Abstract

Objective To investigate the protective effects of human umbilical cord mesenchymal stem cells (hUCMSCs) on liver injury in type 1 non-obese diabetic (NOD) mice. Methods A total of 33 female NOD mice were feeded for 9 weeks. 21 mice with diabetes were randomly divided into diabetic control group and MSC group (10 in each group) . The MSC group was infused with hUCMSCs on the 3rd day after onset. Another 10 mice without diabetes were used as blank control group. The random blood glucose (GLU) level of mice were detected for every week. After 8 weeks, the mice were sacrificed and the liver tissue was harvested for HE staining. AGE was measured by ELISA, and the expression levels of receptor (RAGE) , NF-κB P65, interleukin-6 (IL-6) , and tumor necrosis factor (TNF-α) mRNA were measured by real-time PCR. Statistical analysis was performed by one-way analysis of variance and SNK-q test. P < 0.05 was considered statistically significant. Results After 8 weeks of MSCs treatment, the random blood glucose of mice (11.78±4.10) mmol/L was significantly lower in the MSC group than that in the T1DM group (32.30±1.46) mmol/L, (P < 0.05) . And the liver cells were abnormal and inflammatory cells were seen in the T1DM group, which was significantly improved in the MSC group. The AGEs level (0.72±0.10) μg/ml of the liver tissue of the MSC group was significantly lower than that in the T1DM group (1.35±0.22) μg/ml, (P < 0.05) . At the same time, the mRNA levels of NF-κB P65, IL- 6, TNF-α and RAGE of the MSC group (10.08±1.94, 9.31±1.67, 11.92±1.82, and 3.87±0.27 respectively) were significantly lower than those in the T1DM group (15.46±3.09, 18.04±1.69, 22.12±3.23, and 5.12±0.26 respectively) respectively. The difference was statistically significant (P < 0.05) . Conclusion Human umbilical cord mesenchymal stem cells could reduce blood glucose level, improve pathological injury of liver cells, decrease production of AGEs and some inflammatory factors of diabetic mice. Key words: Human umbilical cord mesenchymal stem cells; Type 1 diabetes; Advanced glycationend products; Liver injury

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