Type 1 diabetes stem-cell-based therapy is one of the best therapeutic approaches for pancreatic damage treatment due to stem cell tissue regeneration. Epigallocatechin gallate (EGCG) is one of the active components found in green tea. Experimental results suggest that EGCG shows beneficial effects on cell protection. This study explores whether a better pancreatic regeneration therapeutic effect could be found in mesenchymal stem cells pretreated with EGCG compared to stem cells without EGCG pretreatment. A cell model confirmed that adipose-derived stem cells (ADSC) incubated with EGCG increase cell viability under high-glucose (HG) stress. This is due to survival marker p-Akt expression. In an animal model, type 1 diabetes induced the activation of several pathological signals, including islet size reduction, extracellular fibrotic collagen deposition, oxidative stress elevation, survival pathway suppression, apoptosis signaling induction, and Sirt1 antioxidant pathway downregulation. Ordinary ADSC transplantation slightly improved the above pathological signals. Further, EGCG-pretreated ADSC transplantation significantly improved the above pathological conditions. Taken together, EGCG-pretreated ADSCs show clinical potential in the treatment of patients with type 1 diabetes through the regeneration of damaged pancreatic tissues.

Aging is one of the causative agents associated with heart failure. Cell-based therapies show potential in the treatment of cardiac aging due to the characteristics of stem cells, including differentiation and the paracrine effect. This study aimed to investigate in detail the mechanism related to biomolecules released from mesenchymal stem cells in the treatment of cardiac aging. In vitro and in vivo models were designed to explore the above hypothesis. Experimental results from the in vitro model indicated that the elevation of oxidative stress, the expression of aging marker p53, and the suppression of antioxidant marker SOD2 could be found in D-galactose-stressed H9c2 cardiomyoblasts. The co-culture of D-galactose-stressed H9c2 with mesenchymal stem cells significantly improved the above pathological signaling. An animal model revealed that the change in cardiac structure, the accumulation of fibrotic collagen, and the activation of the above pathological signaling could be observed in heart tissues of D-galactose-stressed rats. After the rats had received mesenchymal stem cells, all the pathological conditions were significantly improved in D-galactose-stressed hearts. Further evidence indicated that the release of the survival marker IGF-1 was detected in a stem-cell-conditioned medium. Significant increases in cell viability and the expression of SOD2, as well as a reduction in oxidative stress and the suppression of p53, were found in D-galactose-stressed H9c2 cells cultured with a stem-cell-conditioned medium, whereas the depletion of IGF-1 in stem-cell-conditioned medium diminished the antiaging effect on H9c2 cells. In conclusion, the paracrine release of IGF-1 from mesenchymal stem cells increases the expression of antioxidant marker SOD2, and the expression of SOD2 reduces oxidative stress as well as suppresses p53, leading to a reduction in cardiac senescence in D-galactose-stressed rats.

Background: Cardiomyopathy is one of the complications associated with diabetes. Due to its high prevalence, diabetic cardiomyopathy has become an urgent issue for diabetic patients. Various pathological signals are related to diabetic cardiomyopathy progress, including inflammasome. Mesenchymal stem cell transplantation is full of potential for the treatment of diabetic cardiomyopathy because of stem cell cardiac regenerative capability. This study investigates whether mesenchymal stem cell transplantation shows therapeutic effects on diabetic cardiomyopathy through inflammasome signaling regulation. Methods: Wistar male rats were divided into three groups including Sham, T1DM (rats with type 1 diabetes) and T1DM + WJSC (T1DM rats receiving 1 × 10⁶ stem cells per rat). Results: Compared to the Sham, experimental results indicated that several pathological conditions can be observed in heart tissues with T1DM, including structural change, fibrosis, oxidative stress elevation and inflammasome related protein expression. All of these pathological conditions were significantly improved in T1DM rats receiving mesenchymal stem cell transplantation (T1DM + WJSC). Furthermore, the experimental findings suggest that mesenchymal stem cell transplantation exerted antioxidant protein expression in diabetic heart tissues, resulting in a decrease in oxidative stress and inflammasome signaling blockage. Conclusion: These findings imply that mesenchymal stem cell transplantation shows therapeutic effects on diabetic cardiomyopathy through inflammasome regulation induced by oxidative stress.