# Protective Effects of Deer Antler Peptides on D-Galactose-Induced Brain Injury

**Authors:** Sihan Chen, Ying Zong, Jianming Li, Zhongmei He, Rui Du

PMC · DOI: 10.3390/nu17142306 · Nutrients · 2025-07-13

## TL;DR

This study shows that deer antler peptides can protect against brain damage caused by aging, reducing inflammation and oxidative stress in mice.

## Contribution

The study reveals the novel protective mechanism of deer antler peptides in D-galactose-induced brain injury through the TLR4/MyD88/NF-κB pathway.

## Key findings

- DAP reduced oxidative stress and inflammatory factors in serum and brain tissue.
- DAP inhibited the TLR4/MyD88/NF-κB signaling pathway in both in vivo and in vitro models.
- DAP promoted cell proliferation and reduced ROS levels in senescent BV2 cells.

## Abstract

Background/Objectives: The aim of this study was to investigate the role and potential mechanism of deer antler peptides (DAP) in D-galactose (D-gal)-induced brain injury. Methods: In the in vivo study, C57BL/6J mice were intraperitoneally injected with 400 mg/kg D-gal and gavaged with DAP (50 and 200 mg/kg) for 5 weeks. In vitro studies, D-gal (30 μg/mL) induced senescent BV2 cells were used for further research. Results: DAP increased the expression of BDNF and VEGF in the brain tissue of aging mice, reduced the levels of oxidative stress and inflammatory factors in serum, and decreased the pathological damage of brain tissue. In vitro, DAP promoted the proliferation of D-gal-induced senescent BV2 cells, reduced ROS level, and inhibited the release of IL-1β, IL-6 and TNF-α. In addition, DAP significantly reduced the protein expressions of TLR4 and MyD88, and inhibited the phosphorylation of NF-κB. Conclusions: DAP can inhibit the TLR4/MyD88/NF-κB signaling pathway, reduce oxidative stress and inflammation, and promote neovascularization. This indicates the therapeutic potential of DAP as a natural bioactive substance in preventing aging-related brain injury.

## Linked entities

- **Proteins:** BDNF (brain derived neurotrophic factor), VEGFA (vascular endothelial growth factor A), TLR4 (toll like receptor 4), MYD88 (MYD88 innate immune signal transduction adaptor), NFKB1 (nuclear factor kappa B subunit 1), IL1B (interleukin 1 beta), IL6 (interleukin 6), TNF (tumor necrosis factor), ROS1 (ROS proto-oncogene 1, receptor tyrosine kinase)
- **Chemicals:** D-galactose (PubChem CID 206)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Myd88 (myeloid differentiation primary response gene 88) [NCBI Gene 17874], Bdnf (brain derived neurotrophic factor) [NCBI Gene 12064], Vegfa (vascular endothelial growth factor A) [NCBI Gene 22339] {aka L-VEGF, Vegf, Vpf}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Tlr4 (toll-like receptor 4) [NCBI Gene 21898] {aka Lps, Ly87, Ran/M1, Rasl2-8}
- **Diseases:** Brain Injury (MESH:D001930), inflammation (MESH:D007249)
- **Chemicals:** D-Galactose (MESH:D005690), DAP (-)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]
- **Cell lines:** BV2 — Mus musculus (Mouse), Transformed cell line (CVCL_0182), C57BL/6J — Mus musculus (Mouse), Transformed cell line (CVCL_C0MW)

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12298834/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12298834/full.md

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Source: https://tomesphere.com/paper/PMC12298834