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Gallic Acid Pretreatment Mitigates Parathyroid Ischemia-reperfusion Injury Through Signaling Pathway Modulation.

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Gallic Acid Pretreatment Mitigates Parathyroid Ischemia-reperfusion Injury Through Signaling Pathway Modulation.

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Gallic acid pretreatment mitigates parathyroid ischemia-reperfusion injury through signaling pathway modulation.

Nianqiu Liu¹, Hongmin Liang², Yuan Hong³

¹Departments of Breast Surgery, Yunnan Cancer Center, The Third Affiliated Hospital of Kunming Medical University, Kunming, 650000, Yunnan, People's Republic of China.

Scientific Reports

|June 5, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Gallic acid (GA), an antioxidant, protects parathyroid cells from thyroid surgery-induced ischemia-reperfusion injury (IRI). GA pretreatment mitigates cell damage and offers a potential therapy for hypoparathyroidism.

Keywords:

Gallic acid Hypoparathyroidism Ischemia–reperfusion injury Mechanism

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Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging

Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging

Published on: August 17, 2022

Area of Science:

Biochemistry
Cell Biology
Surgical Research

Background:

Thyroid surgery frequently causes parathyroid gland ischemia-reperfusion injury (IRI).
Mechanisms of parathyroid IRI and effective treatments are not fully understood.
Hypoparathyroidism is a potential complication of parathyroid IRI.

Purpose of the Study:

To identify protective agents against parathyroid IRI.
To investigate the protective effects and mechanisms of gallic acid (GA) against parathyroid IRI.
To evaluate GA's potential as a therapeutic strategy for hypoparathyroidism.

Main Methods:

Establishment of a parathyroid IRI model.
Assessment of cell viability and apoptosis using CCK8 assays and flow cytometry.

RNA sequencing (RNA-seq) and bioinformatics analysis to elucidate molecular mechanisms.

Pretreatment with gallic acid (GA).

Main Results:

Hypoxia/reoxygenation induced significant apoptosis and G1 phase arrest, reducing cell proliferation.
GA pretreatment effectively mitigated IRI-induced cell damage and apoptosis.
RNA-seq and bioinformatics revealed GA modulates key signaling pathways (e.g., IL-17, AMPK, MAPK, cAMP, Rap1).

Conclusions:

Gallic acid (GA) exhibits significant antioxidative and protective effects against parathyroid IRI.
GA pretreatment influences multiple critical cellular signaling pathways.
GA presents a promising therapeutic candidate for preventing hypoparathyroidism post-thyroid surgery.