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1.
EfectsofnitricoxideonhepaticdysfunctioninducedbythioacetamindeinratsZhengXiaobin郑晓宾,HanDewu韩德五,MaXuehui马学惠,XuRuiling许瑞龄andZha...  相似文献   

2.
FlunarizineisaselectiveCa2 entryblocker.ItdoesnotinterferewithnormalcellularCa2 homeostasisbutaf fectsCa2 channelopeningswithischemiaorotherpatho logicchanges .Thestudyinvestigatestheprotectiveeffectsofflunarizineonischemiccochleawithauditorybrainstemres…  相似文献   

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Background Although the insulinotropic role of glucagon-like peptide-1 (GLP-1) in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine the effects of GLP-1 on injury of rats cardiac myocytes induced by hypoxia-reoxygenation (H/R) and the possible mechanisms.
Methods The cultured neonatal rats cardiac myocytes were randomly divided into seven groups: the normal control group, the H/R group, the GLP-1+H/R group, the GLP-1+H/R+UO126 (the p42/44 mitogen-activated protein kinase (MAPK) inhibitor) group, the GLP-1+H/R+LY294002 (phosphatidylinositol 3-kinase (PI3K) inhibitor) group, the H/R+UO126 group, and the H/R+LY294002 group. The lactate dehydrogenase (LDH) activity, apoptosis rate of cardiac myocytes, and caspase-3 activity were detected after the injury of H/R.
Results Compared with the normal control group, the activity of LDH, cardiac myocyte apoptosis rate, and caspase-3 activity all increased significantly in the H/R group (P 〈0.01). Compared with the H/R group, these three indices all decreased in the H/R+GLP-1 group (P 〈0.01). However, the changes of LDH activity, apoptosis rate, and caspase-3 activity were inhibited by LY294002 and UO126 respectively.
Conclusions GLP-1 can directly act on cardiac myocytes and protect them from H/R injury mainly by inhibiting their apoptosis. Its mechanism may be through the PI3K-Akt pathway and the MAPK signaling pathway.  相似文献   

4.
Objective To investigate the effects of oral administration of type Ⅱ collagen(C Ⅱ) on adjuvant arthritis (AA)in rats and its mechanisms,and to compare the effects of C Ⅱ with those of the Chinese traditional medicine Tripterygium Polyglycoside administered similarly.Methods Arthritis was induced in rats by immunization using Freund‘s complete adjuvant(FCA).After feeding rats either soluble CⅡ or Tripterygium Polyglycoside,changes in degree of articular swelling and articular histological findings were observed in AA rats.Some correlative immunological indexes were measured,including delayed type hypersensitivity(DTH) reaction,anti-collagen and anti-Mycobacterium tuberculosis(MT)antibody in serum,and levels of IFN-γ and IFN-α in articular steep in rats.Results Oral administration of C Ⅱ was able to alleviate both distinctly articular and general symptoms in AA rats,suppress synovium hyperplasia and inflammatory cells infiltration in arthrosis capsule.The effects brought about by C Ⅱ were stronger than those by Tripterygium Polyglycoside.Oral administration of C Ⅱ inhibited antigen-specific immune response,such as DTH and antibody reaction to C Ⅱ .In addition,the expression of IFN-αand IFN-αin joints were locally downregulated.Conclusions The therapeutic effect of oral administration of C Ⅱ is obvious on adjuvant arthritis in rats.Its remedial mechanisms are likely related to the downregulation of both IFN-γ and TNF-α,and the suppression of cell immunity.  相似文献   

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Previous studies have suggested that glutathione-S-transferase π (GST-π) over-expression in the brain tissue is associated with refractory epilepsy.However,whether the change in GST-π level in the peri...  相似文献   

6.
The changes of immunoreactive neurotensin(ir-NT)contents in the brain areas,pituitary gland and plasma in the traumatized rats were observed in the present study.The results of radioimmunoassay exhibited significant changes of the ir-NT contents inthe hypothalamus,pituitary gland,plasma,injured tissue,hippocampus,central gray andspinal cord in the posttraumatic rats at different intervals.A predominant characteristicsof the changes of ir-NT levels in the brain areas,pituitary gland and plasma was thedramatical decrease at various times except for the hypothalamus,central gray andhippocampus with biphasic alterations.The ir-NT contents in the frontal cortex andpons-medulla also displayed changes to different extent under the acute craniocerebraltrauma condition.These results suggest that NT may play a role in the pathophysiologyof traumatic head injury.  相似文献   

7.
Objective:To observe the therapeutic effect of Yangxue Qingnao Granule(养血清脑颗粒, YXQNG) on cognitive impairment induced by chronic cerebral hypoperfusion and to investigate its impact on oxidative stress,apoptosis,and the cholinergic system.Methods:Adult male Wistar rats were subjected to chronic cerebral hypoperfusion by permanent occlusion of bilateral common carotid arteries(2-VO).Thirty rats were randomly assigned to one of the five treatment groups in a 1:1:1:1:1 ratio:sham operation plus normal saline treatment,2-VO plus normal saline treatment,2-VO plus YXQNG at a dose of 2 g·kg(-1)·d-1 or 4 g·kg(-1)·d-1, or 2-VO plus rivastigmine 2 mgkg-1·d-1.The Morris water maze test was used to assess the spatial memory retrieval.Apoptosis,total antioxide capacity(T-AOC),acetylcholine esterase(AchE) and choline acetyl transferase(ChAT) activities in the hippocampus and the cortex were investigated.Results:In the chronic cerebral hypoperfusion model,the 2-VO plus saline treatment resulted in impaired special learning as shown by the significantly prolonged escape latency and shorter swim time in the first quadrant as compared to the sham operation.The impairment was associated with apoptosis and significant decreases in T-AOC,AchE and ChAT activities in the hippocampus and the cortex.Treatment with YXQNG at either 2 g·kg(-1)·d-1 or 4 g·kg(-1)·d-1 dose,or rivastigmine resulted in significantly shorter escape latencies and longer swim time in the first quadrant.YXQNG at both doses,but not rivastigmine,had significant reduction in apoptosis,and significant increases in T-AOC and ChAT activity in both the hippocampus and the cortex.Unlike rivastigmine,neither dose of YXQNG showed significant reduction in AchE activity.Conclusions:YXQNG ameliorated cognitive impairment induced by chronic cerebral hypoperfusion.The protective effect may be mediated through its regulation of apoptosis and activities of T-AOC and ChAT in the hippocampus and cortex of the rats in the chronic cerebral hypoperfusion model,a mechanism that is different from rivastigmine.  相似文献   

8.
StereologicalandcytochemicalstudyonthepathogenesisofhepatitisinducedbyhalothaneinratsZhengWeiqiang(郑唯强);ZhanRongzhou(詹鎔洲);YuW...  相似文献   

9.
Objective: To explore the effects of Yizhi Capsule (YZC) on learning and memory disorder and β-amyloid peptide induced neurotoxicity in rats.Methods: Various doses of YZC were administered to Sprague-Dawley (SD) rats for 8 consecutive days, twice a day. On the 8th day of the experiment, scopolamine hydrobromide was intraperitoneally injected to every rat and Morris water maze test and shuttle dark avoidance test were carried out respectively to explore the changes of learning and memory capacities in the rats. Besides, after the cerebral cortical neurons of newborn SD rats aged within 3 days were culturedin vitro for 7 days, drug serum containing YZC was added to the cultured neurons before or after β amyloid peptide25–35 (Aβ25–35) intoxication to observe the protective effect of YZC on neurotoxicity by MTT assay and to determine the LDH content in the supernatant.Results: Compared with those untreated with YZC, the rats having received YZC treatment got superiority in shorter time of platform seeking in Morris water maze test, as well as elongated latent period and less times of error in shuttle dark avoidance test. On the cultured neurons, YZC drug serum could effectively increase the survival rate of Aβ25–35 intoxicated neurons and reduce the LDH contents in cultured supernatant.Conclusion: YZC has an action of improving learning and memory disorder, and good protective effect on Aβ25–35 induced neurotoxicity in SD rats. Supported by the Social Development Research Program of Department of Science and Technology of Guangdong Province (No. 2KB04207S)  相似文献   

10.
1Introduction Strokeisoneoftheleadingcausesofdisability worldwide.Effectivetherapeuticsfortherehabilitationof strokesurvivorshaveyettobedeveloped.Bonemarrow stromalcellsormesenchymalstemcells(MSCs)havethe potentialforself renewalanddifferentiationintodiverse celltypes.Anumberofrecentpublicationshavereported thatMSCscannotonlygiverisetobone,cartilage,but alsodifferentiateintomyocytes,hepatocytes,glialcells,andneurons[1,2].Itisindicatedbysomestudiesthat MSCscanpassthroughtheblood brainbarrie…  相似文献   

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Background Our earlier studies indicate that melatonin inhibits the proliferation of prolactinoma and induces apoptosis of pituitary prolactin-secreting tumor in rats. Melatonin has also been shown to induce apoptosis and to reduce the production of ATP in breast tumor cells. This study analyzed the levels of the four mitochondrial respiratory complexes and the production of ATP and also the effects of melatonin treatment of prolactinoma. Methods In the in vivo study, mitochondria were harvested from control pituitaries or prolactinoma collected from the pituitaries of melatonin- and 17-13-estradiol (E2)-treated male rats. In the in vitro study, prolactinoma cells mitochondria were harvested. Activities of the four mitochondrial respiratory complexes were assayed using fluorometer. ATP production of prolactinoma cells was estimated using bioluminescent methods. Results Elevated levels of four mitochondrial respiratory complexes activities and ATP production were recorded in prolactinoma cells. Moreover, in both in vivo and in vitro studies, melatonin inhibited the activities of mitochondrial respiratory complexes and the production of ATP in prolactinoma cells. Conclusions There is a link between mitochondria[ function increase and tumorigenesis. Melatonin induces apoptosis of pituitary prolactin-secreting tumor of rats via the induction of mitochondrial dysfunction and inhibition of energy metabolism.  相似文献   

14.

Objective  

To evaluate the dynamic changes of PECAM-1/CD31 on pulmonary injury induced by ischemia–reperfusion (IR) in rats.  相似文献   

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16.
Objective: To observe the effect of total coptis alkaloids (TCA) on β-amyloid peptide (Aβ25-35) induced learning and memory dysfunction in rats, and to explore its mechanism. Methods: Forty male Wistar rats were randomly divided into four groups: the control group, the model group, the TCA low dose (60 mg/kg) group and the TCA high dose (120 mg/kg) group, 10 in each. Aβ25-35 (5μl, 2μg/μl) was injected into bilateral hippocampi of each rat to induce learning and memory dysfunction. TCA were administered through intragavage for consecutive 15 days. Morris Water Maze test was used to assess the impairment of learning and memory; concentration of malondialdehyde (MDA) in cerebral cortex was determined by thiobarbituric acid reactive substance to indicate the level of lipid peroxidation in brain tissues; activity of manganese-superoxide dismutase (Mn-SOD) in cerebral cortex was determined by xanthine-oxidase to indicate the activity of the enzyme; and NF-κB protein expression in cerebral cortex was measured by SP immunohistochemistry. Results: (1) Morris Water Maze test showed that, during the 4 consecutive days of acquisition trials, the rats in the model group took longer latency and searching distance than those in the control group (P<0.01), which could be shortened by high dose TCA (P<0.05); during the spatial probe trial on the fifth day, the rats in the model group took shorter searching time and distance on the previous flat area than those in the control group (P<0.01), which could be prolonged after TCA treatment (for low dose group, P<0.05; for high dose group, P<0.01). (2) Analysis of cerebral cortical tissues showed that, compared with the control group, MDA level got significantly increased and Mn-SOD activity decreased in the model group (both P<0.01). After having been treated with TCA, the MDA level got significantly decreased (P<0.05 and P<0.01 respectively for low and high dose group), while relative increase of Mn-SOD activity only appeared in high dose group (P<0.05). (3) Immunohistochemistry analysis showed the protein expression of NF-κB got significantly increased after modeling, while high dose TCA can significantly inhibit it. Conclusion: TCA could improve Aβ25-35 induced dysfunction of learning and memory in rats, and its protective mechanism is associated with its actions in decreasing MDA level, increasing Mn-SOD activity and inhibiting the expression of NF-κB in cerebral cortex.  相似文献   

17.
Objective: To investigate the changes of spontaneous and cognitive behavior, and cholinergic M receptors in the brain of mice subjected to chronic mild stress (CMS), and to determine the effect of Ning Shen Ling Granule (宁神灵冲剂, NSL) and dehydroepiandrosterone (DHEA) on them. Methods:CMS model mice were established by applying stress every day for 3 consecutive weeks with 7 kinds of unforeseeable stress sources, and they were medicated for 1 week beginning at the 3rd week of modeling. The changes in behavior were determined by Morris Water Maze and spontaneous movement test, and M-receptor binding activity in cerebral cortex, hippocampus and hypothalamus were measured by radioactive ligand assay with 3H-QNB. Results: (1) The spontaneous movement in CMS model mice was significantly reduced, with the latency for searching platform in Morris Water Maze obviously prolonged (P〈0.01), and these abnormal changes in behavior were improved in those treated with NSL and DHEA. (2) The binding ability of M-receptor in cerebral cortex and hippocampus of CMS mice was significantly decreased as compared with those in the control group (P〈0.05), but could be restored to the normal level after intervention with NSL or DHEA. Conclusion: The decline of spontaneous movement and spatial learning and memory ability could be induced in animals by chronic mild stress, and that may be related to the low activity of central cholinergic M-receptors. Both NSL and DHEA could effectively alleviate the above-mentioned changes.  相似文献   

18.
EffectsoffourtraditionalChinesemedicinalherbsonplasmalevelofIL-6andinducedTNFlevelinburnedratswithwoundinfection¥(衣承东)(陈玉林)(陈...  相似文献   

19.
Apoptosis(programmed cell death) occurs invarious physiological and pathological conditions,exhibits a characteristic mechanism of intracellularsequential reaction and may be involved indetermining clinical outcome.Recent studies showthat propofol can inhibit apoptosis.Kodaka[1]reported that propofol inhibited neuronal apoptosisafter brain ischemia and consequently reduced thedelayed neuronal death in the CA- 1pyramidal celllayer of the hippocampus.Chang[2 ] reported thatpropofol,at a therape…  相似文献   

20.
Efectofmildhypothermiaonthechangesofcerebralbloodflow,brainbloodbarrierandneuronalinjuriesfolowingreperfusionoffocalcerebrali...  相似文献   

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