IL-27 Promotes Human Placenta-Derived Mesenchymal Stromal Cell Ability To Induce the Generation of CD4+IL-10+IFN-γ+ T Cells via the JAK/STAT Pathway in the Treatment of Experimental Graft-versus-Host Disease.

Human mesenchymal stromal cells (MSCs) harbor immunomodulatory properties to induce the generation of suppressive T cells. MSCs have been successfully used in treating graft-versus-host disease (GVHD) accompanied by abundant inflammatory cytokines such as IL-27. This study investigated the effects of IL-27 on the human placenta-derived MSCs (hPMSCs) to induce generation of CD4+IL-10+IFN-γ+ T cells in vitro and in the humanized xenogenic GVHD NOD/SCID model. The results showed that the percentages of CD4+IL-10+IFN-γ+ T cells were significantly increased in activated human PBMC from both healthy donors and GVHD patients with hPMSCs and in the liver and spleen of hPMSC-treated GVHD mice, and the level of CD4+IL-10+IFN-γ+ T cells in the liver was greater than that in the spleen in hPMSC-treated GVHD mice. The serum level of IL-27 decreased and the symptoms abated in hPMSC-treated GVHD. Further, in vitro results showed that IL-27 promoted the regulatory effects of hPMSCs by enhancing the generation of CD4+IL-10+IFN-γ+ T cells from activated PBMC. Activation occurred through increases in the expression of programmed death ligand 2 (PDL2) in hPMSCs via the JAK/STAT signaling pathway. These findings indicated that hPMSCs could alleviate GVHD mice symptoms by upregulating the production of CD4+IL-10+IFN-γ+ T cells in the spleen and liver and downregulating serum levels of IL-27. In turn, the ability of hPMSCs to induce the generation of CD4+IL-10+IFN-γ+ T cells could be promoted by IL-27 through increases in PDL2 expression in hPMSCs. The results of this study will be of benefit for the application of hPMSCs in clinical trials.

Synthesis and Evaluation of Novel 2H-Benzo[e]-[1,2,4]thiadiazine 1,1-Dioxide Derivatives as PI3Kδ Inhibitors.

In previous work, we applied the rotation-limiting strategy and introduced a substituent at the 3-position of the pyrazolo [3,4-d]pyrimidin-4-amine as the affinity element to interact with the deeper hydrophobic pocket, discovered a series of novel quinazolinones as potent PI3Kδ inhibitors. Among them, the indole derivative 3 is one of the most selective PI3Kδ inhibitors and the 3,4-dimethoxyphenyl derivative 4 is a potent and selective dual PI3Kδ/γ inhibitor. In this study, we replaced the carbonyl group in the quinazolinone core with a sulfonyl group, designed a series of novel 2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide derivatives as PI3Kδ inhibitors. After the reduction of nitro group in N-(2,6-dimethylphenyl)-2-nitrobenzenesulfonamide 5 and N-(2,6-dimethylphenyl)-2-nitro-5-fluorobenzenesulfonamide 6, the resulting 2-aminobenzenesulfonamides were reacted with trimethyl orthoacetate to give the 3-methyl-2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide derivatives. After bromination of the 3-methyl group, the nucleophilic substitution with the 3-iodo-1H-pyrazolo[3,4-d]pyrimidin-4-amine provided the respective iodide derivatives, which were further reacted with a series of arylboronic acids via Suzuki coupling to furnish the 2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide derivatives 15a-J and 16a-d. In agreement with the quinazolinone derivatives, the introduction of a 5-indolyl or 3,4-dimethoxyphenyl at the affinity pocket generated the most potent analogues 15a and 15b with the IC50 values of 217 to 266 nM, respectively. In comparison with the quinazolinone lead compounds 3 and 4, these 2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide derivatives exhibited much decreased PI3Kδ inhibitory potency, but maintained the high selectivity over other PI3K isoforms. Unlike the quinazolinone lead compound 4 that was a dual PI3Kδ/γ inhibitor, the benzthiadiazine 1,1-dioxide 15b with the same 3,4-dimethoxyphenyl moiety was more than 21-fold selective over PI3Kγ. Moreover, the introducing of a fluorine atom at the 7-position of the 2H-benzo[e][1,2,4]thiadiazine 1,1-dioxide core, in general, was not favored for the PI3Kδ inhibitory activity. In agreement with their high PI3Kδ selectivity, 15a and 15b significantly inhibited the SU-DHL-6 cell proliferation.

[Effects of Tongbi capsule on joint lesions in rabbits with rheumatoid arthritis].

The purpose of this experiment is to observe the effects of Tongbi capsule on joint lesions in rabbit with rheumatoid arthritis induced by ovalbumin and explore the mechanism in order to provide reference for clinical application of Tongbi capsule. Rheumatoid arthritis in rabbits was induced by subcutaneous injection of emulsions of ovalbumin and Freund's complete adjuvant and intra articular injection of ovalbumin. After successful modeling, 30 New Zealand rabbits with arthritis were randomly divided into model control group, the high, medium and low dose groups of Tongbi capsule (90, 45, 22.5 mg·kg⁻¹) and prednisone group (5 mg·kg⁻¹). Another six normal rabbits were used as normal control group. After 24 hours of modeling, the rabbits in Tongbi capsule groups received intragastric (i.g.) administrations of Tongbi capsule at 90, 45, 22.5 mg·kg⁻¹·d⁻¹, and the rabbits of prednisone group received i.g. administrations of prednisone at 5 mg·kg⁻¹·d⁻¹ for 2 weeks. The rabbits in normal and model groups received the same volume of distilled water at the same time. The swelling degree of rabbit knee joint and local skin temperature were observed daily. After two weeks of administration, pathological changes of rabbit knee joint were examined by magnetic resonance imaging (MRI); the morphological changes of articular cartilage and synovial membrane were observed by microscope; and the contents of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) in serum were detected by enzyme linked immunosorbent assay (ELISA).The results showed that 24 h after modeling, the knee joints of the rabbits were swollen, with red or dark redlocal skin, and fever, elevated local skin temperature and increased diameters of knee joints. Two weeks after modeling, the swelling of rabbit knee joints was obvious in model group; the joint cavities were filled with purulent fluid; joint synovial membranes were obviously thickened, and even joint cavities were fibrotic and cartilage surfaces showed slight defect; the surface of articular cartilage was obvious fibrosis; synovial epithelial cell proliferation was obvious and accompanied by extensive inflammatory cell infiltration; the levels of IL-1 and TNF-α were significantly higher as compared with those seen in model rabbits (P<0.05, P<0.01). After 1 and 2 weeks of administration, knee joint diameters and local skin temperatures were smaller or lower than thosein model group (P<0.05, P<0.01); The lesions of joint cartilage and synovial of all rabbits in each group were less than those in model group; IL-1 and TNF-α levels in serum were also lower than those in model group (P<0.05, P<0.01). The results reveal that high and medium doses of Tongbi capsule can suppress rheumatoid arthritis induced by ovalbumin in rabbits, reduce joint swelling, inhibit synovial epithelial and fiber hyperplasia and inflammatory cell infiltration, and alleviate articular cartilage damage. The mechanism may be associated with decreasing IL-1 and TNF-α levels in serum.

B7-H3 was highly expressed in human primary hepatocellular carcinoma and promoted tumor progression.

B7-H3 has been detected in different cancers and correlated to tumor progression and outcome in cancer patients. In this study, we investigated the expression of B7-H3 in tissues and cells of primary hepatocellular carcinoma (PHC) patients. The research showed that B7-H3 is aberrantly expressed in PHC tissues and cells, and its high expression on HepG2 cells significantly promotes cell proliferation, adhesion, migration, and invasion capacity; moreover, it inhibits the proliferation of CD8(+) T cells. Thus, B7-H3 may have a critical role in PHC and it may enhance tumor escape from the immune surveillance of CD8(+) T cells.

[Scenario Simulation and Effects Assessment of Co-control on Pollution and Carbon Emission Reduction in Beijing].

Focused on the key areas of energy, buildings, industry, and transportation, with 2020 as the base year and 2035 as the target year, we respectively designed the baseline scenario, policy scenario, and enhanced scenario, calculated the emission reduction potential of air pollutants and CO2 of Beijing, and constructed an assessment method of co-control effect gradation index to evaluate the co-control effect of air pollutants and CO2 in the policy scenario and enhanced scenario. The results showed that in the policy scenario and enhanced scenario, the reduction rates of air pollutants emissions will reach 11%-75% and 12%-94%, respectively, and reduction rates of CO2 emissions will reach 41% and 52%, respectively, compared with those from the baseline scenario. Optimizing vehicle structure had the largest contribution to the emission reduction of NOx, VOCs, and CO2, and the emission reduction rates will reach 74%, 80%, and 31% in the policy scenario and 68%, 74%, and 22% in the enhanced scenario, respectively. Replacing coal-fired with clean energy in rural areas had the largest contribution to the emission reduction of SO2; the emission reduction rates will reach 47% and 35% in the policy scenario and enhanced scenario, respectively. Improving the green level of new buildings had the largest contribution to the emission reduction of PM10; the emission reduction rates will reach 79% and 74% in the policy scenario and enhanced scenario, respectively. Optimizing travel structure and promoting green development of digital infrastructure had the best co-control effect. The co-control effect of replacing coal-fired with clean energy in rural areas, optimizing vehicle structure, and promoting green upgrading of the manufacturing industry will be improved to a better status in the enhanced scenario. More attention should be paid to improving the proportion of green trips, implementing the promotion of new energy vehicles, and the green transportation of goods to reduce emissions in the field of transportation. At the same time, with the continuous improvement in electrification level in the end energy consumption structure, the proportion of green electricity should be increased by expanding local renewable energy power production and increasing external green electricity transmission capacity, to enhance the co-control effect of pollution and carbon reduction.

Escin attenuates cerebral edema induced by acute omethoate poisoning.

Organophosphorus exposure affects different organs such as skeletal muscles, the gastrointestinal tract, liver, lung, and brain. The present experiment aimed to evaluate the effect of escin on cerebral edema induced by acute omethoate poisoning. Sprague-Dawley rats were administered subcutaneously with omethoate at a single dose of 60 mg/kg followed by escin treatment. The results showed that escin reduced the brain water content and the amount of Evans blue in omethoate-poisoned animals. Treatment with escin decreased the levels of tumor necrosis factor-alpha (TNF-α), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) in the brain. Escin also alleviated the histopathological change induced by acute omethoate poisoning. The findings demonstrated that escin can attenuate cerebral edema induced by acute omethoate poisoning, and the underlying mechanism was associated with ameliorating the permeability of the blood-brain barrier.

Protective effects of Danshensu on liver injury induced by omethoate in rats.

This study was to evaluate the protective effects of Danshensu on liver injury induced by omethoate in Sprague Dawley rats. The acute omethoate poisoning model was established by administrating subcutaneously with omethoate at a single dose of 60 mg/kg. Danshensu treatment markedly inhibited the increases of aspartate aminotransferase, alanine aminotransferase, cyclooxygenase-2, tumor necrosis factor-alpha, thromboxane B(2), and thromboxane B(2)/6-keto-PGF1alpha ratio induced by omethoate. The histopathological examination further confirmed that administration with Denshensu ameliorated liver injury. The results demonstrated that Danshensu possesses protective action on hepatic injury induced by omethoate and the pharmacological mechanism was related to the anti-inflammatory effect and circulation improvement of Danshensu, at least in part.

Preparation of Zeolite X by the Aluminum Residue From Coal Fly Ash for the Adsorption of Volatile Organic Compounds.

In China, coal fly ash is a large-scale solid waste generated by power plants. The high value utilization of coal fly ash has always been a hot research issue in China for these years. In this paper, the synthesis of zeolite X using aluminum residue from coal fly ash can not only realize the resource utilization of waste, but also achieve the effect of energy saving and emission reduction. Zeolite X prepared by hydrothermal synthesis method have been found to have higher purity and better crystallinity by chemical composition analysis. By comparing and analyzing the adsorption performance of zeolite X and activated carbon on volatile organic compounds, it is found that the adsorption capacity of zeolite X is higher than that of activated carbon, and it has stronger stability. This indicates that the zeolite X synthesized by this environmentally friendly and economical method has a good application prospect in adsorbing volatile organic compounds.

A liposome preparation based on ß-CD-LPC molecule and its application as drug-delivery system.

AIM: The ß-CD-LPC molecule was synthesized based on the conjugation of LPC and ß-CD molecules and it could self-assemble into liposome which was used to encapsulate the Dox to form nanomedicine for the cancer therapy. MATERIALS & METHODS: The anticancer and antitumor effect of ß-CD-LPC-Dox nanomedicine was studied with the vitro and vivo experimental methods. RESULTS: The result showed that ß-CD-LPC liposome had high Dox drug-loading rate and a good sustained-release effect. Cell experiment showed that the ß-CD-LPC-Dox nanomedicine could effectively induce cancer cell apoptosis and in vivo experiments showed that ß-CD-LPC-Dox liposome could effectively inhibit tumor growth and had an effective anticancer activity with lower biotoxicity. CONCLUSION: The ß-CD-LPC-Dox nanomedicine could be applied as a candidate drug to therapy the cancer.

The protective effects of hydrogen on HO-1 expression in the brainafter focal cerebral ischemia reperfusion in rats.

BACKGROUND/AIM: The aim of this study was to investigate whether a hydrogen administration can produce neuroprotective effects after brain ischemia reperfusion in rats. MATERIALS AND METHODS: A brain ischemia reperfusion injury was induced by a 2-h left middle cerebral artery occlusion (MCAO) using an intraluminal filament, followed by 46 h of reperfusion. A hydrogen-rich saline (1 mL/kg body weight i.p.) was administered at the beginning of reperfusion. Saline (1 mL/kg)-treated animals were used as the control. Sham-operated animals were also used. Subsequently, 48 h after the MCAO, histological alternations, heme oxygenase-1 (HO-1) expression, and levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the cerebral cortex and the hippocampus were examined. RESULTS: Hydrogen significantly alleviated brain tissue histological damage, promoted HO-1 expression, upregulated levels of SOD, and decreased the levels of MDA in brain tissue after the ischemia reperfusion injury. CONCLUSION: The results suggest that the neuroprotective effects of hydrogen may be mediated by promoting HO-1 expression and attenuated the oxidative injury.

Synergistic effects of Buyang Huanwu decoction and embryonic neural stem cell transplantation on the recovery of neurological function in a rat model of spinal cord injury.

The aim of the present study was to investigate the therapeutic effect of a combined treatment of Buyang Huanwu decoction (BYHWD), a well-known formula of traditional Chinese medicine, and neural stem cells (NSCs) on spinal cord injury (SCI) and the associated underlying mechanisms. A SCI model was established by surgery via a complete transection of the T10 vertebra of female Sprague-Dawley rats. Gelatin sponges were used to absorb NSCs labeled with the thymidine analog, 5-bromo-2-deoxyuridine (BrdU), and were transferred into the transected spinal cords. BYHWD was administered once a day by introgastric infusion. Motor functions of the hind limbs were evaluated using the 21-point locomotor rating scale developed by Basso, Beattie and Bresnahan (BBB). The fate of the transplanted NSCs under the various conditions was examined by double immunofluorescence staining, using markers for neurons, astrocytes and oligodendrocytes, with BrdU. Ultrastructural changes of the SCI site following the various treatments were examined under a transmission electron microscope. The number of double positive cells for glial fibrillary acidic protein and BrdU in the BYHWD + NSC group was significantly decreased when compared with that in the NSC group (P<0.05). However, the number of cells that were labeled double positive for myelin basic protein and BrdU, as well as neuron specific enolase and BrdU, was greater in the BYHWD + NSC group when compared with the NSC group. Electron microscopy demonstrated that treatment with BYHWD combined with NSCs significantly alleviated demyelination. Results from the BBB motor function test exhibited a significant improvement in the BYHWD + NSC group when compared with the SCI, BYHWD and NSC only groups. In conclusion, the results demonstrated that the traditional Chinese medicine formula, BYHWD, exerted an effect on the differentiation and migration of NSCs. Combining the administration of BYHWD with NSCs was shown to have a synergistic effect on the recovery of neurological function, mitigating the progress of demyelination or ameliorating the recovery of myelination.

Poly (ADP-ribose) synthetase inhibitor has a heart protective effect in a rat model of experimental sepsis.

UNLABELLED: The aim of this study is to investigate whether PARP inhibitor could reduce cell apoptosis and injury in the heart during sepsis. MATERIALS AND METHODS: 60 healthy male Sprague-Dawley (SD) rats were randomly divided into 4 groups---sham group, modal group, 3-AB pretreatment group and 3-AB treatment group, 15 rats per group. The cecal ligation and puncture (CLP) model of sepsis was used. The following were determined--levels of malondialdehyde (MDA), ATP and nicotinamide adenine dinucleotide (NAD+), expression of PARP, Bcl-2, Bax, cytochrome C and caspase 3 activity in the myocardium tissue, levels of serum creatine kinase muscle brain (CK-MB) fraction and troponin I. RESULTS: Histological and molecular analyses showed that myocardial cells apoptosis were associated with mitochondria injury, with an increase in the amount of PARP and a decrease in ATP and NAD+ levels in model group. In addition, the levels of Bax, cytochrome C and caspase 3 activity, serum levels of CK-MB and troponin I increased, but levels of Bcl-2 significantly decreased. Inhibition of PARP upregulated the levels of ATP, NAD + and Bcl-2, and significantly reduced the activation of PARP and caspase 3, decreased the levels of MDA, cytochrome C, CK-MB and troponin I. As a result, apoptosis in the heart was attenuated. CONCLUSION: These results indicate that PARP activation may be involved in apoptosis in the heart induced by sepsis and 3-AB could improve it.

Dihydroartemisinin supresses inflammation and fibrosis in bleomycine-induced pulmonary fibrosis in rats.

Pulmonary fibrosis is a respiratory disease with a high mortality rate and its pathogenesis involves multiple mechanisms including epithelial cell injury, fibroblast proliferation, inflammation, and collagen coagulation. The treatment regimens still fail to recover this disease. We have previously found that dihydroartemisinin inhibits the development of pulmonary fibrosis in rats. This study aimed to determine the mechanisms of dihydroartemisinin in bleomycin-induced pulmonary fibrosis. The experimental rats were divided into six groups as normal saline control group (NS group), bleomycin group (BLM group), dihydroartemisinin-1, -2, or -3 group (DHA-1, DHA-2 and DHA-3 group) and dexamethasone group (DXM group). In BLM group, rats were treated with intratracheal instillation of bleomycin. NS group received the same volume of saline instead of bleomycin. In DHA-1, DHA-2 and DHA-3 group, in addition to intratracheal instillation of bleomycin, respectively, dihydroartemisinin (25 mg/kg, 50 mg/kg, 100 mg/kg daily) was administrated by intraperitoneal instillation. In DXM group, rats were treated with intraperitoneal instillation of dexamethasone as control. Immunocytochemical assay, reverse transcription PCR and western blot were used for detecting the expression of TGF-ß1, TNF-α, α-SMA and NF-κB in lung tissues. What's more, morphological change and collagen deposition were analyzed by hematoxylin-eosin staining and Masson staining. Collagen synthesis was detected by hydroxyproline chromatometry. Results showed that dihydroartemisinin significantly decreased the amount of inflammatory cytokines and collagen synthesis, and inhibited fibroblast proliferation in bleomycin-induced pulmonary fibrosis (P < 0.001). This study provides experimental evidence that dihydroartemisinin could decrease cytokines, alveolar inflammation and attenuates lung injury and fibrosis.

[A negative correlation between B7-H3 expression and the number of CD8+ T cell infiltration in primary hepatocellular carcinoma tissues].

OBJECTIVE: To investigate the relationship between B7-H3 expression and the number of CD8(+) T cell infiltration in primary hepatocellular carcinoma (HCC) tissues. METHODS: The level of B7-H3 expression and the number of CD8(+) T cell infiltration in primary HCC were determined using immunohistochemical staining, and then the correlation between them was analyzed statistically. RESULTS: The immunohistochemical staining showed that the high expression of B7-H3 was found in 26 cases (41.3%), and the low expression in 37 cases (58.7%) of the 63 primary HCC. Fifty-seven cases (90.5%) were positive for B7-H3 expression in HCC tissues, and normal hepatocellular tissues hardly expressed B7-H3 molecules. The number of infiltrating CD8(+) T cells in B7-H3 high expression group was less than that in B7-H3 low expression group. B7-H3 expression was negatively correlated with the number of infiltrating CD8(+) T cells in HCC tissues. Moreover, both B7-H3 expression and CD8(+)T cell infiltration were related with clinical stage, local lymph node metastasis and distant metastasis in HCC patients. CONCLUSION: B7-H3 molecules were highly expressed and negatively correlated with CD8(+) T cell infiltration in primary HCC tissues.

[Expression and clinical significance of soluble B7-H3 in sera of patients with primary hepatocellular carcinoma].

OBJECTIVE: To detect the expression and clinical significance of co-stimulatory molecule B7-H3 in sera and tissues of patients with hepatocellular carcinoma (HCC). METHODS: We collected 63 samples of sera and liver tissue from HCC patients, 5 adjacent normal tissues of hepatic hemangioma as controls, and the other 50 sera samples of healthy people in the same time. The expression of soluble B7-H3 (sB7-H3) in sera from HCC patients and healthy people was detected by ELISA. Immunohistochemistry was performed to analyze the expression of B7-H3 on normal liver and HCC tissues. RESULTS: The level of sB7-H3 from HCC patients was significantly higher than that from healthy people [(4143.47±976.27) pg/mL vs (2076.18±605.42) pg/mL, P<0.05]; and sB7-H3 level was related to clinical stage, distant metastasis and the positive expression of B7-H3 in HCC tissues (P<0.05), while there was no significant difference between its expression and the other clinical pathological parameters, such as the patients' age, gender, histological type, lymphatic metastasis and size of tumor. Furthermore, a positive correlation was found between the level of sB7-H3 and CA19-9 in HCC patients (P<0.05), but it was not associated with AFP and CEA. CONCLUSION: The level of sB7-H3 in HCC patients was significantly higher than that in healthy people, and B7-H3 expression was correlated with clinical pathological indexes, which implicated that detecting the expression of sB7- H3 might be helpful for the diagnosis of primary HCC.

Evaluation of the effect of glutathione on cisplatin antitumor activity and kidney injury at different administration times.

Cisplatin (cis-diamminedichloroplatinum, CDDP) is one of the most potent anticancer drugs. However, the therapeutic value of CDDP is greatly compromised by its dose-limiting nephrotoxicity. This study was performed to investigate whether reduced glutathione (GSH) was able to reduce the kidney injury induced by CDDP and whether it affected the anticancer activity of CDDP in vivo and in vitro. In in vivo experiments, mice were divided into five groups: control, CDDP only and three GSH treatment groups. Blood samples were collected 72 h after CDDP administration to determine the levels of blood urea nitrogen (BUN) and plasma creatinine (Cr). In addition, we examined antioxidative parameters, malondialdehyde (MDA) levels and histopathological changes in the kidney. In order to investigate whether GSH affected the anticancer activity of CDDP, we performed a sulforhodamine B (SRB) assay to determine the anti-proliferative effect in three tumor cell lines of treatment with CDDP alone or combined with GSH and examined the cell morphology. The results revealed that GSH decreased the BUN and Cr levels in plasma, ameliorated the pathological changes induced by CDDP and enhanced the endogenous antioxidant capacities in all three GSH groups. Furthermore, GSH significantly inhibited the growth of the three tumor cell lines when combined with CDDP and did not affect the inhibitory effect of CDDP on the carcinoma cell proliferation. In addition, we found no differences among the three GSH groups. These findings suggest that GSH is able to attenuate the nephrotoxicity induced by CDDP, not only when administered prior to CDDP, but also when administered at the same time as or subsequent to CDDP administration, without affecting the anticancer activity of CDDP. Thus, the administration of GSH is a promising approach for attenuating the nephrotoxicity caused by CDDP.

[Effect of electroacupuncture on proliferation of astrocytes after spinal cord injury].

OBJECTIVE: To explore the mechanism of acupuncture in treatment of spinal cord injury (SCI). METHODS: Adult Wistar rats were used to make SCI model by Allen's method. The SCI rats were treated with electroacupuncture (EA) at acupoints of the Governor Vessel for 3 days, 1 week, 2 weeks or 4 weeks. Normal group and spinal cord injury group were used as controls. The number and morphology of astrocytes in each group were investigated by electron microscope, immunohistochemistry and in situs hybridization methods. The expression of glial fibroblast acid protein (GFAP) mRNA in the injured spinal cord was detected by reverse transcription polymerase (RP-PCR). RESULTS: The mitochondria and ribosomes of astrocytes in the EA group increased. The number of astrocytes increased after SCI, in gray matter being more than that in the white matter, in the caudal being more than that in the rostral. The expression of GFAP mRNA in the EA group was significantly lower than that in the control group. CONCLUSION: Electroacupuncture can inhibit the reactive proliferation of the astrocytes after spinal cord injury and prevent formation of the glial scar.