Objective:To explore the mechanism of dexmedetomidine (DEX) regulating microglial (MG) polarization and neuroinflammation after traumatic brain injury (TBI) in rats.Methods:Forty-two adult male SD rats were randomly (random number) divided into the sham group, TBI group, TBI+DEX group (further divided into 1 d, 3 d and 7 d subgroups), TBI+NF-κB inhibitor (pyrrolidine dithiocarbamate, PDTC) group and TBI+DEX+PDTC group, with 6 animals in each group. The rat TBI model was established according to the modified Feeney free fall method. PDTC was intraperitoneally injected 1 h after modeling with a dose of 100 mg/kg, and DEX was intraperitoneally injected 2 h after modeling with a dose of 100 μg/kg. Modified neurological severity score (mNSS) was used to evaluate rat neurological function, ELISA was used to detect serum inflammatory factors, and rats’ damaged cortex was collected to detect the phenotype markers of MG and protein expressions of MyD88 and NF-κB p65, and immunofluorescence staining was used to observe the expression and nuclear entry of NF-κB p65 in MG in injured cortex. One-way and two-way ANOVA were used to compare the measurement data among multiple groups.Results:Compared with the sham group, the mNSS score was significantly higher in the TBI group, and DEX treatment significantly decreased the mNSS score of TBI rats ( P<0.05). ELISA and Western blot results showed that in the TBI group, the tumor necrosis factor-α (TNF-α), interleukin (IL)-1β in serum and M1 phenotype marker (TNF-α, IL-1β) in brain were increased, the expression of anti-inflammatory factor IL-10 in serum and M2 phenotype markers (arginase-1 and IL-10) in brain were decreased ( P<0.05), and DEX downregulated the expression of TNF-α, IL-1β in serum and M1 phenotype markers in brain, while upregulated the level of L-10 in serum and the M2 phenotype marker in brain ( P<0.05). In addition, the expression of MyD88 and the nuclear translocation of NF-κB p65 were inhibited in the DEX group, and this effect could be enhanced by PDTC. Conclusions:DEX modulates MG activation in TBI rats by inhibiting NF-κB nuclear translocation and reduces neuroinflammation.

目的 探索创伤性脑损伤(traumatic brain injury,TBI)大鼠模型中铁死亡的发生及与其密切相关的基因.方法 将SD大鼠随机分为Sham组和TBI组,采用普鲁士蓝(Perl′s)染色和透射电镜观察TBI大鼠脑组织发生铁沉积和铁死亡的情况;转录组测序初步鉴定TBI大鼠脑组织差异表达基因(differentially express genes,DEGs),将DEGs与数据集GSE111452比较,选择共有的DEGs,再将共有DEGs与铁死亡数据库比对,最终筛选出与铁死亡密切相关的DEGs;最后,通过荧光定量PCR检测大鼠脑组织样本中DEGs的mRNA相对表达量.结果 Perl′s染色结果显示,TBI大鼠脑组织损伤周围区域铁离子沉积现象较Sham组明显;电镜结果显示,TBI大鼠脑组织中神经元形态改变,线粒体萎缩变小,基质颜色变深,膜增厚致密度高,部分外膜模糊并破损,伴有内嵴扩张、减少.测序和信息学分析结果显示,与Sham组比较,TBI大鼠脑组织共有2786个DEGs,与GSE111452数据集交集后发现241个共有DEGs,再与铁死亡相关基因库比对,发现4个与铁死亡相关的DEGs(Slc7a5、Rb1、Fancd2和Pebp1);PCR检测结果显示,TBI大鼠脑组织中Slc7a5和Fancd2基因的mRNA表达水平显著升高,Rb1基因的mRNA表达水平也有升高趋势,但与Sham组比较差异无统计学意义(P>0.05),Pebp1基因的mRNA表达水平显著下降(P<0.05).结论 TBI大鼠脑组织发生了铁死亡,可能与Slc7a5、Rb1、Fancd2和Pebp1基因在TBI大鼠脑组织的差异表达有关.

A method for separation of metal sulfides in molybdenum concentrate by vacuum distillation has been developed. The feasibility for separation was mainly dependent on the differences in saturated vapor pressure between impurity sulfides and molybdenum disulfide, which was determined by theoretical calculation. The main factors including distilling temperature and heating duration were studied by experiments. The volatiles enriched on the graphite condensation plates were also investigated by scanning electron microscope and X-ray diffraction and according to that the volatilization behavior of impurities was analyzed. Multiple impurity sulfides could be removed through one-step vacuum distillation on the premise that MoS2 did not decompose. It's turned out that the contents of impurity elements were efficiently decreased by this method without breaking crystal and layered structure of MoS2.

MSCs-Exo是一种由间充质干细胞(MSCs)分泌的细胞外囊泡,富集多种蛋白质、脂质及核酸等,参与遗传信息传递和功能性转移,运送生物活性分子的作用.近年来研究发现MSCs-Exo在急性呼吸窘迫综合征(ARDS)治疗中对免疫调节、组织修复及抗氧化等方面具有调控作用.该文对MSCs-Exo对ARDS的治疗作用机制及研究进展进行综述,旨在为ARDS的发生、演进和治疗提供新思路.

Objective To examine the effect of autophagy on cerebral damage caused by different models and test the hypothesis that its protection mechanism acts via inhibiting expression of neuroinflammatory mediators. Methods Autophagy was induced by rapamycin treatment. Cerebral damage was induced using models of IL-6 treatment, oxygen glucose deprivation/reoxygenation (OGD/R) in vitro, and middle cerebral artery occlusion (MCAO) in vivo. The effect and mechanism of autophagy was examined and assessed in terms of cell viability, infarction size in brain tissue, neurological score, production of inflammatory mediators IL-1β and IL-6, transcription and protein expression of autophagy markers beclin-1 and LC-3II in different experimental groups. Results Autophagy triggered by rapamycin could protect neurons from IL-6-induced injury and astrocytes from OGD/R-induced injury in vitro and in rat brain tissue from MCAO in vivo. Autophagy significantly increased cell viability, attenuated cerebral infarction and improved neurological scores. It also inhibited production of the IL-1β and IL-6 and elevated the expression of beclin-1 and LC-3II. Conclusions Autophagy can inhibit the inflammatory response and reduce cerebral I/R injury. There was a relationship between the extent of protection and (i) the level of the autophagic response, (ii) the stage of the cerebral I/R injury, and (iii) the time of intervention.

BACKGROUND:Traumatic brain injury (TBI) is a major cause of disability worldwide, without definitive and effective intervention. Dexmedetomidine (DEX) has a neuroprotective effect against TBI; however, the detailed mechanism underlying this effect remains unclear.METHODS:Ten male Sprague Dawley rats were used to establish a TBI model. The rats were randomly divided into two groups: the TBI group (TBI, control group) and the DEX treatment group (DEX). The next day, the neurological function of the rats were evaluated by the modified neurological severity score (mNSS). Then, the rats were sacrificed, and RNA sequencing was performed to identify differentially expressed messenger RNAs (mRNAs) and microRNAs (miRNAs) in brain tissue samples. Additionally, we performed a bioinformatics analysis to explore the candidate genes and pathways that might play important roles in DEX-induced neuroprotection. The most significantly differentially expressed miRNAs and possible hub genes were validated by quantitate reverse transcription-polymerase chain reaction (qRT-PCR) using more samples.RESULTS:In the DEX group, 517 mRNAs (352 up-regulated and 165 down-regulated) and 35 miRNAs (18 up-regulated and 17 down-regulated) were differentially expressed compared to the TBI group. Gene Ontology analysis revealed the up-regulated mRNAs to be significantly enriched in microtubule-based movement or processes, microtubule and tubulin binding. Kyoto Encyclopedia of Genes and Genomes analysis showed that these up-regulated mRNAs were significantly enriched in the B-cell receptor signaling pathway as well as the cell cycle pathway. Also, Lyn and Cdk1 were found to be associated with the B-cell receptor signaling and cell cycle pathways, respectively. Furthermore, the down-regulated miRNAs were significantly enriched in cellular components, although no significant Gene Ontology terms or KEGG pathways were found for the down-regulated mRNAs or up-regulated miRNAs.CONCLUSIONS:Differentially expressed mRNAs and miRNAs were identified after the administration of DEX in a TBI rat model. The B-cell receptor signaling pathway and the cell cycle pathway might be involved in the neuroprotective effect of DEX against TBI, Lyn and Cdk1 might be hub genes.

Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease, but its specific mechanism of action is still unclear. Stromal cell-derived factor-1 and its receptor, chemokine receptor 4 (CXCR4), are important regulators of cell migration. We speculated that the CXCR4/stromal cell-derived factor 1 axis may be involved in the therapeutic effect of neural stem cell transplantation in the treatment of Parkinson’s disease. A Parkinson’s disease rat model was injected with 6-hydroxydopamine via the right ascending nigrostriatal dopaminergic pathway, and then treated with 5 μL of neural stem cell suspension (1.5 × 104/L) in the right substantia nigra. Rats were intraperitoneally injected once daily for 3 days with 1.25 mL/kg of the CXCR4 antagonist AMD3100 to observe changes after neural stem cell transplantation. Parkinson-like behavior in rats was detected using apomorphine-induced rotation. Immunofluorescence staining was used to determine the immunoreactivity of tyrosine hydroxylase, CXCR4, and stromal cell-derived factor-1 in the brain. Using quantitative real-time polymerase chain reaction, the mRNA expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra were measured. In addition, western blot assays were performed to analyze the protein expression of stromal cell-derived factor-1 and CXCR4. Our results demonstrated that neural stem cell transplantation noticeably reduced apomorphine-induced rotation, increased the mRNA and protein expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra, and enhanced the immunoreactivity of tyrosine hydroxylase, CXCR4, and stromal cell-derived factor-1 in the brain. Injection of AMD3100 inhibited the aforementioned effects. These findings suggest that the stromal cell-derived factor-1/CXCR4 axis may play a significant role in the therapeutic effect of neural stem cell transplantation in a rat model of Parkinson’s disease. This study was approved by the Animal Care and Use Committee of Kunming Medical University, China (approval No. SYXKK2015-0002) on April 1, 2014.

The properties and applications of molybdenum disulfide (MoS 2 ) are significantly dependent on its purity. Physical purification is proposed for separating impurities from MoS 2 . Meanwhile, the feasibility of separation of impurities was analyzed by thermodynamic calculations. The effects of the temperature and heating duration on the volatilization of impurities were studied experimentally. The purity of MoS 2 was notably improved by vacuum distillation at optimized processing conditions. The phase of the volatiles and the microstructural change of the residues were investigated and characterized by X-ray diffraction analysis, scanning electron microscopy, electron probe microanalysis, Raman spectroscopy, and atomic force microscopy. Graphical Abstract Vacuum distillation is a scalable one-step approach to separate impurities from molybdenum disulfide. The purity of the residual MoS 2 significantly depends on the distillation temperature and duration. Tiny amounts of impurities were collected and analyzed by phase determination. The transformation to multilayer stacks is attributed to the high temperature used during vacuum distillation.

Cerebral blood flow (CBF) reduction underlies unfavorable outcomes after subarachnoid hemorrhage (SAH). Transient receptor potential melastatin-4 (TRPM4) has a pivotal role in cerebral artery myogenic tone maintenance and CBF regulation under physiological conditions. However, the role of TRPM4 in CBF reduction after SAH is unclear. In this study, we aimed at testing whether TRPM4 would contribute to CBF reduction after SAH in vivo and determining underlying mechanisms. Rat SAH model was established by stereotaxic injection of autologous nonheparinized arterial blood at the suprasellar cistern. A TRPM4 blocker, 9-phenanthrol (9-Phe), was infused through an intraventricular catheter connected to a programmed subcutaneous pump to evaluate the contribution of TRPM4 to SAH outcomes. TRPM4 expression and translocation in cerebral artery myocytes were detected by immunoblotting. Macroscopic currents in cerebral artery myocytes were determined by whole-cell patch clamp. Myogenic tone of cerebral arteries was studied by pressurized myography. Cortical and global CBFs were measured via laser Doppler flowmetry and fluorescent microspheres, respectively. After SAH, TRPM4 translocation and macroscopic current density increased significantly. Furthermore, TRPM4 accounted for a greater proportion of myogenic tone after SAH, suggesting an upregulation of TRPM4 activity in response to SAH. Cortical and global CBFs were reduced after SAH, but were restored significantly by 9-Phe, implying that TRPM4 contributed to CBF reduction after SAH. Collectively, these discoveries show that increased TRPM4 activity has a pivotal role in CBF reduction after SAH, and provide a novel target for the management of cerebral perfusion dysfunction following SAH.

Background/Aims: Parkinson’s disease (PD) is a frequently occurring condition that resulted from the loss of midbrain neurons, which synthesize the neurotransmitter dopamine. In this study, we established mouse models of PD to investigate the expression of microRNA-128 (miR-128) and mechanism through which it affects apoptosis of dopamine (DA) neurons and the expression of excitatory amino acid transporter 4 (EAAT4) via binding to axis inhibition protein 1 (AXIN1). Methods: Gene expression microarray analysis was performed to screen differentially expressed miRNAs that are associated with PD. The targeting relationship between miR-128 and AXIN1 was verified via a bioinformatics prediction and dual-luciferase reporter gene assay. After separation, DA neurons were subjected to a series of inhibitors, activators and shRNAs to validate the mechanisms of miR-128 in controlling of AXIN1 in PD. Positive protein expression of AXIN1 and EAAT4 in DA neurons was determined using immunocytochemistry. miR-128 expression and the mRNA and protein levels of AXIN1 and EAAT4 were evaluated via RT-qPCR and Western blot analysis, respectively. DA neuron apoptosis was evaluated using TUNEL staining. Results: We identified AXIN1 as an upregulated gene in PD based on the microarray data of GSE7621. AXIN1 was targeted and negatively mediated by miR-128. In the DA neurons, upregulated miR-128 expression or sh-AXIN1 increased the positive expression rate of EAAT4 together with mRNA and protein levels, but decreased the mRNA and protein levels of AXIN1, apoptosis rate along with the positive expression rate of AXIN1; however, the opposite trend was found in response to transfection with miR-128 inhibitors. Conclusion: Evidence from experimental models revealed that miR-128 might reduce apoptosis of DA neurons while increasing the expression of EAAT4 which might be related to the downregulation of AXIN1. Thus, miR-128 may serve as a potential target for the treatment of PD.

Traumatic brain injury (TBI) has been suggested to increase the risk of amyotrophic lateral sclerosis (ALS). However, this link remains controversial and as such, here we performed experimental moderate TBI in rats and assessed for the presence of ALS-like pathological and functional abnormalities at both 1 and 12 weeks post-injury. Serial in-vivo magnetic resonance imaging (MRI) demonstrated that rats given a TBI had progressive atrophy of the motor cortices and degeneration of the corticospinal tracts compared with sham-injured rats. Immunofluorescence analyses revealed a progressive reduction in neurons, as well as increased phosphorylated transactive response DNA-binding protein 43 (TDP-43) and cytoplasmic TDP-43, in the motor cortex of rats given a TBI. Rats given a TBI also had fewer spinal cord motor neurons, increased expression of muscle atrophy markers, and altered muscle fiber contractile properties compared with sham-injured rats at 12 weeks, but not 1 week, post-injury. All of these changes occurred in the presence of persisting motor deficits. These findings resemble some of the pathological and functional abnormalities common in ALS and support the notion that TBI can result in a progressive neurodegenerative disease process pathologically bearing similarities to a motor neuron disease.

In this study, we investigated whether Rosemary extract (RE) improved cognitive deficits in repetitive mild Traumatic brain injury (rmTBI) rats and its potential mechanisms. The present results showed that rmTBI caused cognitive deficits, such as increased latency to find platform and decreased time spent in target quadrant in Morris water maze (MWM). These behavioral alterations were accompanying with the increased neuronal degeneration and glial fibrillary acidic protein (GFAP)-positive cells, increased Reactive oxygen species (ROS) generation, decreased activity of Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Catalase (CAT), elevated protein level of IL-1β, IL-6 and TNF-α in hippocampus. Treatment with RE prevented these changes above. Our findings confirmed the effect of rosemary extract on improvement of cognitive deficits and suggested its mechanisms might be mediated by anti-oxidative and anti-inflammatory. Therefore, rosemary extract may be a potential treatment to improve cognitive deficits in rmTBI patients.

This study tested the hypothesis that antinociceptive effects of galanin and its receptors in nucleus accumbens (NAc) of rats with inflammatory pain provoked by subcutaneous injection of 0.1 ml of 2% carrageenin into the sole of the rat's left hindpaw. The hindpaw withdrawal latencies (HWLs) in response to thermal and mechanical stimulation significantly decreased in bilateral hindpaws at 3 and 4 hour after a subcutaneous injection of carrageenin. However intra-NAc injection of 2 and 3 nmol, but not 1 nmol of galanin markedly induced an increase in the HWLs in a dose-dependent way. Western blot also showed, that the expression of galanin receptor 1 (GalR1) and galanin receptor 2 (GalR2) were significantly upregulated in NAc at 3 hour after a subcutaneous injection of carrageenin. In addition, the rats were intra-NAc injected galanin, 5 min later following by intra-NAc injection of galanin receptor antagonist galantide, the galanin-induce antinociceptive effects were suppressed by galantide. The results demonstrated that galanin and its receptors might be involved in antinociception in the NAc of rats with inflammatory pain.

The blood‐brain barrier possesses active transporters carrying brain‐permeable xenobiotics, including many kinds of medicine, back into the blood against injuries. P‐glycoprotein(P‐gp), one kind of important multidrug resistance transporter, is upregulated on capillary endothelium after cerebral ischemia, which may refer as to protect the brain from the poison but may result in the treatment failure of the stroke. Panax notoginseng, a traditional Chinese medicine, has been used for thousands of years to treat ischemic patients. Panax notoginsenoside (PNS) is primarily composed of ginsenosides. Ginsenoside ‐Rg1 is an important part of saponin components in PNS. As such, here we aimed to study the role of PNS and ginsenosides Rg1 against overexpression of P‐glycoprotein in experiment induced cerebral ischemia–reperfusion (I/R) adult in rats. Male SD rats were randomly divided into sham‐injured, vehicle, PNS or Rg1 groups. The expression of P‐gp in cortex, hippocampus, striatum were detected by Imunohisochemistry, Western blot and RT‐PCR. The results show that PNS or Rg1 significantly reduced P‐gp in cortex and striatum infarction area caused by cerebral I/R. The increased expressions of P‐gp caused by cerebral I/R were restored with PNS treatment groups, as well as in Rg1 treatment groups. These results suggest that PNS and Rg1 have similar roles in adjusting overexpression of P‐gp from ischemic/reperfusion damage. PNS could be considered as an inhibitor of P‐gp in brain injuries therapy strategy for use in the case of cerebral ischemic stroke.

Scutellarin (SCU), a flavonoid from a traditional Chinese medicinal plant, is clinically used to treat cardiovascular diseases. In this study, we investigated the vasoprotective effects of SCU against hypoxia reoxygenation (HR) in isolated rat coronary artery (CA). HR treatment significantly impaired acetylcholine (ACh,0.001‐100 µM)‐induced endothelium‐dependent relaxation in isolated CA rings and these effects were reversed by pre‐incubation with SCU (500 µM). SCU pre‐incubation did not affect ACh response in normal CA without HR treatment. HR treatment did not significantly altered nitroglycerin (NTG, 0.001‐10 µM) induced endothelium‐independent vasodilation in CA and SCU (500 µM) had no significant effect on NTG response in CA with or without HR treatment. The PKG inhibitor Rp‐8‐Br‐cGMPS (4 µM) blocked both the vasorelaxative effects of SCU in CA rings without HR treatment and the vasoprotective effects of SCU in HR‐treated CA. These results demonstrate that SCU repairs HR‐induced vascular impairment in endothelium‐dependent vasodilation and might be via activation of the PKG pathway.Grant Funding Source: Supported by grants from the National Natural Science Foundation of China (Nos. 30960450 and 81173110) and Yunnan Provincial Science and Technology Department (Nos. 2011FA022, 2012BC012, 2008CD054, and 2008ZC111M).

Autism is a complex neurodevelopmental disorder that is characterized by social abnormalities. Genetic, dietary and gut-related factors are implicated in autism, however the causal properties of these factors and how they may interact are unclear. Propionic acid (PPA) is a product of gut microbiota and a food preservative. PPA has been linked to autism, and PPA administration to rats is an animal model of the condition. Seizure-prone (FAST) and seizure-resistant (SLOW) rats were initially developed to investigate differential vulnerability to developing epilepsy. However, FAST rats also display autistic-like features, and have been proposed as a genetic model of autism. Here we examined the effects of PPA on social behavior in FAST and SLOW rats. A single intracerebroventricular injection of PPA, or phosphate-buffered saline (PBS), was administered to young-adult male FAST and SLOW rats. Immediately after treatment, rats were placed in same-treatment and same-strain pairs, and underwent social behavior testing. PPA induced social abnormalities in both FAST and SLOW rat strains. While there was no evidence of social impairment in FAST rats that were not treated with PPA, these rats were hyperactive relative to SLOW rats. Post-mortem immunofluorescence analysis of brain tissue indicated that PPA treatment resulted in increased astrogliosis in the corpus callosum and cortex compared to PBS treatment. FAST rats had increased astrogliosis in the cortex compared to SLOW rats. Together these findings support the use of PPA as a rat model of autism, but indicate there are no interactive effects between the PPA and FAST models.

Ischemic postconditioning has been demonstrated to be a protective procedure to brain damage caused by transient focal ischemia/reperfusion. However, it is elusive whether the protection of postconditioning against brain damage and neuroinflammation is via regulating TLR2 and TLR4 pathways. In the present study, we examined the protection of ischemic postconditioning performed immediately prior to the recovery of cerebral blood supply on brain damage caused by various duration of ischemia and tested the hypothesis that its protection is via inhibition of neuroinflammation by modulating TLR2/TLR4 pathways.

BACKGROUND: Permanent or transient implantation of biomaterials can result in biomaterials-centered infections (BCI) in lung cancer patients.OBJECTIVE: To investigate the relationship between BCI and peripheral blood transforming growth factor β1 (TGF-β1) in patients with lung cancer.METHODS: A total of 248 lung cancer patients undergoing in vivo intravascular catheter indwelling > 7 days were included.Quantitative method was used for intubation, bacteriological culture and paired blood culture, and API Staph strips were adopted for positive patients. While enzyme-linked immunosorbent assay was used to detect TGF-β1 levels in the peripheral blood of patients with lung cancer and 75 healthy volunteers as normal controls.RESULTS AND CONCLUSION: Among the 248 patients, there were 82 BCI-positive cases, and 166 BCI-negative cases.Thirteen patients were confirmed to have catheter-related bloodstream infection. There were 48 Gram-positive bacteria, 24Gram-negative bacilli, and 10 fungal. The levels of TGF-β1 were higher in BCI-positive patients than BCI-negative patients (P < 0.05); the levels of TGF-β1 in the BCI-negative group were higher than those in the normal control group (P < 0.05). For lung cancer patients with nosocomial infection induced BCI, there are various species of pathogenic bacteria, and Gram-positive bacteria are more common. To detect TGF-β1 levels in patients with lung cancer is of significance for early prevention of BCI.

Objective: To explore the relationship between the endothelin-B (ET-B) receptors and cerebral ischemia by studying the expression of endothelin-B receptors in the activated microglial cells. Methods: The rat model of middle cerebral artery occlusion (MCAO) was established by minimal invasive craniotomy. Eighty one adult male SD rats were randomly divided into ischemia group including 2 hours, 6 hours, 12 hours, 1 day, 2 days, 3 days and 1 week after ischemia (at each time point, n = 9); a sham operation group (n = 9) and normal control group (n = 9). ET-B receptor immunoreactivity was observed in activated microglial cells following MCAO by double labeling with lectin. The expression of ET-B receptors mRNA and protein were investigated by Western blotting and real-time polymerase chain reactions (RT-PCR). Results: ET-B immunofluorescence was markedly induced in the activated microglial cells in both infarcted and peri-infacted zones by double labeling with lectin at the 1st day, 2nd day, 3rd day and the 1st week, especially at the 3rd day and the 1st week after MCAO. In the control and sham operated rats, microglial cells appeared and relatively unactivated and showed a lack of ET-B immunofluoresecence. ET-B mRNA and protein levels were steadily upregulated from 2 hours to 12 hours (P < 0.05) after MCAO as compared with the controls, peaking at the 6th hours. At the 1st week, ET-B mRNA and protein levels were only marginally elevated above the control level. Conclusion: A major finding of this study is the massive accumulation of activated microglia and the induced expression of ET-B receptors in activated microglial cells following MCAO. It is suggested that ETs via ET-B may act on activated microglia and play an important role in cerebral ischemic injury bearing the receptor.