Sinomenine inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage
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Updated: Apr 30, 2026
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Zhao Yang1, Yongping Liu1, Fang Yuan1
1Department of Neurosurgery, The 476th Hospital of PLA, Fuzhou, Fujian 350025, China.
Abstract:
Intracerebral hemorrhage (ICH) causes morbidity and mortality and commonly follows the reperfusion after an ischemic event. Microglial activation mediated cytokine and protease secretion contributes to brain injury in ICH. Previous studies have shown that sinomenine possesses potent immunoregulatory properties. However, little is known about its exact role in ICH. In the present study, to investigate the effect of sinomenine on microglial cells inflammation, we treated ICH-challenged BV2 microglial cells with sinomenine in vitro, and explored its neuroprotection role in intracerebral hemorrhage in vivo. Changes in inflammatory cytokines, such as TNF-α, IL-1β and IL-6, reactive oxygen species (ROS) and NF-κB activation NF-κB were observed. In addition, the neurological deficit and cerebral water content of ICH mice were studied. The results demonstrated that sinomenine could inhibit the release of these cytokines and attenuate ROS production in a dose-dependent manner, and reduce NF-κB activation. Furthermore, sinomenine markedly inhibited cerebral water content and neurological deficit. In conclusion, our findings suggest that sinomenine played the protective effects through inhibition of microglial inflammation, and the findings also provided a novel therapy to treat ICH induced brain injury.
Insights
Sinomenine effectively reduces brain inflammation and injury following intracerebral hemorrhage (ICH). This study shows sinomenine inhibits microglial activation, decreasing harmful cytokines and reactive oxygen species, offering a potential new treatment for ICH brain damage.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Intracerebral hemorrhage (ICH) leads to significant morbidity and mortality, often exacerbated by microglial activation and subsequent inflammation.
- Sinomenine is known for its immunoregulatory properties, but its specific role in ICH-induced brain injury remains unclear.
Purpose of the Study:
- To investigate the anti-inflammatory effects of sinomenine on microglial cells in vitro.
- To evaluate the neuroprotective potential of sinomenine in an in vivo model of intracerebral hemorrhage.
Main Methods:
- BV2 microglial cells were challenged to induce ICH, then treated with sinomenine.
- In vivo studies involved an intracerebral hemorrhage mouse model treated with sinomenine.
- Assessed inflammatory cytokines (TNF-α, IL-1β, IL-6), reactive oxygen species (ROS), NF-κB activation, neurological deficit, and cerebral water content.
Main Results:
- Sinomenine dose-dependently inhibited the release of inflammatory cytokines and reduced ROS production in microglial cells.
- Sinomenine significantly decreased NF-κB activation.
- Treatment with sinomenine markedly reduced cerebral water content and improved neurological deficits in ICH mice.
Conclusions:
- Sinomenine exerts protective effects against intracerebral hemorrhage by inhibiting microglial inflammation.
- These findings suggest sinomenine as a potential novel therapeutic agent for treating ICH-induced brain injury.
