[Retracted] Role of the AKT pathway in microRNA expression of human U251 glioblastoma cells.

Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the western blots featured in Fig. 3B on p. 670, the bands featured in the U251 and U251­MC lanes for the miR­21 and U6 experiments appeared to be duplicates of each other. Moreover, certain of these data were strikingly similar to data that appeared in another article published at around the same time featuring some of the same authors (again, with apparent duplications of bands within the same gel slices, as they were presented). After having conducted an internal investigation of this matter, the Editor of International Journal of Oncology has judged that the apparently anomalous grouping of the data could not have been attributed to pure coincidence. Therefore, the Editor has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for bringing this matter to our attention. [International Journal of Oncology 36: 665­672, 2010; DOI: 10.3892/ijo_00000542].

Addition of Chelators Increased the Stability of Black Rice Anthocyanins against the Metallic Ions in Tap Water and Improved the Coloration of Steamed Cold Noodles.

The anthocyanins in black rice extract (BRA) are sensitive to metallic ions, which restrict its application in the coloration of steamed cold noodles in China that uses tap water as the solvent. Food-grade chelators were added to check if they could increase the stability of BRA. The results indicated that the color decay of BRA in tap water was mainly caused by Fe3+, Cu2+, and Fe2+, and the addition of chelators could effectively antagonize this effect. Coloration with the BRA solution containing the optimized chelator formulation of 0.01% ethylenediaminetetraacetic acid disodium, 0.08% sodium hexametaphosphate, and 0.064% sodium tartrate conferred comparable appearance and chromatic attributes with those of the noodle colored by deionized water-dissolved BRA. The steamed cold noodles colored by the chelators-containing BRA exhibited increased springiness and decreased starch retrogradation, and possessed potential health functions due to its slightly increased resistant starch content and markedly enhanced antioxidant capacity. Hence, the addition of chelators is a feasible way to increase the color stability of BRA in tap water, and the chelators-supplemented BRA could be used to produce steamed cold noodles with attractive color and health benefits.

Mechanism of synergistic DNA damage induced by caffeic acid phenethyl ester (CAPE) and Cu(II): Competitive binding between CAPE and DNA with Cu(II)/Cu(I).

Caffeic acid phenethyl ester (CAPE) is an active polyphenol of propolis from honeybee hives, and exhibits antioxidant and interesting pharmacological activities. However, in this study, we found that in the presence of Cu(II), CAPE exhibited pro-oxidative rather than antioxidant effect: synergistic DNA damage was induced by the combination of CAPE and Cu(II) together as measured by strand breakage in plasmid DNA and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) formation, which is dependent on the molar ratio of CAPE:Cu(II). Production of Cu(I) and H2O2 from the redox reaction between CAPE and Cu(II), and subsequent OH formation was found to be responsible for the synergistic DNA damage. DNA sequencing investigations provided more direct evidence that CAPE/Cu(II) caused preferential cleavage at guanine, thymine and cytosine residues. Interestingly, we found there are competitive binding between CAPE and DNA with Cu(II)/Cu(I), which changed the redox activity of Cu(II)/Cu(I), via complementary applications of different analytical methods. The observed DNA damage was mainly attributed to the formation of DNA-Cu(II)/Cu(I) complexes, which is still redox active and initiated the redox reaction near the binding site between copper and DNA. Based on these data, we proposed that the synergistic DNA damage induced by CAPE/Cu(II) might be due to the competitive binding between CAPE and DNA with Cu, and site-specific production of OH near the binding site of copper with DNA. Our findings may have broad biological implications for future research on the pro-oxidative effects of phenolic compounds in the presence of transition metals.

Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO2-induced pulmonary fibrosis in rats in vivo.

Silicosis is a serious occupational disease characterized by pulmonary fibrosis, and its mechanism and progression have not been fully elucidated yet. In this study, silicosis models of rat were established by a one-time dusting method, and the rats were sacrificed after 30, 60, and 120 days (herein referred to as the 30, 60, and 120 days groups, respectively). The rats without dust exposure were used as the control. The lungs were removed to observe pathological changes using hematoxylin and eosin and Masson's trichrome staining and transmission electron microscopy, and the degree of collagen type I and III deposition in the lung was evaluated by enzyme-linked immunosorbent assay. The levels of malondialdehyde and superoxide dismutase were measured by spectrophotometry, and the expression levels of fibrosis-related genes (transforming growth factor beta 1, type I collagen, type III collagen) were assessed by real-time quantitative polymerase chain reaction. The results suggested that the rats in the model groups exhibited obvious collagen fibrosis and that the severity of the lung injury increased as the time after exposure to SiO2 increased. There was a significant response to lung inflammation in the model rats, especially in the 30 days group. The degree of lipid peroxidation in bronchoalveolar lavage fluid cells and lung tissues in experiment group rats significantly increased. Among the three fibrosis-related genes, transforming growth factor beta 1was elevated in both bronchoalveolar lavage fluid cells and lung tissues of the experiment group rats, while collagen type I and III were only elevated in lung tissues. Hence, we concluded that as silicosis progressed, inflammation, fibrosis, and the expression of fibrosis-related genes showed different time-dependent changes and that a number of causal relationships existed among them.

Effects of abnormal expression of fusion and fission genes on the morphology and function of lung macrophage mitochondria in SiO2-induced silicosis fibrosis in rats in vivo.

Silicosis is a serious occupational disease affecting millions of related workers. Many studies showed lung macrophages play an important role in the disease. However, the changes of macrophages are not fully characterized and the mechanisms need further investigations. The objectives of this work were to evaluate the effects of abnormal expression of fusion and fission genes on the morphology and function of lung macrophage mitochondria in SiO2-induced silicosis fibrosis in rats. In this study, the rats were injected with 1 mL of SiO2 suspension (100 mg/mL) into the lungs to establish silicosis models, and killed after 30, 60, and 120 days. The rats which were injected with normal saline (1 mL) into lungs were used as control. The lungs of rats were taken for pathological observation. Lung macrophages were collected to measure the number, activity, level of MDA and SOD, and relative content of fusion (Mfn1, Mfn2) and fission (Fis, DRP) genes. Subsequently, mitochondria were extracted from the macrophages to measure the changes of function, including MDA, SOD, ATP, and ATPase. We found that silica dust inhalation led to the proliferation of collagen fibers in the lung tissue. During this process, the number and activity of macrophages increased, the degree of lipid peroxidation increased, and the expression of mitochondrial fusion and fission genes was abnormal. Moreover, the mitochondrial lipid peroxidation level in macrophages increased, the production of ATP and the activity of ATPase decreased, and the abnormal forms of mitochondria occurred. Our results indicated that the morphology and function of mitochondria in macrophages changed during the progress of silicosis, which were related to the abnormal expression of fusion and fission genes.

Paraburkholderia caffeinitolerans sp. nov., a caffeine degrading species isolated from a tea plantation soil sample.

A Gram-stain negative, facultatively anaerobic, non-sporulating, non-motile and rod-shaped bacterium, designated CF3T, was isolated from a tea plantation soil sample and its taxonomic position was determined using polyphasic taxonomy. Strain CF3T displayed optimum growth at 25 °C, pH 5.0 and in the presence of 0-1 % NaCl. Comparative phylogenetic analysis of the 16S rRNA, recA and gyrB gene sequences showed that the isolate belongs to the genus Paraburkholderia, showing high levels of similarity with respect to Paraburkholderia oxyphila OX-01T (98.3, 95 and 93 %, respectively) and Paraburkholderia sacchari IPT101T (98.2, 95 and 95 %, respectively). The predominant ubiquinone was determined to be Q-8, and the polar lipids are phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, one unidentified amino-phospholipid, three unidentified amino-lipids and three unidentified polar lipids. The major fatty acids were found to be C16:0, C17:0 cyclo, summed feature 8 (C18:1 ω7c and/or C18:1 ω6c) and summed feature 3 (C16:1 ω7c and/or C16:1 ω6c). The DNA G+C content was found to be 63.8 mol% and the DNA-DNA relatedness values between strain CF3T and its two close relatives P. oxyphila OX-01T and P. sacchari IPT101T was 41 and 40 %, respectively. Based on phylogenetic analysis, phenotypic and genotypic data, it is concluded that the isolate represents a novel species of the genus Paraburkholderia, for which the name Paraburkholderia caffeinitolerans sp. nov. is proposed. The type strain is CF3T (= LMG 28688T = CGMCC 1.15105T).

Killer cell immunoglobulin-like receptor genotypes and haplotypes with susceptibility to pulmonary tuberculosis infection.

BACKGROUND: Killer cell immunoglobulin-like receptors (KIRs) are expressed on natural killer (NK) cells and T cells and organized in highly polymorphic families. Genetic diversity is an important characteristic of KIR genes. The aim of the study was to investigate the influence of KIR genotypes and halotypes on the risk of pulmonary tuberculosis (PTB). METHODS: A sequence specific primer polymerase chain reaction (SSP-PCR) was employed to amplify the KIR genes and pseudogenes in 139 pulmonary tuberculosis (PTB) patients and 30 healthy controls. The innovative point of our study was the subdivision of the patient group according to sputum smear test (positive and negative). KIR genotype and haplotype frequencies were compared between the PTB group and the control group by Chi-square test, and p < 0.05 was regarded as statistically significant. RESULTS: The genotype AH and FZ14 may be associated with the clearance of Mycobacterium. In addition, haplotype B may be the susceptive haplotype that facilitated the clearance of Mycobacterium and haplotype A may be protective haplotype of PTB. CONCLUSIONS: Therefore, the diversity of genotypes and haplotypes induced an inflammatory reaction that resulted in continuous infection.

Systematic review on Epstein-Barr virus (EBV) DNA in diagnosis of nasopharyngeal carcinoma in Asian populations.

OBJECTIVE: To conduct a meta-analysis to investigate the value of EBV DNA in diagnosis of nasopharyngeal cancer (NPC) in Asian populations, and provide important evidence for screening. METHODS: Prospective or respective case-control or cohort studies regarding the detection role of EBV DNA for NPC were included in our study. We conducted a comprehensive literature search in PubMed, EMBASE, and the Chinese Biomedical Database (CBM database between January 1980 and March 2012. RESULTS: A total of 18 studies with 1492 NPC cases and 2641 health controls were included. Almost of the included studies were conducted in China, and only one other conducted in Thailand. The overall results demonstrated that the pooled sensitivity, specificity, positive likelihood (+ LR) and negative likelihood (-LR) were 0.73 (0.71-0.75), 0.89 (0.88-0.90), 8.84 (5.65-13.84) and 0.19(0.11-0.32), respectively. The overall EBV DNA detection showed the largest area of 0.932 under the summary receiver operator curve (SROC). The accuracy of detection by plasma for NPC (0.86) was higher than in serum (0.81), with largest areas under the SROC of 0.97 and 0.91, respectively. CONCLUSION: Our results demonstrated the EBV DNA detection in plasma or serum has high sensitivity and specificity in diagnosis of NPC, especially in Chinese populations with a high risk of cancer.

MicroRNA-21 expression is regulated by ß-catenin/STAT3 pathway and promotes glioma cell invasion by direct targeting RECK.

AIMS: MicroRNA-21 (miR-21) expression is increased in many types of human malignancy, including glioma. Recent studies report that miR-21 regulates cell invasion by targeting RECK, however, the underlying transcriptional regulation of miR-21 in glioma cells remains elusive. RESULTS: Here, we identify a positive correlation between miR-21 expression and pathological grade in glioma tissues. We demonstrate that ß-catenin pathway regulates miR-21 expression in human umbilical vein endothelial cell and glioma cells, and that this regulation is signal transducer and activator of transcription 3 (STAT3)-dependent. Further, chromatin immunoprecipitation and luciferase reporter analysis demonstrate that miR-21 is controlled by an upstream promoter containing a conserved STAT3 binding site. Notably, knockdown of miR-21-inhibited cell invasion by increasing RECK expression and decreased tumor growth in a xenograft model. CONCLUSION: These data provide compelling evidence that ß-catenin regulation of miR-21 via STAT3 plays a role in glioma cell invasion and proliferation and indicate that STAT3 is a potential therapeutic target for glioma intervention.

[A preliminary study on the relationship between HLA-Cw polymorphism and susceptibility to pulmonary tuberculosis].

OBJECTIVE: To analyze the relationship between HLA-Cw polymorphism and susceptibility to pulmonary tuberculosis (PTB), and therefore to explore the susceptible or resistant genes of PTB. METHODS: A hundred and twelve patients who were confirmed to have secondary PTB in Shandong Chest Hospital from May 2010 to May 2011 were selected as the PTB group, including 62 males and 50 females aged 19 - 69 years (mean 41.7). According to the acid-fast staining results, PTB patients were divided into a smear-negative group (SN group, 77 cases) and a smear-positive group (SP group, 35 cases). A hundred and ten subjects who underwent physical examination in Shandong Chest Hospital at the same period were selected as the control group, including 59 males and 51 females aged 21 - 67 years (mean 38.3). After genomic DNA was extracted, genotyping of HLA-Cw was conducted by sequence specific primer polymerase chain reaction (PCR-SSP) method. Then Hardy-Weinberg (H-W) equilibrium was tested, and gene frequencies(%) were estimated = 1-(1-phenotype frequencies)(1/2). Gene frequencies were compared between the PTB group and the control group, and between the SN group and SP group by χ(2) test. According to Bonferroni's principle, α was divided by the number of alleles (n = 8), and P < 0.006 25 was regarded as statistically significant. RESULTS: The frequency of HLA-Cw08 was significantly higher in PTB patients (43.6%, 75/112) compared with the controls (27.4%, 52/110), χ(2) = 8.790, P < 0.006 25. Among PTB patients, HLA-Cw04 had a significantly higher frequency in the SP group (20.7%, 13/35) than in the SN group (4.7%, 7/77), while HLA-Cw08 had a significantly lower frequency in the SP group (22.5%, 14/35) than in the SN group (54.4%, 61/77), χ(2) = 12.909, 16.732, both P < 0.006 25. CONCLUSIONS: HLA-Cw polymorphism is related to susceptibility to PTB. HLA-Cw08 may be one of the susceptible genes for PTB, and HLA-Cw04 and 08 may be related to MTB infectious status and clinical outcomes.

MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma.

BACKGROUND: MiR-221 and miR-222 (miR-221/222) are frequently up-regulated in various types of human malignancy including glioblastoma. Recent studies have reported that miR-221/222 regulate cell growth and cell cycle progression by targeting p27 and p57. However the underlying mechanism involved in cell survival modulation of miR-221/222 remains elusive. RESULTS: Here we showed that miR-221/222 inhibited cell apoptosis by targeting pro-apoptotic gene PUMA in human glioma cells. Enforced expression of miR-22/222 induced cell survival whereas knockdown of miR-221/222 rendered cells to apoptosis. Further, miR-221/222 reduced PUMA protein levels by targeting PUMA-3'UTR. Introducing PUMA cDNA without 3'UTR abrogated miR-221/222-induced cell survival. Notably, knockdown of miR-221/222 induces PUMA expression and cell apoptosis and considerably decreases tumor growth in xenograft model. Finally, there was an inverse relationship between PUMA and miR-221/222 expression in glioma tissues. CONCLUSION: To our knowledge, these data indicate for the first time that miR-221/222 directly regulate apoptosis by targeting PUMA in glioblastoma and that miR-221/222 could be potential therapeutic targets for glioblastoma intervention.

Role of the AKT pathway in microRNA expression of human U251 glioblastoma cells.

Activation of the AKT (serine-threonine kinase) pathway is a common feature in glioblastoma cells. Downstream factors of the AKT pathway are involved in cell proliferation, apoptosis, cellular migration and angiogenesis. Micro-RNAs (miRNAs) are highly conserved small non-coding RNAs that block targeted mRNA expression at the post-transcriptional level. The aim of this study was to investigate the role of the AKT pathway in regulating miRNA. The changes of miRNA expression profile in human glioblastome U251 cells after AKT small interfering RNA transfection were examined by a microarray, and confirmed by Northern blotting. Down-regulation of AKT expression by siRNA decreased the activity of AKT pathway in U251 cells. Interruption of AKT pathway suppressed the expression of NF-kappaB and c-Myc, furthermore, the expression of a set of miRNAs was also changed after AKT siRNA transfection. There are putative binding sites of NF-kappaB and c-Myc in the promoters of several up-regulated miRNAs, indicating these transcription factors may also be involved in the regulation of miRNA expression, thus affecting the activity of AKT pathway in tumorigenesis. We provide new components of the regulatory function of AKT pathway to better understand the regulatory network mediated by downstream transcription factors. The understanding of the regulatory function of AKT pathway is crucial in tailored therapy of gliomas.

[The relationship between monocyte chemoattractant protein-1 gene polymorphisms and the susceptibility to pulmonary tuberculosis].

OBJECTIVE: To explore the possible relationship between the -2518 A/G single nucleotide polymorphisms in monocyte chemoattractant protein-1 (MCP-1) gene of Chinese Han population and the susceptibility to pulmonary tuberculosis. METHODS: A 1:1 matched case-control study was conducted from March 2008 to August 2008. The - 2518 MCP-1 A/G polymorphisms were detected in 167 pairs of subjects by reaction-restriction fragment length polymorphism (PCR-RLFP) technique. General characteristics, current disease history, past medical history and related environmental factors of tuberculosis were collected using a questionnaire designed by ourselves. Univariate analyses and multivariate conditional logistic analyses were conducted. RESULTS: The genotype frequencies of AA, GA and GG in the case group and the control group were 21/167 (12.6%), 62/167 (37.1%), 84/167 (50.3%) and 42/167 (25.2%), 83/167 (49.7%), 42/167 (25.1%), respectively. There was a significant difference in genotype frequencies between the case and the control groups in the univariate analysis (chi2 = 24.041, P<0.01). The significant association remained after adjusting environmental factors between genotype GG (OR 1.989, 95% CI 1.154 - 3.428, chi2 = 6.124, P<0.05) and the susceptibility to pulmonary tuberculosis. CONCLUSION: The -2518 MCP-1 GG genotype might be associated with susceptibility to pulmonary tuberculosis in Chinese Han population.

[Inhibitory effect of knocking down microRNA-221 and microRNA-222 on glioma cell growth in vitro and in vivo].

OBJECTIVE: To study the inhibitory effect of knocking down microRNA(miR)-221 and miR-222 on human glioma cell growth and its possible mechanism. METHODS: miRNA-221/222 antisense oligonucleotides (antisense miR221/222) were transfected into human glioma U251 cells by lipofectamine. Northern blot analysis was conducted to detect the mRNA expression of miR-221/222 in the control and transfected cell groups. The proliferation activity of cells was determined by MTT assay. Cell invasion ability was examined by transwell assay, and cell cycle kinetics and apoptosis were detected with flow cytometry. The expression of relevant proteins was analyzed by Western blotting. The therapeutic efficacy of antisense miR221/222 on the growth of xenograft tumors in nude mice were also observed. RESULTS: In the antisense miR-221/222-transfected cells, the expression of miR-221/222 was significantly reduced; the cell invasion ability was suppressed, cell cycle was blocked at G(0)/G(1) phase, and apoptotic cells were increased. The growth of xenograft tumors treated with antisense miR-221/222 was also inhibited. In antisense miR-221/222 treated tumor cells, the expression of bcl-2 was down-regulated while connexin43, p27, PUMA, caspase-3, PTEN, TIMP3 and Bax up-regulated, and p53 expression not changed. CONCLUSION: There is a significant inhibitory effect of antisense miR-221/222 on the growth of human glioma U251 cells. miR-221/222 may be considered as a candidate target for gene therapy of human gliomas.

[Experimental study on combined effect of low temperature and vibration on peripheral circulation function and peripheral nerve function].

OBJECTIVE: To study the combined effect of low temperature and vibration on function of peripheral circulation and nerve. METHODS: 64 rabbits were divided into control group, low temperature group, vibration group and combined effect group randomly, 16 each group. The changes of concentration of ET, Ang II, NO in plasma and SCV, amplitude of sensory nerve action potential, latency of sensory nerve action potential, MCV, distal amplitude of motor nerve, and distal latency of motor nerve were measured before and after experiment. RESULTS: After experiment, the concentration of ET, Ang II, NO and SCV, amplitude of sensory nerve action potential, latency of sensory nerve action potential, MCV, distal amplitude of motor nerve, and distal latency of motor nerve were (68.84+/-14.81) pg/ml, (544.01+/-70.20) pg/ml, (123.73+/-9.58) nmol/ml, (25.36+/-6.96) m/s, (1.84+/-0.65) microV, (4.05+/-1.04) m/s, (27.40+/-6.05) m/s, (1.60+/-0.52) microV, (3.51+/-1.30) m/s respectively in low temperature group; (70.22+/-15.02) pg/ml, (540.77+/-68.25) pg/ml, (129.46+/-11.99) nmol/ml, (27.69+/-6.16) m/s, (2.19+/-0.53) microV, (3.86+/-0.89) m/s, (30.03+/-5.21) m/s, (1.65+/-0.49) microV, (3.36+/-l.11) m/s respectively in vibration group; (88.47+/-13.20) pg/ml, (687.38+/-101.44) pg/ml, (70.66+/-4.99) nmol/ml, (20.82+/-3.65) m/s, (1.21+/-0.64) microV, (5.05+/-0.94) m/s, (19.97+/-4.37) m/s, (1.09+/-0.49) microV, (4.49+/-1.26) m/s respectively in combined effect group; compared with pre-experiment, the concentration of ET and Ang II in low temperature group, vibration group and combined effect group were increased after experiment, and the NO was decreased (P<0.05); the nerve conduct velocity and amplitude was decreased and the latency was delayed (P<0.05). After experiment, the concentrations of ET and Ang II in combined effect group were higher than low temperature group and vibration group, and the concentration of NO in combined effect group was lower than low temperature group and vibration group (P<0.05). After experiment, the SCV and MCV in combined effect group were slower than low temperature group and vibration group; the amplitude of sensory nerve action potential and distal amplitude of motor nerve were less than low temperature group and vibration group; the latency of sensory nerve action potential and distal latency of motor nerve in combined effect group was longer than low temperature group and vibration group. The factorial analysis results indicated the synergistic effect between low temperature and vibration (P<0.05). CONCLUSION: Vibration-induced peripheral vascular impairment and nerve impairment would be intensified by low temperature.

[Effects of low temperature on functions of learning, memory and activities of ATPase in brain tissue of mice].

OBJECTIVE: To explore the effects of low temperature on the functions of learning and memory and activities of ATPase in brain tissue of mice. METHODS: 120 mice were randomly divided into 3 groups of A, B, and C with different cold exposure time. After low temperature test, learning and memory ability and activities of ATPase in brain tissue of the mice were measured. RESULTS: Compared with corresponding control group, in the test of learning ability, the total electric shock period [(41.00 +/- 12.06), (45.90 +/- 13.61) min], the total electric times (85.00 +/- 15.81, 89.00 +/- 17.29), and the error reaction times (33.60 +/- 10.69, 39.00 +/- 11.63) were increased in group A and group C significantly (P < 0.01, P < 0.05), but the rate of right reaction (53.60% +/- 11.23%, 54.59% +/- 6.14%) were decreased in group A and group C significantly (P < 0.01, P < 0.05). In the test of memory ability, the total electric shock period [(19.00 +/- 4.62), (51.70 +/- 15.19) min] in group A and group C were increased significantly (P < 0.05, P < 0.01), the rate of right reaction (86.17% +/- 6.34%, 65.92% +/- 8.17%) in group A and group C were decreased significantly (P < 0.05). In test of activities of ATPase in brain tissue, the activities of Na(+)-K(+)-ATPase and activities of Ca(2+)-Mg(2+)-ATPase in brain tissue in group A and group C were decreased significantly (P < 0.05, P < 0.01). CONCLUSION: Low temperature could decrease the functions of learning and memory and the activities of Na+-K+-ATPase and Ca(2+)-Mg(2+)-ATPase in brain tissue of mice.

[Effect of captopril on the nervous function in rabbits exposed to vibration].

OBJECTIVE: To study the effect of captopril on the nervous function in rabbits exposed to vibration. METHODS: Rabbits were divided into vibration group, intervention group, and control group. Vibration group and intervention group were exposed to (tested by) vibration. Captopril was given to intervention group from the 11th day of vibration exposure. Somatosensory evoked potential (SEP) and motor nervous conduction function (MCF) were measured and analyzed in each group before and after vibration exposure. RESULTS: The latent periods of N1, P1 and N2 of SEP in vibration group after vibration exposure were (30.76 +/- 4.26), (41.91 +/- 6.67), and (45.29 +/- 5.81) ms respectively, and in intervention group after vibration exposure were (27.00 +/- 3.04), (35.07 +/- 4.20) and (41.15 +/- 3.19) ms respectively. Compared with intervention group before and after exposure, and control group, the latent periods of each wave of SEP were delayed significantly (P < 0.05). The nervous conduction velocity, the distant wave amplitude, and the distant potential period of sciatic nerve in vibration group after vibration exposure were significantly different from those in intervention group [(35.69 +/- 4.37) m/s, (1.55 +/- 0.73) microV, (8.16 +/- 0.71) ms respectively vs (52.20 +/- 5.13) m/s, (2.89 +/- 0.36) microV, (7.26 +/- 0.77) ms respectively (P < 0.01)]. CONCLUSION: Captopril may improve the impairment of nervous functions to a certain degree in rabbits exposed to vibration.