# Polysaccharide fraction from Triplostegia glandulifera Wall and its renoprotective effect in streptozotocin-induced diabetic mice by attenuating oxidative stress

## TL;DR

A polysaccharide from a traditional Chinese plant shows kidney-protecting effects in diabetic mice by reducing oxidative stress.

## Contribution

The study identifies and evaluates a low molecular weight polysaccharide fraction (TGB) from Triplostegia glandulifera for its renoprotective effects in diabetic nephropathy.

## Key findings

- TGB reduced oxidative stress and abnormal cell proliferation in high-glucose-induced kidney cells.
- TGB improved glucose-lipid metabolism and kidney function in diabetic mice.
- TGB showed better activity than TGC due to its lower molecular weight and antioxidant properties.

## Abstract

Triplostegia glandulifera Wall (T. glandulifera) is an ethnomedicine commonly used by ethnic minorities in Yunnan, China, to treat kidney disease. However, there are few reports on the renoprotective effects of this substance, and the active ingredients remain unclear. In this study, we extracted the polysaccharide fractions TGB and TGC using the water extraction-alcohol precipitation method and determined their molecular weight (Mw) and monosaccharide composition. The study investigated the protective effects of TGB and TGC fractions against diabetic nephropathy (DN) using an in vitro high glucose-induced HRMCs model and an in vivo STZ-induced diabetic mouse model. HPLC analysis revealed that TGB contained D-galacturonic acid, D-glucose, D-galactose, and D-arabinose, and had a lower Mw than TGC. In vitro, TGB showed concentration-dependent antioxidant activity and effectively reduced abnormal proliferation and while attenuating oxidative stress in HRMCs. In mice with diabetes, TGB corrected the dysregulation of glucose-lipid metabolism and alleviated oxidative stress in the kidneys. Additionally, it improved renal function and reduced renal tissue damage. The study suggests that the low Mw polysaccharides (TGB) have better activity against DN through the antioxidative stress mechanism.