# Preclinical evidence of ginkgo biloba extract on diabetic nephropathy: a systematic review and meta-analysis

## TL;DR

This study reviews preclinical evidence showing that Ginkgo biloba extract may help treat diabetic nephropathy by reducing inflammation and oxidative stress.

## Contribution

The study provides the first comprehensive preclinical meta-analysis on Ginkgo biloba extract's dose-time effect in diabetic nephropathy.

## Key findings

- GBE significantly reduces markers of kidney damage and inflammation in diabetic nephropathy models.
- GBE improves oxidative stress indicators and fibrosis while modulating glycolipid metabolism.
- Optimal GBE dosage for treatment is 36–200 mg/kg/d for 8–12 weeks.

## Abstract

Diabetic nephropathy (DN) is one of the common complications of diabetes, which is the leading cause of end-stage renal disease worldwide. Ginkgo biloba extract (GBE) has shown effectiveness in DN animal models and represents a promising therapeutic candidate. However, a comprehensive preclinical meta-analysis remains to be conducted, and the dose-time effect of GBE in the treatment of DN has not been evaluated.

To evaluate the therapeutic effectiveness, mechanism and dose-time effect of GBE for DN by systematic review and meta-analysis.

Seven databases (PubMed, Web of science, Embase, CBM, CNKI, Wanfang and VIP databases) were searched in this systematic review up to July 2025. Study quality was assessed using SYRCLE bias risk tool. STATA 14.0 software was employed to evaluate fasting blood glucose serum creatinine (SCr), blood urea nitrogen 24-h urine protein (24 h Upro), kidney index and indicators related to inflammatory response, oxidative stress, fibrosis, and glycolipid metabolism. The dose-time effect of Ginkgo biloba extract was evaluated by three-dimensional dose-time-effect analysis.

30 pertinent articles were included in the meta-analysis. Comparative analysis revealed that GBE exhibited statistically significant effect in reducing FBG, SCr, BUN, 24 h Upro, and KI. Furthermore, it also improved inflammatory indicators such as interleukin 1β (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), as well as oxidative stress indicators like superoxide dismutase (SOD), malondialdehyde (MDA), antioxidation capability (AOC) and glutathione peroxidases (GSH-Px). Additionally, GBE showed positive effect in alleviating fibrosis and reducing serum total cholesterol (TC) and advanced glycation end products (AGEs). The dose-time-effect diagram showed that the rational dose of GBE for DN treatment was 36–200 mg/kg/d for 8–12 weeks.

GBE may delay the progression of DN through multimodal mechanisms, including inhibition of inflammatory responses, attenuation of oxidative stress, suppression of fibrotic pathways, and modulation of glycolipid metabolism.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420250652386.