Title : Glycyrrhizin Attenuates Hypoxic-Ischemic Brain Damage by Inhibiting Ferroptosis and Neuroinflammation in Neonatal Rats via the HMGB1/GPX4 Pathway.

Pub. Date : 2022

PMID : 35432719






6 Functional Relationships(s)
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Protein Name
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1 Herein, glycyrrhizin (GL), an HMGB1 inhibitor, was used to investigate the relationship between ferroptosis and HMGB1. Glycyrrhizic Acid high mobility group box 1 Homo sapiens
2 Herein, glycyrrhizin (GL), an HMGB1 inhibitor, was used to investigate the relationship between ferroptosis and HMGB1. Glycyrrhizic Acid high mobility group box 1 Homo sapiens
3 Western blot analysis revealed that GL markedly suppressed the expression of HMGB1 and increased the level of GPX4 in the context of HIBD. Glycyrrhizic Acid high mobility group box 1 Homo sapiens
4 More importantly, GL may improve oxidative stress imbalance and mitochondrial damage, alleviate the downstream production of inflammatory factors, and ultimately reduce ferroptosis and damage to cortical neurons following HIBD via the HMGB1/GPX4 pathway. Glycyrrhizic Acid high mobility group box 1 Homo sapiens
5 In conclusion, we showed for the first time that GL could suppress the occurrence of neuronal ferroptosis and reduce neuronal loss in HIBD via the HMGB1/GPX4 pathway. Glycyrrhizic Acid high mobility group box 1 Homo sapiens
6 These findings highlight the potential of HMGB1 signaling antagonists to treat neuronal damage by suppressing ferroptosis, provide new and unique insights into GL as a neuroprotective agent, and suggest new prevention and treatment strategies for HIBD. Glycyrrhizic Acid high mobility group box 1 Homo sapiens