| 徐宣萍,陆仲夏,王盛楠,等.壳寡糖对脓毒血症小鼠保护作用的研究[J].中国海洋药物,2026,(5):-. |
| 壳寡糖对脓毒血症小鼠保护作用的研究 |
| Study on the protective effect of chitooligosaccharide on septic mice |
| 投稿时间：2025-04-29 修订日期：2025-06-10 |
| DOI： |
| 中文关键词: 壳寡糖 脓毒血症 肝损伤 |
| English Keywords:chitooligosaccharide sepsis liver injury |
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| 中文摘要: |
| 目的 评估壳寡糖（chitooligosaccharide，COS）对脓毒血症小鼠的保护作用，并探究相关机制。方法 采用动态光散射、Zeta电位和咪唑-锌染色检测COS对内毒素脂多糖（lipopolysaccharide，LPS）的分子粒径、电荷和迁移能力的影响。同时，应用流式细胞术、Western Blot、细胞计数试剂盒-8和乳酸脱氢酶，评价COS对LPS与细胞的结合及Toll样受体4的激活能力、细胞活力和毒性的作用。通过腹腔注射E.coil ATCC25922建立脓毒血症小鼠模型，观察并绘制不同组小鼠的生存曲线。采用苏木精-伊红染色检测小鼠肝脏的形态。根据试剂盒提供的方法检测血清中谷丙转氨酶、谷草转氨酶含量。结果 COS与LPS混合后能显著改变LPS的分子粒径和所带电荷，并抑制LPS的迁移能力。COS能够抑制LPS与细胞的结合以及Toll样受体4的激活，并有效减少了LPS诱导的细胞毒性。脓毒血症小鼠的生存期在COS干预后明显延长，且脓毒血症小鼠的抗菌能力在COS干预后明显增强。COS下调了血清中肝脏损伤生化指标的水平，减轻了肝脏损伤。结论 COS通过与LPS直接作用抑制LPS对免疫系统的激活，凭借其抗炎及器官保护功能减少脓毒血症小鼠的死亡。 |
| English Summary: |
| Objective Sepsis poses a significant threat to human life, health, and safety. This study aimed to evaluate the protective effects of chitooligosaccharide (COS) on septic mice and to explore the underlying mechanisms involved. Methods Dynamic light scattering, zeta potential analysis, and imidazole-zinc staining were employed to assess the effect of COS on the molecular size, charge, and migration ability of endotoxin (lipopolysaccharide, LPS). At the same time, flow cytometry, Western Blot, Cell Counting Kit-8 and lactate dehydrogenase was employed to assess the effect of COS on the binging affinity of LPS to cells, the activation of Toll-like receptor 4, cell viability and toxicity. A sepsis mouse model was established through intraperitoneal injection of E. coli ATCC25922, and the survival curves of various groups of mice were observed and plotted. Hematoxylin-eosin staining was utilized to examine the morphology of the mouse liver. Additionally, the levels of alanine aminotransferase and aspartate aminotransferase in serum were assessed according to the methods outlined in the provided kit. Results The combination of COS with LPS significantly altered the molecular particle size and charge of LPS, and inhibit its migration ability. COS was shown to inhibit the binding of LPS to cells and the activation of TLR4, effectively reducing LPS-induced cytotoxicity. Furthermore, the survival duration of septic mice was notably extended after COS intervention, and their antibacterial capacity was markedly enhanced following COS treatment. Additionally, COS reduced the levels of biochemical markers indicative of organ damage in serum and mitigated liver damage. Conclusion COS directly binds to LPS, suppressing its immune-activating effects. Through its dual mechanisms of anti-inflammation and organ protection, COS significantly decreases mortality rates in murine sepsis models. |
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