Publications by authors named "Jing Wei Xiao"

7 Publications

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Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway.

Neural Regen Res 2021 Jan;16(1):150-157

Department of Toxicology, Key Lab of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.

Acrylamide has been shown to be neurotoxic. Brain-derived neurotrophic factor (BDNF) can alleviate acrylamide-induced synaptic injury; however, the underlying mechanism remains unclear. In this study, dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma (NB-1) cells were exposed with 0-100 μg/mL acrylamide for 24-72 hours. Acrylamide decreased cell viability and destroyed synapses. Exposure of co-cultured NB-1 cells and Schwann cells to 0-100 μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF, suggesting that Schwann cells can activate self-protection of neurons. Under co-culture conditions, activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect. Exogenous BDNF can increase expression of TrkB, Erk1/2, and synapsin I, while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes. Taken together, Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway, indicating that BDNF plays an important role in this process. Therefore, exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury. This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control, a division of the Chinese Center for Disease Control and Prevention (approval No. EAWE-2017-008) on May 29, 2017.
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http://dx.doi.org/10.4103/1673-5374.286976DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7818888PMC
January 2021

Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats.

Biomed Environ Sci 2017 Jun;30(6):432-443

Department of Toxicology, Key Lab of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Objective: To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.

Methods: Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated.

Results: The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P < 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P < 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups.

Conclusion: Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.
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http://dx.doi.org/10.3967/bes2017.057DOI Listing
June 2017

[Effects of acrylamide on synaptic plasticity of rat neuron].

Zhonghua Yu Fang Yi Xue Za Zhi 2011 Nov;45(11):1022-5

National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Objective: To explore effects of acrylamide on synaptic plasticity of rat neuron and its mechanisms.

Methods: 24 Wistar rats were divided into control and test groups randomly, 12 rats in each group. The ratio of male and female in each group was 1:1. Acrylamide (30 mg/kg) was administered to rats by intraperitoneal injection in test group and normal saline (5 g/kg) was given to rats in control group. The neurobehavioral and pathologic changes of heart, liver, spleen, lung and kidney were observed. Changes of parameters in synapse were recorded by electron microscope. As an important target of synapse, change of Synapsin I was measured by immunohistochemical method.

Results: Compared with the control group (male: 1.00 ± 0.00; female: 1.00 ± 0.00), the gait score was increased significantly in ACR treated group (male: 2.50 ± 0.55, t = -7.24, P < 0.01; female: 3.17 ± 0.41, t = -12.19, P < 0.01). No obvious pathological changes of heart, liver, spleen, lung and kidney were found in all rats. Compared with the control group (male: (0.41 ± 0.09) µm; female: (0.40 ± 0.06) µm), the length of active zone of synapse was decreased significantly in ACR treated group (male: (0.15 ± 0.05) µm, t = 6.59, P < 0.05; female: (0.14 ± 0.07) µm, t = 7.26, P < 0.05). The width and postsynaptic density of synapse in ACR treated group had no significant difference with control group. The location of Synapsin I of control group and ACR treated group was both in gray matter of spinal dorsal horn. Compared with the control group (male: 195.40 ± 12.30; female: 195.19 ± 6.71), the concentration of Synapsin I was decreased significantly in ACR treated group (male: 60.90 ± 29.19, t = 10.40, P < 0.05; female: 67.56 ± 20.23, t = 15.65, P < 0.05).

Conclusion: Neuronal synaptic plasticity was found in damage of nervous system induced by acrylamide in rats, which might be associated with the expression of Synapsin I.
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November 2011

[Effect of vinyl chloride on reproductive and endocrine system of male rats].

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2010 Jul;28(7):517-20

Zhejing Provincial Center for Disease Control and Prevention, Hangzhou 310051, China.

Objective: To explore the effect of vinyl chloride on reproductive and endocrine system of male rats.

Methods: Male SD rats were administered with vinyl chloride at dose of (0, 10, 100, 1000 mg/kg) for 14 and 28 days, respectively. The levels of testosterone (T), inhibin B, luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2) were measured in serum and testis homogenates. Histopathological examinations were performed for testis with electron microscopy.

Results: Compared with the control group after 14-day exposure, T and E2 serum levels of 1000, 100, 10 mg/kg groups decreased, InhB and LH levels of three dose groups increased. LH serum levels of 100 mg/kg increased significantly statistically compared with control group (P < 0.05). After 28-day exposure, T serum levels of 100, 1000 mg/kg groups were (10.90 +/- 1.56), (8.52 +/- 2.85) ng/ml respectively (P < 0.05), InhB serum levels of 100, 1000 mg/kg groups were (31.40 +/- 6.21), (28.39 +/- 5.67) pg/ml respectively. Both of T and InhB serum levels of 100, 1000 mg/kg groups decreased significantly (P < 0.05). Serum FSH levels of 10, 100, 1000 mg/kg groups decreased significantly compared with control group (P < 0.05). Compared with groups of 14-day exposure, serum InhB and LH levels of 10, 100, 1000 mg/kg groups decreased significantly statistically after 28 days. T and InhB testis levels of 100, 1000 mg/kg groups were 8.05 +/- 2.19),(6.75 +/- 1.94) ng/mg pro and (39.32 +/- 5.55), (35.53 +/- 8.71) pg/mg pro respectively, which decreased significantly compared with control group (P < 0.05). Leydig cell and Sertoli cell were damaged according to histopathological examinations.

Conclusion: Vinyl chloride has adverse effects on reproductive and endocrine system of male rats and may change their serum and testis homogenate levels of hormones.
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July 2010

[Study of L-02 hepatocyte apoptosis induced by hexavalent chromium associated with mitochondria function damage].

Wei Sheng Yan Jiu 2006 Jul;35(4):416-8

Institute for Occupational Health and Poison Control, China CDC, Beijing 100050, China.

Objective: To explore the effect of hexavalent chromium on apoptosis of L-02 hepatocytes and the functions of mitochondria. METHODS L-02 hepatocytes in all tests were incubated with 0,2,4,8,16,32 [see text] 64 micromol/L of Cr(VI) for 6h. Apoptosis of L-02 hepatocytes in the presence of Cr(VI) was quantified by flow cytometry (FCM). The permeability transition pore (FTP) of mitochondria and mitochondrial membrane potential as indicators of mitochondrial damage were measured by fluorescent spectrometer.

Results: Concentration-dependent decrease in cell apoptosis rate of Cr(VI)-treated L-02 hepatocytes were observed. The results of permeability transition pore (PTP) of mitochondria, mitochondrial membrane potential in all concentrations of Cr(VI) had significant difference when compared to the control cells (P < 0.05).

Conclusion: The results demonstrated that L-02 hepatocytes apoptosis induced by Cr(VI) associated with mitochondrial damages.
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July 2006

[Protective effect of reduced glutathione on cytotoxicity induced by hexavalent chromium [Cr(VI)] in L-02 hepatocyte].

Wei Sheng Yan Jiu 2006 Jul;35(4):414-5

Institute for Occupational Health and Poison Control, China CDC, Beijing 100050, China.

Objective: To explore the effect of reduced glutathione (GSH) on cytotoxicity induced by hexavalent chromium (Cr(VI)) in L-02 hepatocyte.

Methods: The test has three groups:the groups of (Cr(VI), the groups of GSH, the groups of Cr (VI) and GSH. The survival rate of L-02 hepatocyte is assessed on the reductions of tetrazolium dye (MTT).

Results: Significant cytotoxicities of L-02 hepatocyte were observed at the concenations of 2,4,8,16,32 and 64 micromol/L Cr (VI). Concentration-dependent decrease in cell survival rate of Cr (VI)-treated L-02 hepatocytes were observed (r = -0.910) Protective effect on all concentrations of Cr(VI) (2 - 64 micromol/L) at the dose of 20 micromol/LGSH were found.

Conclusion: The results demonstrated that proper concentrations of GSH could have protective effect on cytoxicity induced by Cr(VI) in L-02 hepatocyte. GSH of too low or too high concentrations don't has this effect.
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July 2006

[Effects of styrene on the dopaminergic transmitter content and monoamine oxidase activity in different sections of rat brain].

Wei Sheng Yan Jiu 2006 Jul;35(4):399-401

Institute of Occupational Health and Poison Control, China Center for Disease Control and Prevention, Beijing 100050, China.

Objective: To observe the effect on dopaminergic transmitter content and of monoamine oxidase (MAO) activity at dose of experiment in different sections of rat brain exposed bu acutely and subacutely styrene.

Methods: Rats were administrated orally with styrene of at dose of 600mg/kg for acute, 150, 300 and 600mg/kg for subacute experiment; recovery group were observed after 3 weeks exposure of styrene and intervened group were injected intraperitoneally at dose of 600mg/kg Levodopa (L-dopa) ; the urinary metabolites of styrene mandelic acid (MA) and phenylglyoxylic acid (PGA) were monitered as inner dosage, and the content of dopamine (DA) and activity of MAO were evaluated.

Results: The result indicated that the content of urinary MA and PGA were associated with dosage positively, and MA may be more sensitive as inner dosage of styrene exposure since the background of PGA. Levels of DA in retina, hypophysis and striatum were decreased after styrene exposure, the activities of MAO in hypophysis were increased and were reduced in retina and striatum.

Conclusion: It was suggested dopaminergic system could be participated in styrene neurotoxicity.
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July 2006
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