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壳寡糖可保护培养的海马神经元免受谷氨酸诱导的神经毒性。

Chitooligosaccharides protect cultured hippocampal neurons against glutamate-induced neurotoxicity.

作者信息

Zhou Songlin, Yang Yumin, Gu Xiaosong, Ding Fei

机构信息

Jiangsu Key Laboratory of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong, JS 226001, PR China.

出版信息

Neurosci Lett. 2008 Oct 31;444(3):270-4. doi: 10.1016/j.neulet.2008.08.040. Epub 2008 Aug 19.

Abstract

Chitooligosaccharides (COSs), the biodegradation product of chitosan, have demonstrated a diverse array of biological activities. Here we report the protective effect of COSs (M.W. 800) against glutamate-induced neurotoxicity in cultured hippocampal neurons. The cell viability assessments, together with Hoechst 33342 staining and flow cytometry for cell apoptosis analysis, indicated that glutamate (125 microM)-induced cell apoptosis in cultured hippocampal neurons was attenuated in a concentration-dependent manner by COSs pretreatment. After measurement with Fluo 4-AM, COSs were found to depress glutamate-induced elevation in intracellular calcium concentration (Ca(2+)). The enzymatic assay indicated that COSs antagonized glutamate-evoked activation of caspase-3. These results collectively suggest that COSs prevent cultured hippocampal neurons from glutamate-induced cell damage by interfering with an increase in Ca(2+) and inhibiting caspase-3 activity.

摘要

壳寡糖(COSs)是壳聚糖的生物降解产物,已显示出多种生物活性。在此,我们报告了分子量为800的壳寡糖对培养的海马神经元中谷氨酸诱导的神经毒性的保护作用。细胞活力评估,以及用于细胞凋亡分析的Hoechst 33342染色和流式细胞术表明,壳寡糖预处理以浓度依赖的方式减轻了谷氨酸(125微摩尔)诱导的培养海马神经元细胞凋亡。用Fluo 4-AM测量后,发现壳寡糖可抑制谷氨酸诱导的细胞内钙浓度(Ca(2+))升高。酶活性测定表明,壳寡糖可拮抗谷氨酸诱发的caspase-3激活。这些结果共同表明,壳寡糖通过干扰Ca(2+)的增加并抑制caspase-3活性,防止培养的海马神经元受到谷氨酸诱导的细胞损伤。

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