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Published on: August 15, 2025
Anti-diabetic effect mediated by Ramulus mori polysaccharides
Lingyuan Xu1, Fenglian Yang2, Junli Wang3
1Department of Pharmacy, Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, Guangxi 533000, PR China.
Abstract:
Diabetes mellitus is a complicated metabolic disease, whose pathogenesis is related to apoptosis within pancreatic tissue. In this study, the potential therapeutic benefits of Ramulus mori polysaccharides (RMP) on streptozotocin (STZ)-induced diabetic mice were evaluated. Our experiments indicated that RMP lowered hyperglycemia and increased insulin levels in diabetic mice. Histopathological examination revealed that RMP contributed to the reduction of STZ-lesioned pancreatic cells. In addition, the serum level of HbA1c was decreased. RMP treatment also showed increased Bcl-2 expression and reduced Bax protein level in pancreatic tissue. Furthermore, intrapancreatic expressions of p-JNK, p-p38 and cleaved-caspase-3 were down-regulated by RMP treatment. Collectively, the findings demonstrate that RMP exerts the pronounced hypoglycemic effect via regulation of the intrapancreatic JNK/p38 pathway to protect against STZ-induced apoptosis in pancreatic tissue, eventually ameliorating metabolic function in the pancreas.
Insights
Ramulus mori polysaccharides (RMP) effectively treat diabetes by lowering blood sugar and increasing insulin in mice. RMP protects pancreatic cells from damage and reduces apoptosis, improving metabolic function.
Area of Science:
- Metabolic disease research
- Endocrinology
- Pharmacology
Background:
- Diabetes mellitus is a complex metabolic disorder.
- Pancreatic beta-cell apoptosis contributes to diabetes pathogenesis.
- Streptozotocin (STZ) is commonly used to induce experimental diabetes.
Purpose of the Study:
- To evaluate the therapeutic potential of Ramulus mori polysaccharides (RMP) in a mouse model of diabetes.
- To investigate the effects of RMP on pancreatic cell apoptosis and metabolic function.
Main Methods:
- Induction of diabetes in mice using streptozotocin (STZ).
- Administration of RMP to diabetic mice.
- Assessment of glycemic control (blood glucose, HbA1c, insulin levels).
- Histopathological examination of pancreatic tissue.
- Analysis of apoptosis-related protein expression (Bcl-2, Bax) and signaling pathways (JNK, p38, caspase-3).
Main Results:
- RMP treatment significantly lowered hyperglycemia and increased insulin levels in STZ-induced diabetic mice.
- Histological analysis showed RMP reduced STZ-induced pancreatic cell damage.
- RMP decreased HbA1c levels.
- RMP modulated Bcl-2 and Bax protein expression, indicating an anti-apoptotic effect.
- RMP downregulated the expression of p-JNK, p-p38, and cleaved-caspase-3 in pancreatic tissue.
Conclusions:
- RMP demonstrates significant hypoglycemic effects in experimental diabetes.
- RMP protects pancreatic tissue from STZ-induced apoptosis, likely through the regulation of the JNK/p38 signaling pathway.
- RMP holds promise as a therapeutic agent for ameliorating pancreatic metabolic dysfunction in diabetes.
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