Maraviroc Attenuates Neuronal Apoptosis by Inhibiting CCR5-Mediated Microglial Activation After Subarachnoid Hemorrhage.

Jiasen Ye, Hangyang Li, Zhenghong Peng, Zuoyue Duan, Qiang Chen, Yong Jiang, Tianqi Tu, Jianhua Peng

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Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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8 authors.

Jiasen Ye *Department of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China.

Hangyang Li *Department of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China.

Zhenghong Peng *Laboratory of Neurological Diseases and Brain Function, The Affiliated Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, China.

Zuoyue DuanLaboratory of Neurological Diseases and Brain Function, The Affiliated Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, China.

Qiang ChenDepartment of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China.

Yong JiangDepartment of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China.

Tianqi TuDepartment of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China. tutianqineurosci@sina.com.

Jianhua PengDepartment of Neurosurgery, The Affiliated Hospital, Southwest Medical University, NO. 25 of Taiping Street, Luzhou, 646000, Sichuan, China. pengjianhua@swmu.edu.cn.

Funding

National Natural Science Foundation of China 82271306

6 · The paper itself

Abstract

Subarachnoid hemorrhage (SAH) triggers robust neuroinflammatory responses that contribute to secondary brain injury, with microglia acting as central mediators; however, the upstream regulators governing microglial activation remain incompletely understood. To address this, we investigated the role of C-C chemokine receptor 5 (CCR5) using a murine endovascular perforation SAH model. Expression profiling revealed that CCR5 is rapidly upregulated after SAH, with prominent expression in microglia in the cortex and perilesional region. We then evaluated the therapeutic efficacy of pharmacological inhibition using the intranasal CCR5 antagonist maraviroc (MVC). MVC treatment successfully shifted microglia toward an anti-inflammatory phenotype and reduced pro-inflammatory cytokines. This inflammatory modulation attenuated brain edema, suppressed neuronal apoptosis, and significantly improved both early and long-term neurological outcomes. Furthermore, in vitro experiments confirmed that MVC reverses oxyhemoglobin-induced pro-inflammatory microglial polarization, indirectly protecting neurons from microglia-dependent injury. Collectively, these findings identify CCR5 as an important regulator of microglia-associated neuroinflammation after SAH and suggest that MVC exerts neuroprotection, at least in part, through modulation of the CCR5-related inflammatory microenvironment.

Indexed as

ApoptosisCCR5 Receptor AntagonistsMaravirocMicrogliaNeuronsReceptors, CCR5Subarachnoid HemorrhageAnimalsMaleMiceMice, Inbred C57BLNeuroinflammatory DiseasesNeuroprotective AgentsCCR5 protein, mouseCCR5 Receptor AntagonistsMaravirocNeuroprotective AgentsReceptors, CCR5CCR5MaravirocMicrogliaNeuroinflammationSubarachnoid hemorrhage

Identifiers

PMID42159851

DOI10.1161/strokeaha.123.044422

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.