocardial hypertrophy induced by pressure overload.     

Effects of acute and chronic hypobaric hypoxia on spatial learning and memory functions in adult rats

AIM: To explore the effects of acute and chronic hypobaric hypoxia on spatial learning and memory functions in adult rats. METHODS: Three separate experiments were carried out. In the first experiment, 30 adult male SD rats were divided into control group (group A) and acute hypoxia group (group B, 7 000 m, 72 h). Learning and memory functions were tested by Morris water maze. The spatial acquisition was performed 4 trails per day, 3 days to reach asymptotic performance. The platform was removed on the 4th day, using a novel start position during the probe trail. The data of escape latency, time in platform quadrant and times of passing platform were recorded. In the second experiment, 26 adult male SD rats were divided into control group (group C) and chronic hypoxia group (group D, 6 000 m, 35 d). The spatial acquisition was performed 4 trails per day, 5 days to reach asymptotic performance. The platform on the 6th day was removed, using a novel start position during the probe trail. The data of escape latency, time in platform quadrant and times of passing platform were recorded. In the third experiment, after trained with Morris water maze by using the method as the second experiment, 30 adult male SD rats were divided into control group (group E) and acute hypoxia group (group F, 7 000 m, 72 h), and 2 h later, the memory functions were reevaluated. RESULTS: In the first day after acute hypoxia exposure, the escape latency in group B was significantly shorter than that in group A. However, the escape latency in the following days and the and times of passing platform was not significantly different. No difference of the escape latency in the following days and the time of passing platform between group C and D was observed. Memory tests didn’t show any difference between group E and F. CONCLUSION: Either acute or chronic hypobaric hypoxia does not affect the spatial learning and memory functions in adult rats.     

Change of synapsins in hippocampal formation during spacial learning and memory in rats

AIM and METHODS: The immunohistochemical method was used to study the on synapsin express in hippocampal formation during spatial learning and memory in rats.RESULTS: (1) In control group there are diffuse brown granules without any obvious granular product in hippocampal formation and in model group there are synapsin products in the hippocampal formation ,especially in the subregion CA3 , CA4 and the dentate gyrus after water maze trained for one week. After two weeks water maze trained the hippocampal formation appear the same distribution of the product granules with darker staining. (2) The light dendity of synapsin products between the model and the control groups showed significant differences, that in the model group was highter than that in the control group (P＜0.05). The light dendity of synapsin products increased with the training time from the first week to the second week in the model group. And there is no increase with the training time from the second week to the third week . The light dendity is higher in the CA3, CA4 subregion and the dentate gyrus than the CA1 and CA2 subregion (P＜0.05).CONCLUSIONS: (1) As mentioned above, it is believed that the new synapes are formed in the hippocampal formation of the rat by spacial learning and memory training. (2) The CA3, CA4 subregion and the dentate gyrus are correlated with the spacial learning and memory.     

Effect of cerebral ischemic preconditioning on NOS activity and NO content in the CA1 region of the hippocampus in rats

AIM: To explore the role of NO in the induction of brain ischemic tolerance (BIT) by observing changes of NOS activity and NO2-/NO3- content following a transient cerebral ischemia. METHODS: The rat 4-vessel occluding brain ischemic model was used. 140 male Wistar rats were divided into sham, cerebral ischemic preconditioning (CIP), ischemic insult and CIP+ischemic insult groups. An occlusion of the 4 vessels for 3 min was normally used as CIP, and a relative long one for 10 min was used as ischemic insult. When CIP was followed by ischemic insult, the interval between them was 3 d. The CA1 region of the hippocampus of rats was dissected out at 0 h, 2 h, 16 h, 24 h, 36 h, 72 h and 7 d after the last time of ischemia to assay its NOS activity and NO2-/NO3- content. RESULTS: The NOS activity and NO2-/NO3- content began to increase at 16 h, peaked at 24 h and decreased to basal level at 36 h of reperfusion after CIP. The duration of the up-regulation of NOS activity and NO2-/NO3- content was much shorter than that of BIT, which usually takes place 1-7 d after CIP. The pattern of upregulation of the NOS activity and NO2-/NO3- content was similar to the CIP group, but the maximum (24 h) was much more than that in CIP group (P<0.05). In the CIP＋ischemic insult group, the NOS activity and NO2-/NO3- content increased at 2 h of reperfusion, but the maximum (24 h) were much lower than that in ischemic insult group (P<0.05). CONCLUSION: A moderate increase in NOS activity and NO production after CIP might participate in the induction of BIT by triggering a series of cellular signal transduction. In addition, inhibiting effect of CIP on over-production of NO caused by ischemic insult might be another way to induce BIT.     

Distinct effects of different β-adrenoceptor stimulation patterns on car-diac AMP-activated protein kinase activity

AIM: To investigate the cardiac AMP-activated protein kinase (AMPK) activity and the effects of AMPK activator on cardiac structure and function in the mice with different β-adrenoceptor (β-AR) stimulation patterns. METHODS: Male BALB/c mice were subcutaneously injected with AMPK activator (AICAR, 250 mg· kg^-1·d^-1) or saline, and infused with β-AR agonist isoproterenol (ISO, 5 mg·kg^-1·d^-1) for 14 d. The cardiac functions were evaluated by echocardiography or hemodynamic method, and the hearts were harvested after infusion cessation immediately or 3 d later. Phosphorylated AMPK (p-AMPK) was measured by Western blot. RESULTS: Sustained ISO infusion increased p-AMPK level. AICAR did not further increase p-AMPK but attenuated ISO-induced increase in heart weight. Sustained ISO infusion increased cardiac systolic function as indicated by left ventricular fractional shortening (FS) and maximum rate of pressure rise (+dp/dt_max). The cardiac systolic function was not further increased by AICAR. The cardiac diastolic function as indicated by left ventricular end-diastolic pressure (LVEDP) was not different in each group. In contrast, cardiac p-AMPK level was similar between the control mice and the mice with sustained ISO infusion and ceased infusion for 3 d. In this model, AICAR improved the cardiac systolic and diastolic functions, which were impaired by ISO. Moreover, the increased pattern of p-AMPK level was similar with that of heart rate upon ISO stimulation. CONCLUSION: Sustained ISO infusion increases p-AMPK. After ISO infusion cessation for 3 d, p-AMPK is decreased to the basal level. β-AR-induced inotropic effects should be avoided to investigate the cardioprotective role of AMPK activation in the β-AR stimulation models.     

Differential regulating effect on estrogen receptor α and β expression in female rat hippocampus and cortex regions between different types of estrogen regents

AIM: To study the regulatory effect two different estrogen reagents on expressions of estrogen receptor α and β in female rat hippocampus and cortex regions. METHODS: 12 cycles after ovariectomy, female rats were orally injected with premarin or progynova for 3 cycles before sacrificed. Semiquantitative RT-PCR was used to detect the ERs mRNA expression and SP immunohistochemistry was performed to measure the ERs protein distribution and expression. RESULTS: In premarin group, ER α mRNA levels in both hippocampus and cortex tissues decreased significantly compared with control. ER α protein level in hippocampus was lower than that in the control. However, ER α protein level in cortex had no statistical difference. ER β mRNA in the two regions and ER β protein in cortex had no statistical differences compared with control, while ER β protein level in hippocampus was higher than that in the control. In progynova group, both mRNA and protein levels of ER β increased significantly in the two regions compared with the control, and ER α mRNA level also increased in hippocampus, but ER α mRNA level in cortex and ER α protein levels in the above two regions showed no statistical differences. CONCLUSION: There were differential regulatory effects on ER α and ER β expression in female rat cognitive regions between the two different types of estrogen reagents, which may be one of the mechanisms of varied effects in different estrogen replacement therapy reagents.     

Influences of Vit-E on the mtDNA damage and Ca2+ homostasis of hippocampus and antioxidative ability in brain of aging mice induced by D-galactose

AIM: To study the influences of vitamin E (Vit-E) on the mtDNA damage and Ca²⁺ homeostasis in hippocampus and antioxidative ability in aging brain induced by D-galactose.METHODS: D-galactose (1 000 mg·k^-1·d^-1 ) was injected into mice hypodermically for 8 weeks to induce aging animal model, and Vit-E (100 mg·kg^-1; 250 mg·kg^-1) was administered for 6 weeks by ig at the 3rd week of making model. After Vit-E treatment for 8 weeks, water maze test was used to determine the ability of mice’s learning and memory. The activities of glutathione peroxidase (GSH-Px) and succinate dehydrogenase (SDH), the content of nitric oxide (NO) and activity of nitric oxide synthase (NOS) in the brain tissue were detected separately. Fura-2/AM, double-wave-length fluorospectrophotometer and PCR method were used to measure the concentration of calcium ion and mtDNA mutation in the hippocampus cells.RESULTS: Administration of Vit-E improved significantly the ability of learning and memory in model mice, inhibited the activity of NOS and decreased the amount of NO, and increased the activities of GSH-Px and SDH respectively in brain tissues, decreased the concentration of calcium ion (P<0.01, P<0.05), and prevented the damage of mtDNA in hippocampus.CONCLUSION: Vit-E can enhance the antioxidative ability, regulate the homeostasis of Ca²⁺ and inhibit the damage of mtDNA caused by oxidative stress in aging brain, and improve the ability of learning and memory in aging mice.     

Effects of dexmedetomidine on behaviors and expression of BDNF and mTOR in hippocampus of depressive rats

AIM: To investigate the effects of dexmedetomidine (DEX) on the behaviors and the expression of brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR) in the hippocampus of depressive rats. METHODS: Sprague-Dawley (SD) rats were randomly divided into 5 groups: sham operation group, model group, and DEX (2.5, 5 and 10 μg/kg) groups. The rats were randomly selected in each group (n=12). The rat depression model was established by chronic unpredictable mild stress and ovariectomy. The rats in DEX groups received daily DEX treatment via intraperitoneal injection for 21 d. The forced swimming immobility time (FSIT) and open-field test were used to evaluate the antidepressant effect of DEX. Escape latency and times of crossing the flat were evaluated by Morris water maze. The histological changes of hippocampal neurons were determined by Nissl staining. The mRNA levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) were detected by RT-qPCR. The protein expression of IL-1β, IL-6, TNF-α and BDNF, and the phosphorylation levels of protein kinase A (PKA), cAMP response element-binding protein (CREB), tropomyosin-related kinase B (TrkB), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt) and mTOR in hippocampus were evaluated by Western blot. RESULTS: Compared with model group, the FSIT was significantly reduced and the spontaneous activity was markedly increased in DEX groups. The damage of the hippocampal neurons was obviously attenuated, the escape latency was obviously decreased, and times of crossing the flat were markedly increased (P<0.05 or P<0.01). The levels of IL-1β, IL-6 and TNF-α were obviously decreased, and the protein levels of p-PKA, p-CREB, BDNF, p-TrkB and p-PI3K, p-Akt, p-mTOR in hippocampal tissues were obviously increased (P<0.05 or P<0.01). CONCLUSION: Dexmedetomidine improves the behaviors and the spatial learning and memory ability of depressive model rats, which may be related to its anti-inflammatory effects, as well as up-regulating the protein levels of BDNF and p-TrkB, and activating PI3K/Akt/mTOR signaling pathway in the hippocampus.     

Behavior changes of learning and memory related to the levels of NO and nNOS in brain of rats with acute alcoholism

AIM: In order to investigate the molecular mechanism of alcoholism acting on learning and memory, the dysfunction of learning and memory function was observed and the content of nitric oxide (NO) and neuronal nitric oxide synthase (nNOS) were determined in rats with acute alcoholism.METHODS: The mature male Sprague-Dawley rats were randomly divided into two groups. The experimental group animals were intraperitoneally administered with ethanol. The control group animals were injected with saline in the same way. The tests of learning and memory were performed at Y-maze after 6 h. Then brains were removed and the content of NO in brain tissue and nNOS expression in hippocampus CA1, corpus striatum were determined, respectively.RESULTS: (1) The training times to reach qualifying standards of Y-maze in experimental group (34.33±13.04) were higher than those in control group (27.50±8.79, P<0.05). (2) The content of NO in experimental group (23.09±9.60) in hippocampus CA1 was significantly increased (P<0.01) compared with that in control group (8.46±5.67). The content of NO in experimental group (19.46±8.25) in corpus striatum was also higher than that in control group (8.22±4.46, P<0.01). (3) The levels of nNOS expression in experimental group (34.33±13.04) in hippocampus CA1 increased significantly (P<0.05) compared with that in control group (27.50±8.79). nNOS positive neurons in experimental group (18.22±7.47) in corpus striatum were also higher than those in control group (10.15±4.24, P<0.05).CONCLUSION: These findings suggest that the mechanism of ethanol neurotoxicity may be partly involved in the signal pathway of NOS and NO in the brain.     

Effect of Jieyuwan on depression-like behaviors and expression of BDNF in hippocampus and prefrontal cortex of WKY rats

AIM:To investigate the mechanism of depression and its development, and to study the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus and prefrontal cortex of Wistar-Kyoto (WKY) rats treated with Jieyuwan. METHODS:Adult male WKY rats were used as an animal model of endogenous depression. Wistar rats of the same strain were selected as control group. WKY rats were randomly divided into model group, citalopram group and Jieyuwan group. After intragastric administration for 21 d, the changes of depression-like behaviors were observed by sucrose preference test and forced swimming test. Immunofluorescence and Western blot were used to detect the expression of BDNF in the hippocampus and prefrontal cortex. RESULTS:WKY rats showed significant depression-like behaviors, and the expression of BDNF was significantly decreased in the hippocampus and prefrontal cortex (P<0.01). The reduction of neuronal axons in hippocampus was also observed. After drug treatment, the depression-like behaviors of WKY rats were significantly attenuated, and the expression of BDNF and the number of axons were increased (P<0.01). CONCLUSION:Jieyuwan effectively attenuates the depression-like behaviors of WKY rats, and BDNF is a key factor in its antidepressant effect. Our findings further confirm the involvement of BDNF in the development of depression.     

Gene and protein alterations in the hippocampus of rats with temporal lobe epilepsy

AIM:To examine the expression profiles of both genes and proteins in hippocampus of rats with temporal lobe epilepsy (TLE) for revealing the molecular mechanisms of TLE and looking for the candidate targets and new therapeutic approaches in clinical practice.METHODS:Rat temporal lobe epilepsy was induced by administration of lithium chloride and pilocarpine (LiCl-PILO).The expression spectra of genes and proteins were constructed through the techniques of cDNA microarray,two-dimensional (2D) electrophoresis and Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS).Subsequently,the differentially expressed genes and proteins were identified and analyzed.RESULTS:There were 192 genes of differential expression observed in hippocampal tissues of LiCl-PILO-induced temporal lobe epilepsy,and 159 genes have been registered in Genbank database,in which 84 genes were up-regulated while 75 genes were down-regulated.78 protein spots of differential display were screened out,in which 31 proteins were detected to be down-regulated and 47 were up-regulated.Finally,5 proteins were identified.CONCLUSION:These genes and proteins found in our study may play pivotal roles in the pathogenic mechanisms of epilepsy and may promise new therapeutic targets for refractory epilepsy in the future.     

Pretreatment with external trigeminal nerve electrostimulation inhibits seizures and decreases expression of IL-1β and TNF-α in hippocampus with status epilepticus induced by pentylenetetrazol in rats

AIM:To observe the effect of pretreatment with external trigeminal nerve electrostimulation (eTNS) on behavioral changes and the expression of interleukin-1β (IL-1β) and 　tumor necrosis factor α (TNF-α) in hippocampus of pentylenetetrazol (PTZ)-treated rats. METHODS:The rats were randomly divided into control group, PTZ group and eTNS group, and kindled by PTZ after administered 7 d, 14 d and 28 d of consecutive fake electrostimulation or eTNS. Subsequently, the severity and duration of seizure were quantitatively evaluated. The concentrations of IL-1β and TNF-α in hippocampus were detected by the methods of ELISA and immunohistochemisty. RESULTS:Compared with PTZ group, treatment with eTNS significantly inhibited the severity and duration of seizure (P<0.05), and significantly reduced the content of IL-1β and TNF-α in the hippocampus after status epilepticus (P<0.05 or P<0.01). CONCLUSION:Pretreatment with eTNS may provide a new approach for prevention and treatment of epileptogenesis.     

Expression and effect of glucocorticoid receptor β on children with idiopathic nephrotic syndrome

AIM: To elucidate the significance of glucocorticoid(GC) receptor isoform β(GRβ)in children with idiopathic nephrotic syndrome(INS), and to evaluate the effect of sera from GC-resistant INS on the expression of GRβ. METHODS: The percentage of GRβ positive staining peripheral blood mononuclear cells(PBMC) and the quantity of nuclear protein of GRβ in PBMC were detected by immunocytochemistry and Western blotting assay, respectively. The effect of sera isolated from children with GC-resistant INS on GRβ expression was examined by cell culture in vitro. RESULTS: The number of GRβ positive staining PBMC and the quantity of nuclear protein of GRβ in children with GC-resistant INS were significantly higher than those in patients with GC-sensitive INS(P<0 01). The quantity of GRβ protein in nuclei of PBMC in children with GC-resistant INS was significantly higher than that in normal control and children with GC-sensitive INS. After 24 hours incubation with sera from children with GC-resistant INS, the percentage of GRβ positive PBMC and the quantity of nuclear GRβ protein in children with GC-sensitive INS and normal control increased significantly(P<0.05). CONCLUSION: Increased expression of GRβ is closely related with the GC resistance in children with INS, and high expression of GRβ is mediated, at least in part, by certain humoral factors in the serum.     

Effects of gypenosides on cell cycle-related protein expression and calcium homeostasis in hippocampal neurons of rats treated with β-amyloid protein fragmant 1-40

AIM：To observe the effects of gypenosides on the expression of cell cycle-related protein and calcium homeostasis in the hippocampal neurons in the animal model of Alzheimer’s disease (AD) induced by Aβ₁-40.METHODS：The animal model of AD was established through injection of Aβ₁-40 into hippocampus in rats.The ability of learning and memory were verified by the performance of Y-shape maze task.With the method of immunohistochemical staining coupled integral absorbance analysis,the expression of cell cycle related protein in hippocampus was determined in rats.The contents of cytoplasm Ca2+ were determined using Fura-2/AM-fluorescence method.The effects of gypenosides on above indices were studied.RESULTS：Compared with the controls,the learning and memory ability of Aβ₁-40-injected rats were lower,the expression of cyclin A and cyclin B₁ protein in rat hippocampus neurons had hoisted,the contents of calcium in hippocampus were increased significantly.Gypenosides,however,improved all the indexes in varying degrees.CONCLUSION：These results imply that gypenosides improves the learning and memory ability of the rats treated with Aβ₁-40,reverses the expression of cell cycle-related protein and maintains the calcium homeostasis in hippocampus neurons.