Schisandra chinensis polysaccharide attenuates diabetic islet cell injury by promoting autophagy via suppression of the PI3K/AKT/mTOR signaling cascade.

BACKGROUND

Schisandra chinensis polysaccharide (SCP) has demonstrated antidiabetic properties in previous studies; however, the mechanisms underlying its regulation of autophagy in pancreatic protection remain poorly understood. This study investigated how SCP modulates autophagic pathways to alleviate diabetic pathology.

METHODS

Diabetic rats were administered SCP orally, followed by histopathological and biochemical assessments of pancreatic islet function and tissue damage. Beta-TC-6 pancreatic β-cells were exposed to SCP to evaluate cellular viability, insulin secretion, and autophagic processes using immunohistochemistry, Western blotting, immunofluorescence, and transmission electron microscopy.

RESULTS

SCP dose-dependently attenuated diabetes-associated weight loss, reduced hyperglycemia, and improved β-cell function. Histological examination revealed amelioration of pancreatic islet disorganization, diminished collagen deposition, and reduced basement membrane thickening. Mechanistically, SCP enhanced autophagic activity in pancreatic tissues and Beta-TC-6 cells by inhibiting the PI3K/AKT/mTOR signaling cascade, with high-dose SCP exhibiting efficacy comparable to that of metformin. Chloroquine co-treatment abolished these effects, confirming autophagy dependence.

CONCLUSION

This study demonstrates that SCP alleviates diabetes by restoring β-cell function and inducing protective autophagy via the inhibition of the PI3K/AKT/mTOR pathway. These findings indicate SCP as a potential candidate for diabetes therapy.