Effect of MSCs on vascular endothelial growth factor (VEGF), C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), triglyceride, pancreatic beta cells and insulin resistance in Oobese Type 2 diabetic rat m

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Aim to investigate the potential of SG followed by injection of MSCs in type 2 diabetic rats with obesity in improving IR. Methods This study used a pre and post-control group design with 24 rats divided into three groups: Control (C), SG, and SG + MSCs (SG+M). On day 10, the level of vascular endothelial growth factor (VEGF), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), triglyceride (TG), pancreatic beta cells, and homeostasis model assessment of IR (HOMA-IR) was evaluated using qRT-PCR, ELISA, and immunohistochemistry. Results A significant decrease of TNF-α (1.179 pg/mL), CRP(209 pg/mL), and TG levels (82,83  15,02pg/mL) in all treatment groups on day 10, in which SG + M group showed optimum inhibition was found (p < 0.05). This result was in line with the optimum increase of VEGF (8,1500 ± 2,47397) and pancreatic beta cell(10,1783±0,47) in SG + M group (p < 0.05). Moreover, our study also revealed the optimum decrease of HOMA-IR in SG+M group on day 10 (49,8233 ± 1,07303). Conclusion A combination of SG and MSCs can optimally improve insulin resistance by inhibiting TNF-α, CRP, and TG level and upregulating VEGF and pancreatic beta cell in an obese T2DM rat model.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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