Anti-inflammatory and antioxidant potential capacities of AD-MSCs and BM-MSCs in suppressing pancreatic β-cells auto-immunity and apoptosis in rats with T1DM induced model

Since Type 1 diabetes (T1DM) occurs when beta-cells mass is reduced to less than 20% of the normal level due to autoimmune destruction of cells resulting in the inability to secrete insulin, preservation or replenishment of the functional beta-cells mass has become a major therapeutic focus for this diabetic type treatment. Thus, this 4-week work plan was designed to determine which mesenchymal stem cells (MSCs) type is more appropriate to alleviate pancreatic hazards resulting from diabetes induction; via tracking a comparative study between MSCs derived from adipose tissue (AD-MSCs) and from bone marrow (BM-MSCs) in management of T1DM considering their immunomodulatory, anti-apoptotic and antioxidative roles. Rats were divided randomly into 4 groups; control, STZ-diabetic (D), D+AD-MSCs, and D+BM-MSCs groups. Both stem cells types in this study were allogenic. Herein, both oxidative stress and antioxidant markers were evaluated using colorimetric analysis, while inflammatory, immune and apoptotic markers were assessed through flow cytometric analysis. Results showed that diabetic rats treated with either AD-MSCs or BM-MSCs exhibited marked pancreatic antioxidant and anti-inflammatory activities that were able to initiate pancreatic immunomodulation and reducing beta-cells apoptotic death, thus, help to restore their normal insulin secretion and hypoglycemic abilities. However, AD-MSCs injection was shown to be superior as a pancreatic regenerative tool in overcoming diabetes; owing to their marked antioxidant, anti-inflammatory, immunomodulatory, and anti-apoptotic characteristics over BM-MSCs treatment.

Automated summary

This study determined the superiority of AD-MSCs injection as a pancreatic regenerative tool in treating type 1 diabetes. AD-MSCs exhibited significant antioxidant, anti-inflammatory, and anti-apoptotic characteristics, reducing beta-cell death and restoring normal insulin secretion and hypoglycemic abilities.