# Gallic acid pretreatment mitigates parathyroid ischemia–reperfusion injury through signaling pathway modulation

**Authors:** Nianqiu Liu, Hongmin Liang, Yuan Hong, Xiaokai Lu, Xin Jin, Yuting Li, Shiying Tang, Yihang Li, Weihan Cao

PMC · DOI: 10.1038/s41598-024-63470-5 · Scientific Reports · 2024-06-05

## TL;DR

Gallic acid pretreatment helps protect parathyroid glands during surgery by reducing injury caused by oxygen loss and recovery.

## Contribution

This study shows gallic acid mitigates parathyroid ischemia–reperfusion injury through modulation of multiple signaling pathways.

## Key findings

- GA pretreatment reduces apoptosis and G1 phase arrest in parathyroid cells under hypoxia/reoxygenation.
- RNA-seq reveals GA modulates IL-17, AMPK, MAPK, and other signaling pathways.
- GA shows potential as a therapeutic strategy for preventing hypoparathyroidism.

## Abstract

Thyroid surgery often results in ischemia–reperfusion injury (IRI) to the parathyroid glands, yet the mechanisms underlying this and how to ameliorate IRI remain incompletely explored. Our study identifies a polyphenolic herbal extract—gallic acid (GA)—with antioxidative properties against IRI. Through flow cytometry and CCK8 assays, we investigate the protective effects of GA pretreatment on a parathyroid IRI model and decode its potential mechanisms via RNA-seq and bioinformatics analysis. Results reveal increased apoptosis, pronounced G1 phase arrest, and significantly reduced cell proliferation in the hypoxia/reoxygenation group compared to the hypoxia group, which GA pretreatment mitigates. RNA-seq and bioinformatics analysis indicate GA’s modulation of various signaling pathways, including IL-17, AMPK, MAPK, transient receptor potential channels, cAMP, and Rap1. In summary, GA pretreatment demonstrates potential in protecting parathyroid cells from IRI by influencing various genes and signaling pathways. These findings offer a promising therapeutic strategy for hypoparathyroidism treatment.

## Linked entities

- **Chemicals:** gallic acid (PubChem CID 370)
- **Diseases:** hypoparathyroidism (MONDO:0001220)

## Full-text entities

- **Genes:** RAP1A (RAP1A, member of RAS oncogene family) [NCBI Gene 5906] {aka C21KG, G-22K, KREV-1, KREV1, RAP1, SMGP21}, PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562] {aka AMPK, AMPK alpha 1, AMPKa1}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}
- **Diseases:** hypoparathyroidism (MESH:D007011), parathyroid (MESH:D010279), hypoxia (MESH:D000860), IRI (MESH:D015427)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC11153493/full.md

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11153493/full.md

## References

72 references — full list in the complete paper: https://tomesphere.com/paper/PMC11153493/full.md

---
Source: https://tomesphere.com/paper/PMC11153493