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Neurodegeneration, demyelination, and astrogliosis in rat spinal cord by chronic lead treatment

机译:慢性铅治疗的大鼠脊髓脱髓鞘,脱髓鞘和星分激

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摘要

Abstract Early exposure to lead (Pb) has been associated with an elevated risk of developing neurodegenerative diseases. There is evidence that neuronal damage in chronic Pb exposure can be caused by the convergence of glial damage. Apoptosis may be a possible mechanism of Pb‐induced cell death in the central nervous system. We tested cellular damage and apoptosis in the spinal cord of Wistar rats treated with Pb. Twelve rats were divided into two groups ( n ?=?6): the control group was treated with only drinking water and the other group received 500?ppm of Pb acetate. After 3 months of Pb treatment, all animals were euthanized and spinal cords were extracted. Morphology was evaluated by Nissl and Kluver‐Barrera stainings. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Specific antibodies were used to evaluate Pb damage in oligodendrocytes, astrocytes, and microglia. A large number of apoptotic bodies was observed in the white matter of the Pb‐treated group. The Pb‐treated group also showed a reduced number of neurons and oligodendrocytes but had an increased number of astrocytes compared with the nontreated group. Our results demonstrate that chronic Pb treatment induces neurodegeneration, demyelination, and astrogliosis in the rat spinal cord.
机译:摘要早期暴露于铅(PB)与发育神经变性疾病的风险升高有关。有证据表明慢性Pb暴露中的神经元损伤可能是由胶质损伤的收敛引起的。细胞凋亡可能是中枢神经系统中PB诱导的细胞死亡的可能机制。我们在用Pb处理的Wistar大鼠的脊髓中测试了细胞损伤和细胞凋亡。将十二只大鼠分为两组(n?=β6):对照组仅用饮用水处理,另一组接受500〜ppm的pb乙酸盐。在3个月的PB治疗后,所有动物都被安乐死,并提取脊髓。通过NISSL和Kluver-Barrera染色来评估形态。通过末端脱氧核苷酸转移酶DUTP切口末端标记测定检测细胞凋亡。使用特异性抗体评估寡核细胞,星形胶质细胞和小胶质细胞的PB损伤。在PB处理组的白质中观察到大量凋亡体。 PB治疗组还表现出减少的神经元和少突胶质细胞,但与非处理基团相比具有增加的星形胶质细胞。我们的结果表明,慢性PB治疗诱导大鼠脊髓中的神经变性,脱髓鞘和星形症。

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