# Ganoderma lucidum and Robinia pseudoacacia Flower Extract Complex Alleviates Kidney Inflammation and Fibrosis by Modulating Oxidative Stress

## TL;DR

A plant extract complex reduces kidney inflammation and fibrosis by targeting oxidative stress in both cells and mice models.

## Contribution

NEPROBIN, a combination of Ganoderma lucidum and Robinia pseudoacacia flower extract, shows therapeutic potential for chronic kidney disease.

## Key findings

- NEPROBIN reduced oxidative stress and inflammation in renal cells.
- NEPROBIN mitigated kidney damage and fibrosis in mice fed an adenine diet.
- NEPROBIN lowered blood and urine markers of kidney dysfunction in treated mice.

## Abstract

Chronic kidney disease (CKD) is characterized by functional and structural abnormalities, with its progression strongly influenced by oxidative stress and inflammatory responses, ultimately leading to renal fibrosis. This study aimed to investigate the effects of a Ganoderma lucidum and Robinia pseudoacacia flower extract complex (NEPROBIN) through in vitro and in vivo experiments. In vitro experiments with NRK52E renal tubular epithelial cells demonstrated that NEPROBIN significantly alleviates H2O2-induced oxidative stress and suppresses lipopolysaccharide (LPS)-induced activation of the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways. Additionally, NEPROBIN reduced LPS-induced NF-κB transcriptional activity and downregulated the expression of cytokines and chemokines in these cells. We further investigated the effects of NEPROBIN in vivo. Kidney damage was induced in mice using a 0.25% adenine diet (AD), and the mice were orally treated with NEPROBIN at doses of 100, 200, and 400 mg/kg/day for two weeks. NEPROBIN treatment significantly reduced AD-induced elevations in blood urea, serum creatinine, and urinary β2-microglobulin levels. Markers of oxidative stress and kidney damage were notably lower in the kidneys of NEPROBIN-treated mice. Furthermore, NEPROBIN effectively mitigated the AD-induced inflammatory response in the kidneys, with a marked reduction in cytokine and chemokine expression. This decrease in inflammation was associated with a significant reduction in tubulointerstitial fibrosis. Overall, NEPROBIN alleviated renal damage and fibrosis by directly targeting renal oxidative stress and inflammation, highlighting its potential as a therapeutic agent for CKD.