壳寡糖调节NOD小鼠的血脂异常和氧化应激

为了探究壳寡糖(COS)延缓NOD小鼠自发性糖尿病进程的可能机制,研究不同剂量COS对血脂异常和氧化应激的影响。持续灌胃不同剂量COS28w后,测定各组小鼠血糖、血脂和氧化应激等指标,并进行组织学检查。结果显示,各剂量COS均使NOD小鼠进入糖尿病前期和糖尿病阶段的时间有一定的延后,且可将其处于糖尿病前期的时间段(Control组为9 w)分别延长为10 w、13 w和16 w;可分别使小鼠血清T-CHO降低了37.10%、46.68%和62.72%(p0.01),使TC降低了35.01%、45.06%和60.62%(p0.01),使LDL-C降低了31.21%(p0.05)、51.68%和72.48%(p0.01),但对HDL-C无显著影响,改善了血脂异常;使小鼠肝组织内SOD和GSH-Px比活力有所提高,尤其是在COS-H组分别提高了94.69%和167.59%(p0.01),同时使MDA降低48.41%(p0.05),有效减轻氧化应激引起的氧化损伤;组织学检查显示COS使胰腺系数有所增加,肝脏系数逐步下降,脂肪空泡有所减少,对胰腺组织完整性具有一定的保护作用。据此推测,COS可通过调节血脂异常、抵抗血糖异常引起的体内氧化应激、保护组织等途径延缓自发性糖尿病发生发展的进程。

Chitooligosaccharides Regulate Dyslipidemia and Oxidative Stress in NOD Mice

To explore the possible mechanism underlying the ability of chitooligosaccharides (COS) to delay the progression of spontaneous diabetes in NOD mice, the effects of different doses of COS on dyslipidemia and oxidative stress were studied. After continuous intragastric administration of different doses of COS for 28 weeks, the indicators including blood glucose, blood lipids and oxidative stress of mice in each group were determined, and the histological examination was carried out. The results showed that COS at each dose could delay the time for NOD mice to enter the prediabetic and diabetic phases, and extend the time period of prediabetic phase to 10 W, 13 W and >16 W, respectively (9 w for the control group); COS at the three doses could decrease the level of T-CHO by 37.10%, 46.68% and 62.72%, respectively (p<0.01), level of TC by 35.01%, 45.06% and 60.62%, respectively (p<0.01), and level of LDL-C by 31.21% (p<0.05), 51.68% and 72.48%, respectively (p<0.01), although insignificant effect of COS on HDL-C was found. These results indicate that COS can improve dyslipidemia, increase the specific activities of SOD and GSH-Px in the liver tissues of mice (especially increased by 94.69% and 167.59%, respectively, in the COS-H group; p<0.01), and decreased the MDA concentration (by 48.41%; p<0.05), thereby reducing effectively oxidative stress-induced oxidative damage. Histological examination showed that COS increased the pancreatic coefficient, decreased gradually the liver coefficient, reduced fat vacuoles, providing a certain protective effect on the integrity of pancreatic tissue. According to these results, COS can delay the development of spontaneous diabetes through regulating dyslipidemia, resisting oxidative stress in the body caused by abnormal blood sugar, and protecting the tissues.