Neuroinflammation and Anxiety-Related Pathology: Apoptosis, Pyroptosis, and the Preclinical Potential of Paeoniflorin
- 1School of Traditional Chinese Medicine, Inner Mongolia Medical University, Hohhot 010110, China
Abstract
Anxiety disorders have a multifactorial pathophysiology involving neurotransmitter signaling, stress-responsive neuroendocrine systems, and distributed neural circuits. Neuroinflammation has emerged as an important component of this network, although its contribution varies across anxiety phenotypes and experimental contexts. Apoptosis and pyroptosis may contribute to cellular injury in selected preclinical models, but their causal roles in human anxiety disorders remain incompletely established. This review examines inflammatory signaling and cell-death pathways relevant to anxiety-related pathology and critically evaluates the evidence for paeoniflorin (PF), a monoterpene glycoside derived from Paeonia species. Particular attention is given to the tryptophan–kynurenine pathway, regional differences across amygdala, hippocampal, and prefrontal networks, and interactions among the hypothalamic–pituitary–adrenal axis, glucocorticoid signaling, and peripheral-to-central immune communication. PF-related changes in inflammatory, apoptotic, and pyroptotic markers are considered alongside neurochemical, neuroendocrine, and behavioral outcomes, with direct PF findings distinguished from evidence involving other interventions or disease models. Available studies support further investigation of PF as a preclinical candidate, rather than establishing clinically meaningful anxiolytic efficacy. Limitations in model validity, causal inference, dosing, bioavailability, and biomarker validation are discussed to guide mechanistic research and future clinical translation.
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BibTeX
@article{li2026neuroinflammation,
title = {{Neuroinflammation and Anxiety-Related Pathology: Apoptosis, Pyroptosis, and the Preclinical Potential of Paeoniflorin}},
author = {Chen Li and Qiumei Dong and Yajing Hou},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219549},
url = {https://www.mdpi.com/1422-0067/27/21/9549},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Neuroinflammation and Anxiety-Related Pathology: Apoptosis, Pyroptosis, and the Preclinical Potential of Paeoniflorin
AU - Chen Li
AU - Qiumei Dong
AU - Yajing Hou
PY - 2026
DA - 2026/10/26
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219549
UR - https://www.mdpi.com/1422-0067/27/21/9549
AB - Anxiety disorders have a multifactorial pathophysiology involving neurotransmitter signaling, stress-responsive neuroendocrine systems, and distributed neural circuits. Neuroinflammation has emerged as an important component of this network, although its contribution varies across anxiety phenotypes and experimental contexts. Apoptosis and pyroptosis may contribute to cellular injury in selected preclinical models, but their causal roles in human anxiety disorders remain incompletely established. This review examines inflammatory signaling and cell-death pathways relevant to anxiety-related pathology and critically evaluates the evidence for paeoniflorin (PF), a monoterpene glycoside derived from Paeonia species. Particular attention is given to the tryptophan–kynurenine pathway, regional differences across amygdala, hippocampal, and prefrontal networks, and interactions among the hypothalamic–pituitary–adrenal axis, glucocorticoid signaling, and peripheral-to-central immune communication. PF-related changes in inflammatory, apoptotic, and pyroptotic markers are considered alongside neurochemical, neuroendocrine, and behavioral outcomes, with direct PF findings distinguished from evidence involving other interventions or disease models. Available studies support further investigation of PF as a preclinical candidate, rather than establishing clinically meaningful anxiolytic efficacy. Limitations in model validity, causal inference, dosing, bioavailability, and biomarker validation are discussed to guide mechanistic research and future clinical translation.
SN - 1422-0067
ER -