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Updated: Mar 12, 2026
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Pinostrobin attenuates microglia-mediated neuroinflammation after subarachnoid hemorrhage through modulation of the
Qi Liu1, Yihan Wang2, Bingchuan Wang1
1Department of Neurosurgery, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, No. 89, Xianglin Road Section 1, Longmatan District, Luzhou, China.
Abstract:
Subarachnoid hemorrhage (SAH) is a life-threatening neurological emergency associated with high mortality and poor functional outcomes. Early brain injury (EBI) within the first 72 h critically influences prognosis, with excessive microglial activation representing a key contributor to neuroinflammation and secondary neuronal damage. Identifying pharmacological agents capable of modulating microglia-driven inflammatory responses remains an important therapeutic challenge. In this study, we investigated the potential anti-inflammatory mechanisms of pinostrobin (PIN), a natural flavonoid with reported neuroprotective properties. By integrating bioinformatics, network pharmacology, and machine learning approaches (LASSO, random forest, and SVM), MYC and CTSL were identified as candidate targets potentially linking PIN to SAH-related inflammatory pathways. Molecular docking and 50-ns molecular dynamics simulations suggested stable interactions between PIN and these proteins. Furthermore, in vitro evidence from LPS-stimulated BV2 microglial cells demonstrated that PIN reduced the expression of MYC, CTSL, NF-κB p65, and IL-1β, accompanied by attenuation of microglial inflammatory activation. Collectively, these findings suggest that PIN may modulate neuroinflammatory cascades relevant to EBI after SAH, potentially through regulation of the MYC-CTSL axis. This study provides integrative, hypothesis-generating insights into the microglia-targeted anti-inflammatory potential of PIN in the context of SAH.
Insights
Pinostrobin (PIN) shows potential in reducing inflammation after subarachnoid hemorrhage (SAH). This natural flavonoid may target microglial activation, offering a new avenue for treating early brain injury (EBI) and improving outcomes.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Subarachnoid hemorrhage (SAH) is a critical neurological emergency with high mortality.
- Early brain injury (EBI) significantly impacts SAH prognosis, driven by microglial activation and neuroinflammation.
- Targeting microglia-driven inflammation is a key challenge in SAH therapeutics.
Purpose of the Study:
- To investigate the anti-inflammatory mechanisms of pinostrobin (PIN), a natural flavonoid.
- To explore PIN's potential in modulating microglia-driven inflammatory responses in the context of SAH.
- To identify potential molecular targets of PIN relevant to SAH-induced neuroinflammation.
Main Methods:
- Bioinformatics, network pharmacology, and machine learning (LASSO, random forest, SVM) were used to identify candidate targets.
- Molecular docking and molecular dynamics simulations assessed PIN's interaction with identified targets.
- In vitro studies utilized LPS-stimulated BV2 microglial cells to evaluate PIN's effects on inflammatory markers.
Main Results:
- MYC and CTSL were identified as candidate targets linking PIN to SAH inflammatory pathways.
- PIN demonstrated stable interactions with MYC and CTSL proteins.
- In vitro, PIN reduced MYC, CTSL, NF-κB p65, and IL-1β expression, attenuating microglial activation.
Conclusions:
- Pinostrobin exhibits potential anti-inflammatory effects relevant to early brain injury following SAH.
- PIN may exert its neuroprotective effects by modulating the MYC-CTSL axis in microglia.
- This study offers hypothesis-generating insights into pinostrobin as a microglia-targeted therapy for SAH.
