# Polygonati Rhizoma Polysaccharides Ameliorated Diabetic Kidney Disease in db/db Mice via Inhibiting TGFβ /Smad2 Signaling Pathway

**Authors:** Xiyu Mei, Zeming Ren, Ziyun Gao, Sisi Chen, Xuan Chen, Qingyun Zhou, Yeling Tong, Guanhai Dai

PMC · DOI: 10.1002/fsn3.70677 · 2025-07-18

## TL;DR

A plant-based treatment improved kidney disease in diabetic mice by reducing inflammation and oxidative stress.

## Contribution

This study is the first to show that Polygonati Rhizoma polysaccharides reduce diabetic kidney disease via the TGFβ/Smad2 pathway.

## Key findings

- PP reduced kidney dysfunction and damage in diabetic db/db mice.
- PP improved lipid metabolism and reduced oxidative stress in diabetic mice.
- PP inhibited TGFβ/Smad2 signaling and increased Smad7 expression in mouse kidneys.

## Abstract

Polygonati Rhizoma polysaccharides (PP) are the active components isolated from medicine food homology (MFH) Chinese herb Polygonati Rhizoma. Diabetic kidney disease (DKD) is a serious diabetic complication occurring in the later stage of diabetes. We have previously reported the hypoglycemic effect of PP on early‐stage type 2 diabetes (T2D). This study evaluated the effect of PP on DKD and investigated the underlying mechanisms. PP was mainly composed of L‐fucose, L‐rhamnose, D‐glucose, and D‐mannose. Ten‐week‐old Leprdb/Leprdb (db/db) compared with control Leprdb/Lepr+ (db/+) mice were given vehicle or PP for 16 weeks. Our results showed that PP alleviated renal dysfunction (BUN, Cr, microalbumin) and pathological damage in db/db mice. PP improved lipid homeostasis (TG, NEFA, and HDL) and reversed oxidative stress (CAT, MDA, SOD, and GSH) in the serum of db/db mice. Besides, PP reduced the Masson‐positive area and expression of TGFβ in the kidneys from db/db mice. Furthermore, PP upregulated the expression of Smad7 and abrogated the phosphorylation of Smad2 in the kidneys from db/db mice. In conclusion, PP ameliorated kidney dysfunction and fibrosis through attenuating dyslipidemia, anti‐oxidative stress, and inhibiting the activation of TGFβ/Smad2 signaling pathway in db/db mice. The study provides a theoretical basis for further elucidation of the effect and mechanism of PP in attenuating DKD.

PP ameliorated diabetic kidney disease in T2D db/db mice. PP improved the lipid metabolism and attenuated the oxidative stress in T2D db/db mice. PP increased the expression of Smad7 and inhibited the activation of TGFβ/Smad2 signaling pathway in kidneys from T2D db/db mice.

## Linked entities

- **Genes:** SMAD2 (SMAD family member 2) [NCBI Gene 4087], SMAD7 (SMAD family member 7) [NCBI Gene 4092], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040]
- **Chemicals:** PP (PubChem CID 5460699), BUN (PubChem CID 91971254), Cr (PubChem CID 23976), TG (PubChem CID 2723601), NEFA (PubChem CID 57426056), HDL (PubChem CID 6323542), MDA (PubChem CID 1614), GSH (PubChem CID 124886)
- **Diseases:** Diabetic kidney disease (MONDO:0005016), Type 2 diabetes (MONDO:0005148)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Cat (catalase) [NCBI Gene 12359] {aka 2210418N07, Cas-1, Cas1, Cs-1}, Lepr (leptin receptor) [NCBI Gene 16847] {aka B219, LEP-R, LEPROT, Leprb, Modb1, OB-RGRP}, Smad2 (SMAD family member 2) [NCBI Gene 17126] {aka 7120426M23Rik, Madh2, Madr2, Smad-2, mMad2}, Smad7 (SMAD family member 7) [NCBI Gene 17131] {aka Madh7}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}
- **Diseases:** fibrosis (MESH:D005355), dyslipidemia (MESH:D050171), diabetic complication (MESH:D048909), T2D (MESH:D003924), DKD (MESH:D003928), diabetes (MESH:D003920), kidney dysfunction (MESH:D007674)
- **Chemicals:** PP (-), NEFA (MESH:D005230), L-fucose (MESH:D005643), L-rhamnose (MESH:D012210), D-glucose (MESH:D005947), Cr (MESH:D002857), D-mannose (MESH:D008358), lipid (MESH:D008055), TG (MESH:D013866), MDA (MESH:D015104)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12274161/full.md

---
Source: https://tomesphere.com/paper/PMC12274161