Therapeutic Evaluation of Eleutheroside B from Eleutherococcus senticosus in Streptozotocin-Induced Renal Dysfunction

Authors

  • M. Ezhilarasi
  • Swarnalatha S
  • Karthi J

Keywords:

Diabetic nephropathy, Eleutherococcus senticosus, Eleutheroside B, Eleutheroside E, Inflammation, Oxidative stress

Abstract

Diabetic nephropathy is a major small-blood-vessel complication of diabetes, mainly caused by increased oxidative stress and inflammation that damage the kidneys. In this study, we explored the ability of Eleutheroside B, a natural compound obtained from the roots of Eleutherococcus senticosus, to protect kidney function and reduce blood glucose levels in a streptozotocin (STZ)-induced diabetic mouse model. The roots were authenticated and extracted using a hydroalcoholic solvent, and the active compound was identified and characterized through UV, FT-IR, and NMR analyses. Diabetic mice received oral doses of the extract at 100 mg/kg and 300 mg/kg for 28 days, with metformin (200 mg/kg) serving as a standard reference. Various physiological, biochemical, and histological parameters were measured to assess kidney protection. Treatment with E. senticosus led to notable improvements in body weight, reduction in excessive urination, and normalization of the kidney index, with effects increasing at higher doses. The extract markedly reduced blood glucose and creatinine levels, while simultaneously boosting albumin and insulin concentrations. It also helped rebalance oxidative stress indicators and inflammatory mediators such as MDA, TNF-α, IL-1β, and IL-6, bringing them closer to normal values. Microscopic examination of kidney tissue further revealed clear protection of both glomerular and tubular architecture. The higher dose of the extract demonstrated effects comparable to metformin, highlighting its strong antioxidant and anti-inflammatory properties. Overall, these findings indicate that Eleutheroside B from E. senticosus holds considerable promise as a protective agent against diabetic kidney damage by targeting oxidative and inflammatory pathways.

Published

2025-12-30