Effect of Acupuncture on CXCL8 Receptors in Rats Suffering from Embryo Implantation Failure简

To observe the effect of acupuncture on CXCL8 receptors（CXCR1 and CXCR2） in rat endometrium experiencing embryo implantation failure, 72 pregnant rats were randomly divided into four groups： normal group（N）, embryo implantation failure group（M）, acupuncture treatment group（A）, and progestin treatment group（W）. Then the rats in each group were equally randomized into a day-6（D6） group, a day-8（D8） group, and a day-10（D10） group. The rats in group M, group A, and group W were treated with mifepristone-sesame oil solution on day 1, while the rats in group N were injected with the same amount of sesame oil. Meanwhile, ＂Housanli＂ and ＂Sanyinjiao＂ were selected for acupuncture. From day 1 to the time of death, the rats in group A were fastened up and then acupuncture was administered while the rats in group N and group M were only fixed, and the rats in group W were given progestin. The number of implanted embryos was calculated. The expression of CXCR1 and CXCR2 in rat endometrium was detected by immunohistochemistry, Western blotting and real-time PCR. Compared to group N, the average number of implanted embryos, the protein and mRNA expression of CXCR1（D6, D8 and D10）, and the protein and mRNA expression of CXCR2（D8 and D10） in rat endometrium were significantly decreased in group M. Compared to group M, there was significant elevation in the average number of implanted embryos, the protein expression（D6, D8 and D10） and mRNA expression（D8） of CXCR1 in rat endometrium of group A, and the protein expression（D8 and D10） and mRNA expression（D8） of CXCR2 in rat endometrium of group W. These findings indicated that acupuncture can increase the number of implanted embryos in rats of embryo implantation failure, which may be relevant with up-regulation the expression of CXCR1 and CXCR2 at maternal-fetal interface of rats with embryo implantation failure.     

Influence of neurotrophin-3 on Bcl-2 and Bax expressions in spinal cord injury of rats

Objective： To study the protective mechanisms of neurotrophin-3 （NT-3） on the spinal cord injury. Methods：Totally 105 SD rats were randomly divided into 3 groups： control group, experimental group and sham operation group. Rats from the former 2 groups were inflicted to animal model of acute spinal cord injury according to Allen＇s （WD） by situating a thin plastic tube in the subarachnoid space below the injury level for perfusion. Rats in experimental group received 20 ul NT-3 （200 ng） from the tube at 0, 4, 8, 12, 24 h and 3, 7 d after injury, and those in control group got an equal volume of normal saline at the same time. The animals in sham operation group only received opening vertebral plate and tube was put in subarachnoid space. The rats were sacrificed at 4, 8, 12, 24 h and 3, 7, 14 d post injury （n=5）. The expression levels of Bcl-2 and Bax proteins in spinal cord of rats were detected by immunohistochemistry assay. Results： The level of Bax protein in control group significantly increased as compared with those in sham operation group, and the peak reached at 8 h after spinal cord injury. The Bcl-2 proteins were always weakly positive. The Bax proteins in NT-3 group significantly decreased but the Bcl-2 proteins obviously increased as compared with those in control group. Conclusion： NT-3 can protect spinal cord from injury in vivo. One of the mechanisms is that NT-3 can inhibit abnormal expression of Pax protein, and increase the expression of Bcl-2 protein, then inhibit apoptosis after spinal cord injury.     

Recombinant human growth hormone secreted from tissue-engineered bioartificial muscle improves left ventricular function in rat with acute myocardial infarction

Background Experimental studies and preliminary clinical studies have suggested that growth hormone （GH） treatment may improve cardiovascular parameters in chronic heart failure （CHF）. Recombinant human GH （rhGH） has been delivered by a recombinant protein, by plasmid DNA, and by genetically engineered cells with different pharmacokinetic and physiological properties. The present study aimed to examine a new method for delivery of rhGH using genetically modified bioartificial muscles （BAMs）, and investigate whether the rhGH delivered by this technique improves left ventricular （LV） function in rats with CHE Methods Primary skeletal myoblasts were isolated from several Sprague-Dawley （SD） rats, cultured, purified, and retrovirally transduced to synthesize and secrete human rhGH, and tissue-engineered into implantable BAMs. Ligation of the left coronary artery or sham operation was performed. The rats that underwent ligation were randomly assigned to 2 groups： CHF control group （n=6） and CHF treatment group （n=6）. The CHF control group received non-rhGH-secreting BAM （GFP-BAMs） transplantation, and the CHF treatment group received rhGH-secreting BAM （GH-BAMs） transplantation. Another group of rats served as the sham operation group, which was also randomly assigned to 2 subgroups： sham control group （n=6） and sham treatment group （n=6）. The sham control group underwent GFP-BAM transplantation, and the sham treatment group underwent GH-BAM transplantation. GH-BAMs and GFP-BAMs were implanted subcutaneously into syngeneic rats with ligation of the left coronary artery or sham operation was performed. Eight weeks after the treatment, echocardiography was performed, hGH, insulin-like growth factor-1 （IGF-1） and TNF-a levels in rat serum were measured by radioimmunoassay and ELISA, and then the rats were killed and ventricular samples were subjected to immunohistochemistry. Results Primary rat myoblasts were retrovirally transduced to secrete rhGH and tissue-engineered into implantable BAMs containing parallel arrays of postmitotic myofibers. In vitro, they secreted 1 to 2 lug of bioactive rhGH per day. When implanted into syngeneic rat, GH-BAMs secreted and delivered rhGH. Eight weeks after therapy, LV ejection fraction （EF） and fractional shortening （FS） were significantly higher in CHF rats treated with GH-BAMs than in those treated with GFP-BAMs （（65.0i-6.5）% vs （48.1±6.8）%, P 〈0.05）, （（41.3±7.4）% VS （26.5±7.1）%, P 〈0.05）. LV end-diastolic dimension （LVEDD） was significantly lower in CHF rats treated with GH-BAM than in CHF rats treated with GFP-BAM （P 〈0.05）. The levels of serum GH and IGF-1 were increased significantly in both CHF and sham rats treated with GH-BAM. The level of serum TNF-α decreased more significantly in the CHF treatment group than in the CHF control group.Conclusions rhGH significantly improves LV function and prevents cardiac remodeling in rats with CHF. Genetically modified tissue-engineered bioartificial muscle provides a method delivering recombinant protein for the treatment of heart failure.     

Matrix metalloproteinase-8 inhibitors mitigate sepsis-induced myocardial injury in rats

Background Sepsis-induced myocardial injury （SIMI） is caused by a variety of mechanisms. The aim of the study is to investigate the effects of metalloproteinase-8 （MMP-8） on SIMI and its mechanisms in rats. Methods Forty male Sprague Dawley rats were randomly divided into four groups： MMP-8 inhibitor （M81）, dexamethasone （DEX）, sepsis, and sham groups. The sepsis model was established by cecal ligation and puncture （CLP）. Rats in the M81 group immediately received an intraperitoneal injection of M81 （0.1 mg/kg） after CLP. Rats in the DEX group immediately received an intraperitoneal （IP） injection of DEX （2 mg/kg）. Rats in the sepsis and sham groups received intraperitoneal injections of normal saline. Rats were sacrificed 12 hours after CLP. Paraffin sections were stained with hematoxylin and eosin to observe the myocardium. The myocardial ultrastructure was observed with transmission electron microscopy. MMP-8, tumor necrosis factor-Q （TNF-a）, and interleukin-113 （IL-113） were detected by immunohistochemistry. The expression of MMP-8 was measured by Western blotting. TNF-a and IL-113 levels in serum and myocardial tissue were determined by enzyme-linked immunosorbent assay. Results Compared with the sham group, the myocardium in the sepsis group was seriously injured. MMP-8, TNF-α and IL-1β expression was higher in the sepsis group than in the sham group, Treatment with M81 or DEX, however, attenuated sepsis induced histopathological changes in the heart, and was associated with significant reductions in serum and myocardial levels of TNF-a and IL-113 （P 〈0.05）. M81 significantly inhibited MMP-8 expression in myocardial tissue （P 〈0.05）. In addition, treatment with DEX was not associated with a change in myocardial levels of MMP-8 （P 〉0.05）. Conclusion MMP-8 inhibitor attenuated myocardial injury in septic rats, which might be related to reduced expression of TNF-α and IL-1β.     

Lithium improves memory by decreasing A-beta production and tau phosphorylation in rats chronically exposed to aluminum

Objective： To investigate the effects of lithium on cognitive function and metabolism of Amyloid-beta Protein Precursor （APP） and tau phosphorylation in rats chronically exposed to aluminum. Methods： Twenty-four chronically aluminum-exposed rats were randomly divided into 2 groups： a lithium-treatment group and a non-treatment group （n=12 per group）. Lithium chloride was administered to the lithium-treatment group via gastric gavage daily for 6 weeks （200 mg/kg·d LiCl）, while the non-treatment group was administered the same volume of sodium chloride by the same means. An additional control group （n=12） received no intervention. Memory function was evaluated by the Morris water maze test. Aβ was measured by immunohistochemical staining, while total APP, phosphorylated-tau protein, CDK5 and PP2A were determined by Western Blotting. Results： （1） Compared to the non-treatment group, the lithium-treatment group had a significantly shorter mean escape latency and a lower proportion of random navigation pattern in the spatial probe test （P〈0.05）. After the platform was taken away, the rats in the lithium-treatment group crossed the platform quadrant significantly more and stayed longer in the platform quadrant than those in the non-treatment group （P〈0.05）. （2） The number of Aβ positive neurons in the hippocampus and cortex was significantly less in the lithium-treatment group than in the non-treatment group （P〈0.05）, but the content of APP was not different between groups （P=0.730）. （3） Phosphorylation of tau protein decreased significantly in the lithium-treatment group than that in the non-treatment group （P〈0.05）. The content of CDK5 in the lithium-treatment group was significantly less than that in the non-treatment group in the cortex and hippocampus, while there was no difference in the content of PP2A between the 2 groups. The expression of CDK5 was significantly correlated with phosphorylated tau （r=0.871, P=0.024） in the lithium-treatment group. Conclusion： Lithium may improve memory function in rats chronically exposed to aluminum by decreasing both the production of Aβ and tau phosphorylation, with the latter results from inhibiting expression of CDK5.     

Thioredoxin and impaired spatial learning and memory in the rats exposed to intermittent hypoxia

Background  Obstructive sleep apnea (OSA) can cause cognitive dysfunction and may be a reversible cause of cognitive loss in patients with Alzheimer’s disease (AD). Chronic exposure to intermittent hypoxia (IH), such as encountered in OSA, is marked by neurodegenerative changes in rat brain. We investigated the change of thioredoxin (Trx), spatial learning and memory in rats exposed to chronic intermittent hypoxia (CIH).

Methods  Forty healthy male Sprague-Dawley (SD) rats were randomly divided into four groups of ten each: a CIH+normal saline (CIH+NS group), a N-acetylcystein-treated CIH (CIH+NAC) group, a sham CIH group (sham CIH+NS), and a sham NAC-treated sham CIH (CIH+NAC) group. Spatial learning and memory in each group was assessed with the Morris water maze. Real-time PCR and Western blotting were used to examine mRNA and protein expression of Trx in the hippocampus tissue. The terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling (TUNEL) method was used to detect the apoptotic cells of the hippocampus CA1 region.

Results  CIH-rats showed impaired spatial learning and memory in the Morris water maze, including longer mean latencies for the target platform, reduced numbers of passes over the previous target platform and a smaller percentage of time spent in the target quadrant. Trx mRNA and protein levels were significantly decreased in the CIH-hippocampus, meanwhile, an elevated apoptotic index revealed apoptosis of hippocampal neurons of rats exposed to CIH. The rats, which acted better in the Morris water maze, showed higher levels of the Trx mRNA and protein in the hippocampus; apoptotic index of the neurons in the hippocampus of each group was negatively correlated with the Trx mRNA and protein levels.

Conclusion  The Trx deficit likely plays an important role in the impaired spatial learning and memory in the rats exposed to CIH and may work through the apoptosis of neurons in the hippocampus.

     

Effect of anterior nucleus of thalamus stimulation on glucose metabolism in hippocampus of epileptic rats

Background  Electrical stimulation of the anterior nucleus of the thalamus (ANT) appears to be effective against seizures. In this study, we investigated changes in glucose metabolism during high-frequency stimulation of ANT in epileptic rats.

Methods  Three groups of rats were used: (1) a stimulation group (n=12), (2) a sham stimulation group (n=12) with seizures induced by stereotactic administration of kainic acid (KA), and (3) a control group (n=12) with sham surgery. Concentric bipolar electrodes were stereotaxically implanted unilaterally in the ANT. High-frequency stimulation was performed in each group except the sham stimulation group. Microdialysis probes were lowered into the CA3 region of the hippocampus unilaterally but bilaterally in the stimulation group. The concentrations of glucose, lactate, and pyruvate in dialysate samples were determined by an ISCUS microdialysis analyzer.

Results  The extracellular concentrations of lactate and lactate/pyruvate ratio (LPR) of epileptic rats were significantly higher than in control rats (P=0.020, P=0.001; respectively). However, no significant difference in the concentration of glucose and pyruvate was found between these groups (P >0.05). Electrical stimulation of ANT induced decreases in lactate and LPR in the ipsilateral hippocampus (KA injected) of the stimulation group (P <0.05), but it did not influence the glucose metabolism in the contralateral hippocampus (P >0.05).

Conclusions  This study demonstrated that the glycolysis was inhibited in the ipsilateral hippocampus of epileptic rats during electrical ANT stimulation. These findings may provide useful information for better understanding the mechanism of ANT-deep brain stimulation.

     

Efficacy of Topical versus Oral 5-Aminosalicylate for Treatment of 2,4,6-Trinitrobenzene Sulfonic Acid-induced Ulcerative Colitis in Rats简

5-aminosalicylic acid（5-ASA） is drug of choice for the treatment of ulcerative colitis（UC）. In this study, the efficacy of topical versus oral 5-ASA for the treatment of UC was examined as well as the action mechanism of this medication. A flexible tube was inserted into the rat cecum to establish a topical administration model of 2,4,6-trinitrobenzene sulfonic acid（TNBS）-induced UC. A total of 60 rats were divided into sham operation group（receiving an enema of 0.9% saline solution instead of the TNBS solution via the tube）, model group, topical 5-ASA group, oral Etiasa group（a release agent of mesalazine used as positive control） and oral 5-ASA group（n=12 each）. Different treatments were administered 1 day after UC induction. The normal saline（2 mL） was instilled twice a day through the tube in the sham operation group and model group. 5-ASA was given via the tube in the topical 5-ASA group（7.5 g/L, twice per day, 100 mg/kg）, and rats in the oral Etiasa group and oral 5-ASA group intragastrically received Etiasa（7.5 g/L, twice per day, 100 mg/kg） and 5-ASA（7.5 g/L, twice per day, 100 mg/kg）, respectively. The body weight was recorded every day. After 7 days of treatment, blood samples were drawn from the heart to harvest the sera. Colonic tissues were separated and prepared for pathological and related molecular biological examinations. The concentrations of 5-ASA were detected at different time points in the colonic tissues, feces and sera in different groups by using the high pressure liquid chromatography（HPLC）. The results showed that the symptoms of acute UC, including bloody diarrhea and weight loss, were significantly improved in topical 5-ASA-treated rats. The colonic mucosal damage, both macroscopical and histological, was significantly relieved and the myeloperoxidase activity was markedly decreased in rats topically treated with 5-ASA compared with those treated with oral 5-ASA or Etiasa. The mRNA and protein expression of IL-1β, IL-6, and TNF-α was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. The concentrations of 5-ASA in the colonic tissue were significantly higher in the topical 5-ASA group than in the oral 5-ASA and oral Etiasa groups. It was concluded that the topical administration of 5-ASA can effectively increase the concentration of 5-ASA in the colonic tissue, decrease the expression of proinflammatory cytokines, alleviate the colonic pathological damage and improve the symptoms of TNBS-induced acute UC in rats.     

Echinacoside Alleviates Cognitive Impairment in Cerebral Ischemia Rats through α7nAChR-Induced Autophagy

Objectives:To evaluate the effect of echinacoside(ECH) on cognitive dysfunction in post cerebral stroke model rats.Methods:The post stroke cognitive impairment rat model was created by occlusion of the transient middle cerebral artery(MCAO).The rats were randomly divided into 3 groups by a random number table:the sham group(sham operation),the MCAO group(received operation for focal cerebral ischemia),and the ECH group(received operation for focal cerebral ischemia and ECH50 mg/kg per day), with...     

Change of p16~(INK4a) and PNCA Protein Expression in Myocardium after Injection of hIGF-1 Gene Modified Skeletal Myoblasts into Post-infarction Rats

This study examined the change of p16^INK4a and PNCA protein expression in myocardium after injection of hIGF-1 gene modified skeletal myoblasts into post-infarction rats. HIGF-1 gene modified skeletal myoblasts （hIGF-1-myoblasts） were injected into hind limb muscles of 18 post-infraction rats （experimental group）. Primary-myoblasts were injected into 18 post-infraction rats （control group） and 12 non-infarction rats （sham group）. Expression of p16INK4a and PCNA pro- tein in myocardiums were separately detected immunocytochemically 1, 2 and 4 weeks after the inuection. The level of hIGF-1 and rIGF-1 protein in serum and myocardium were detected by en- zyme-linked immunosorbent assay （ELISA）. Compared with the sham group, the percentage of p^16INK4a and PCNA positive cells reached a peak after 1 week in the control group and the experimental group （P〈0.01）. Moreover, the percentage of p16^INK4a-positive cells in the experimental group was lower than in control group whereas the percentage of PCNA-positive cells was lower in the control group than in the experimental group （P〈0.01）. The percentage of p16^INK4a-positive cells in the experimental group and the percentage of PCNA-positive cells in the control group were close to that in the sham group from the 2nd week （P〉0.05）. ELISA analysis disclosed that the myocardium level of rIGF-1 protein increased gradually in the controls and especially in the experimental group （P〈0.01）. The serum level of rIGF-1 decreased significantly in post-infraction rats, but these conditions were improved in the experimental group （P〈0.01）. The hIGF-1 protein in serum and myocar- dium were detected from the 1st week to the 4th week in the experimental group. Statistical analysis revealed significant associations of myocardium level of hIGF-1 protein with expression of p^16INK4a and PCNA protein （r=–0.323, P〈0.05; r=0.647, P〈0.01）. It is concluded that genetically hIGF-1-myoblast provides a means for constant synthesis and re     

Effects of Bone Marrow-derived Mesenchymal Stem Cells on TGF-β and MCP-1 in Injured Lung of Rats

The primary objective of the present study is to investigate the therapeutic effect of bone marrow-derived mesenchymal stem cells （MSCs） on bleomycin （BLM）-induced lung injury of rats and the effect on transforming growth factor-β （TGF-β） and monocyte chemoattractant protein-1 （MCP-1）. MSCs were isolated from SD rats. The recipients rats were divided randomly into four groups： lung injury group, MSC treatment group, MSC control group and normal control group. Rats of lung injury group and MSC treatment group were perfused with BLM of 5mg/kg （0.2-0.3ml） intratracheally, others were perfused with normal saline. After twelve hours, rats of MSC treatment group and MSC control group were injected MSCs of 0.5×10^6per rat into tail vein. Haematoxylin-eosin staining was used to observe the morphology in lung tissue. ELISA was used to detect the contents of TGF-β and MCP-1 in serum and bronchoalveolar lavage fluid （BALF）. Collagen content of the lung tissue was assessed by hydroxyproline （HYP） concentration. It was found that the thickness of alveolar wall and lung interstitium were significantly reduced in the rats of MSC treatment group compared with the lung injury group. HYP content in lung interstitium, TGF-β and MCP-1 in serum and BALF were increased significantly in rats of lung injury group two weeks after BLM perfusion, but they were reduced significantly in the rats of MSC treatment group compared with the injured rats. These observations provide evidence that MSCs engraftment could alleviate bleomycin-induced lung injury and fibrosis in rats and the therapeutic effects might relate with the decrease of TGF-β and MCP-1.     

Antioxidant Mechanism of Xiaojin Pill(小金丸) for Treatment of Peyronie's Disease in Rats Based on Matrix Metalloproteinases

Objective: To evaluate the effects of Xiaojin Pill(小金丸) in the treatment of Peyronie's disease(PD) in a rat model. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into four groups with 6 in each: sham operation, PD model, vehicle control and Xiaojin Pill groups. The rats in the sham operation group received penile tunica albsginea(TA) injection with 50 μL vehicle, while the rats in the other 3 groups received 50 μL penile TA injection of 50 μg transforming growth factor(TGF)-β1. Forty-two days after the injection, rats in the vehicle control and Xiaojin Pill groups received 0.5 mL water and Xiaojin Pill solution(107 mg/kg of body weight), respectively by gavage for 28 days, while those in the sham operation and PD model groups did not receive any intervention. After intervention, the expressions of matrix metalloproteinase 2/9(MMP2/9), nitric oxidesynthase(NOS), superoxide dismutase(SOD) and malondialdehyde(MDA) were measured. Results: Rats in the PD model and vehicle control groups presented obvious fibrosis in corpus cavernosum(CC) and demonstrated a significantly increased expressions of MMP2 and MMP9 in the CC compared with the sham operation group(all P0.01). In contrast, the expressions of MMP2 and MMP9 in the Xiaojin Pill group were significantly down-regulated(both P0.01). In addition, the levels of NOS and MDA in CC were significantly increased while the activity of SOD was decreased in the PD model and vehicle control groups compared with the sham operation group(al P0.01). After Xiaojin Pil treatment, the levels of MDA, NOS and SOD appeared to be corrected(al P0.01). Conclusions: Xiaojin Pill could reduce fibrosis in the CC by decreasing the expressions of MMPs, NOS and MDA, and by increasing the activity of SOD. Therefore, Xiaojin Pill might be a therapeutic option for PD.     

Eiectroacupuncture Prevents Cognitive Deficits Caused by Topiramate （TPM） in Rats

Objective Recent studies have demonstrated that acupuncture is feasible to treat cognitive impairments. The objective of this study was to present behavioral evidence that electro-acupuncture （EA） could improve the learning and memory of TPM administrated rats. Methods The pattern of TPM-induced cognitive deficits in rats was made by administration of TPM intragastrically for 3 weeks. Of them the rats which showed damage in learning and memory （n=45） were randomly allocated to 3 groups： Impaired group （n=15）, EA group （n=15） and placebo-EA group （n=15）. Moreover, normal group （n=15） was set as control groups. EA stimulation was provided at acupoints located in either the midline of the back or of the head： Gv-20 （Baihui）, Gv-14 （Dazhui）. Morris water maze test was employed to assess spatial discriminative ability per group respectively and to analyze the curative effects of EA. Results Compared to the normal group, obvious cognitive deficits were found in the impaired and placebo-EA groups, and the statistic analysis showed that there were significant differences between normal and impaired groups in ANOVA. In the EA group, shortened mean escape latency was detected compared with the impaired effect on cognitive group during the same trial days; search strategy changed from random pattern adopted by impaired and placebo-EA rats to tendency or linear pattern popular in the normal group. Conclusion The present results suggested that EA exerted a protective impairment caused by TPM in rats, and EA has a specificity of cure. EA as a potential clinic method in treating TPM-induced cognitive impairment should be developed and investigated in the future.     

The Influences of Electroacupuncture on the Quantitative Changes of Ultra Structure in CA3 Sector of the Hippocampus of VD Rats

Objective To observe the effect of electroacupuncture （EA） on learning and memory and the pathology morphologic of nerve and the quantitative changes of synapses in CA3 sector of the hippocampus on vascular dementia （VD） rats. Methods The VD rats were modeled with method of global ischemia reperfusion by 4 vascular occlusion （4-vo）. Morris water maze tests were used for a behavioral study. The changes of the ultra structure parameter in CA3 sector of the hippocampus were studied with transmission electron microscope and picture analysis system. Results The model group animals needed more escape time than the control group, and they did not swim longer in platform quadrant than in the others in the Morris water tests. In the control group and electro-acupuncture group, the modality configuration of cells in CA3 sector of the hippocampus was normal, and the normal and abnormal chromatin was obvious. The configuration of endoplasmic reticulum, chondriosome and synapses was normal. The front and back membrane of the synapses was clear. In the VD group, the cells were atrophied and dwindled. The front and back membrane of the synapses was illegible. The clearance, PSD and interphase curvature on area of Gray type Ⅰ synapses in CA3 sector of the hippocampus in VD rats were decreased significantly. In the EA group, the animals cut the escape time mostly and they swam more times in platform quadrant than in other three quadrants. The interphase curvature, cleft and PSD on area of Gray type Ⅰ synapses in CA3 sector of the hippocampus were increased significantly. Conclusion EA can improve learning and memory of VD rats by restraining the disappearance of nerve cells, and influencing the structure parameter of synapses in CA3 sector of the hippocampus.     

Inactivation of the Rho-ROCK signaling pathway to promote neurologic recovery after spinal cord injuries in rats

Background After injury,axonal regeneration of the adult central nervous system （CNS） is inhibited by myelin-derived growth-suppressing proteins.These axonal growth inhibitory proteins are mediated via activation of Rho,a small GTP-binding protein.The activated form of Rho,which is bound to GTP,is the direct activator of Rho kinase （ROCK） through serial downstream effector proteins to inhibit axonal regeneration.The objective of this study was to observe the therapeutic effect of inactivation of the Rho-ROCK signaling pathway to promote neurologic recovery after spinal cord injuries in rats.Methods One hundred and twenty adult female Sprague-Dawley rats were randomly divided into three groups.Laminectomies alone were conducted in 40 rats in the sham group.Laminectomies and spinal cord transections were performed in 40 rats in the control group （treated with normal saline administered intraperitoneally）.Laminectomies and spinal cord transections were performed in 40 rats in the fasudil-treated group （treated with fasudil administered intraperitoneally）.Neurologic recovery was evaluated before surgery and 3 days,and 1,2,3,and 4 weeks after surgery using the Basso-Beattie-Bresnahan （BBB） scale of hind limb movement.At the same time,the expression of RhoA mRNA was determined with RT-PCR.Histopathologic examinations and immunofiuorescence staining of NF were performed 1 month after surgery.Results Compared with the control group,the BBB scores of the fasudil-treated group were significantly increased and the expression of RhoA mRNA was significantly decreased.In the fasudil-treated group,a large number of NF-positive regenerating fibers was observed; some fibers crossed the slit of the lesion.Conclusion Inactivation of the Rho-ROCK signaling pathway promotes CNS axonal regeneration and neurologic recovery after spinal cord injuries in rats.     

Effects of isoflurane on ICAM-1 expression and neutrophils infiltration in rats with liver ischemia and reperfusion injury

Objective： To establish a rat model of warm partial hepatic ischemia-reperfusion （IR）, and investigate the protective and anti-inflammatory effects of isoflurane on warm hepatic ischemia-reperfusion injury （IRI） in rats. Methods： Thirty-two female Sprague-Dawley rats were divided equally into 4 groups （n-8）： PB-Sham group in which the rats were anesthetized by intraperitoneal injection of pentobarbital sodium （1.0%, 40 mg/kg, PB） and received a sham operation without occlusion of liver blood flow; PB-IR group whose rats underwent partial hepatic IR after anesthesia; Iso-Sham group in which inhalation of 1.0 MAC isoflurane and sham operation was performed; Iso-IR group in which 1.0 MAC isoflurane was inhaled for 4 h and IR was performed. Rat model of warm partial hepatic IR was established by clamping the hepatic arteries and hilar vessels distributing to the left and median lobes to induce partial hepatic ischemia （70%） for 60 rain followed by reperfusion for 3 h. The rats were killed 3 h after declamping, and specimens of liver tissue and blood were obtained. The serum ALT and AST were detected as liver damage markers. Viability of myeloperoxidase （MPO） in liver was measured. The protein level of ICAM-1 in the liver was detected by immunohistochemistry and Western blotting. Results： Rats treated with 1.0 MAC isoflurane during warm partial （70%） hepatic ischemia 60 rain and 3 h reperfusion had significantly lower serum ALT and AST compared with rats anesthetized with pentobarbital sodium subjected to hepatic IRI. The expression of ICAM-1 in hepatic tissue was significantly increased by hepatic IRI after pentobarbital sodium anesthesia. Isoflurane significantly inhibited protein expression of ICAM-1 in hepatic IR injury compared with pentobarbital sodium anesthesia. Viability of liver MPO was significantly increased by hepatic IRI after pentobarbital sodium anesthesia; Isoflurane can significantly inhibit MPO alteration in rat liver ischemia-reperfusion injury compared with rats anesthetized with pentobarbital sodium. Conclusion： Isoflurane anesthesia can attenuate liver IR injury in rats that maybe by inhibiting ICAM-I expression and reducing the infiltration of neutrophils.     

Effect of neurotrophin-3 on SOD and MDA in rats after acute spinal cord injury

Objective：To investigate the effect of neurotrophin-3 on the expressions of SOD and MDA in the injured spinal cord of rats. Methods： Totally 105 SD rats were randomly divided into 3 groups （n= 35）： sham group, control group and experimental group. Animal model of acute spinal cord was inflicted with Allen＇s method by a thin plastic tube situated in subarachnoid space below the injury level for perfusion. Rats in experimental group received 20μl NT-3 （200ng） from the tube at 0, 4, 8, 12, 24 h and 3, 7 d after injury, and those in control group got the equal volume of normal saline at the same time points. The animals in sham group only received opening vertebral plate and putting tube in subarachnoid space. The rats were sacrificed at 4, 8, 12, 24 h, and 3, 7, 14 d postinjury （n=5）. And the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in blood were observed with colorimetric method. Results： The serum level of SOD reduced obviously and the level of MDA raised obviously in rats after the injury, and the activity of SOD reached the lowest on day 3 and the concentration of MDA reached peak at the 7 d. In the experimental group, the SOD level was obviously higher （P〈0. 01）, and MDA level was lower than the control （P〈0. 01）. Conclusion： NT-3 can mitigate secondary injury of spinal cord in vivo. One of mechanisms is that inhibits abnormal expression of MDA and elevates the activity of SOD, thus the injury of free radical and lipid peroxidation is attenuated.