Zhou Songlin, Yang Yumin, Gu Xiaosong, Ding Fei
Jiangsu Key Laboratory of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong, JS 226001, PR China.
Neurosci Lett. 2008 Oct 31;444(3):270-4. doi: 10.1016/j.neulet.2008.08.040. Epub 2008 Aug 19.
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.
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。
