Multiplex Immunofluorescence-Based Investigation of the Interventional Effect of Bisdemethoxycurcumin on Glial Cell Polarization in Radiation-Induced Brain Injury
- 1School of Pharmacy, Shanxi Medical University, Taiyuan 030001, China
Abstract
Radiation-induced brain injury (RIBI) is a severe and common complication following radiotherapy for intracranial tumors, primarily manifested as brain tissue damage, neuroinflammation, and cognitive dysfunction. Currently, clinically effective therapeutic options remain lacking, severely compromising patient prognosis and quality of life. Bisdemethoxycurcumin (BDMC) is a highly stable active derivative of curcumin with antioxidant, anti-inflammatory, and neuroprotective properties. However, the therapeutic effect and underlying mechanisms of BDMC against RIBI remain poorly defined. Objective: To investigate the neuroprotective effects of BDMC on RIBI in rats and to elucidate the molecular mechanisms that regulate glial cell polarization. Methods: Forty SPF-grade male Sprague–Dawley (SD) rats were randomly assigned to four groups (n = 12 per group): control, model, amifostine (AMF) and BDMC. A rat RIBI model was established by whole-brain irradiation with a single dose of 30 Gy X-rays, followed by the respective drug interventions. After 4 consecutive weeks of treatment, body weight was recorded, and brain water content and oxidative-stress indicators in brain tissue were quantified. Hematoxylin–eosin (HE) staining was performed to assess pathological injury in brain tissues. Multiplex immunohistochemistry (mIHC) was employed to quantitatively analyze the polarization states of microglia and astrocytes in the cerebral cortex, hippocampus, and thalamus. Results: Radiation-induced RIBI induced body-weight loss, cerebral edema, and cerebral oxidative-stress disturbance in rats, accompanied by neuronal edema, degeneration, and necrosis. Concurrently, microglia and astrocytes were activated in multiple brain regions, with glial polarization shifting toward the pro-inflammatory CD86+ microglia and C3+ astrocyte states and disrupting the cerebral microenvironment. BDMC intervention improved the overall condition of the rats, attenuated cerebral edema and oxidative-stress damage, and ameliorated neuronal pathological lesions. Furthermore, BDMC suppressed excessive glial activation, reversed the CD86+ microglia/CD206+ microglia and C3+ astrocyte/S100A10+ astrocyte polarization imbalance, and attenuated neuroinflammation. Conclusion: BDMC exerts significant neuroprotective effects in RIBI rats, potentially through the inhibition of cerebral oxidative stress and the maintenance of glial cell polarization homeostasis across multiple brain regions.
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BibTeX
@article{zhang2026multiplex,
title = {{Multiplex Immunofluorescence-Based Investigation of the Interventional Effect of Bisdemethoxycurcumin on Glial Cell Polarization in Radiation-Induced Brain Injury}},
author = {Tianrui Zhang and Ziying Geng and Jianhua Chen and Jianhua Li and Zongtai Han and Fangping Han and Jianguo Li},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16101424},
url = {https://www.mdpi.com/2218-273X/16/10/1424},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Multiplex Immunofluorescence-Based Investigation of the Interventional Effect of Bisdemethoxycurcumin on Glial Cell Polarization in Radiation-Induced Brain Injury
AU - Tianrui Zhang
AU - Ziying Geng
AU - Jianhua Chen
AU - Jianhua Li
AU - Zongtai Han
AU - Fangping Han
AU - Jianguo Li
PY - 2026
DA - 2026/10/01
JO - Biomolecules
DO - 10.3390/biom16101424
UR - https://www.mdpi.com/2218-273X/16/10/1424
AB - Radiation-induced brain injury (RIBI) is a severe and common complication following radiotherapy for intracranial tumors, primarily manifested as brain tissue damage, neuroinflammation, and cognitive dysfunction. Currently, clinically effective therapeutic options remain lacking, severely compromising patient prognosis and quality of life. Bisdemethoxycurcumin (BDMC) is a highly stable active derivative of curcumin with antioxidant, anti-inflammatory, and neuroprotective properties. However, the therapeutic effect and underlying mechanisms of BDMC against RIBI remain poorly defined. Objective: To investigate the neuroprotective effects of BDMC on RIBI in rats and to elucidate the molecular mechanisms that regulate glial cell polarization. Methods: Forty SPF-grade male Sprague–Dawley (SD) rats were randomly assigned to four groups (n = 12 per group): control, model, amifostine (AMF) and BDMC. A rat RIBI model was established by whole-brain irradiation with a single dose of 30 Gy X-rays, followed by the respective drug interventions. After 4 consecutive weeks of treatment, body weight was recorded, and brain water content and oxidative-stress indicators in brain tissue were quantified. Hematoxylin–eosin (HE) staining was performed to assess pathological injury in brain tissues. Multiplex immunohistochemistry (mIHC) was employed to quantitatively analyze the polarization states of microglia and astrocytes in the cerebral cortex, hippocampus, and thalamus. Results: Radiation-induced RIBI induced body-weight loss, cerebral edema, and cerebral oxidative-stress disturbance in rats, accompanied by neuronal edema, degeneration, and necrosis. Concurrently, microglia and astrocytes were activated in multiple brain regions, with glial polarization shifting toward the pro-inflammatory CD86+ microglia and C3+ astrocyte states and disrupting the cerebral microenvironment. BDMC intervention improved the overall condition of the rats, attenuated cerebral edema and oxidative-stress damage, and ameliorated neuronal pathological lesions. Furthermore, BDMC suppressed excessive glial activation, reversed the CD86+ microglia/CD206+ microglia and C3+ astrocyte/S100A10+ astrocyte polarization imbalance, and attenuated neuroinflammation. Conclusion: BDMC exerts significant neuroprotective effects in RIBI rats, potentially through the inhibition of cerebral oxidative stress and the maintenance of glial cell polarization homeostasis across multiple brain regions.
SN - 2218-273X
ER -