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Published on: July 3, 2014
Sinomenine Protects against Early Brain Injury by Inhibiting Microglial Inflammatory Response via Nrf2-Dependent
Chuanjing Fu1, Heng Xin2, Zhengting Qian2
1Department of Neurosurgery, Jiangsu Hospital of Traditional Chinese Medicine, Nanjing 210029, China.
Abstract:
Microglial activation and sustained inflammation plays an important role in the processes of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Sinomenine (SIN) has been demonstrated to have neuroprotective effects in the traumatic brain injury (TBI) model. However, the role of SIN in SAH-induced EBI and its latent mechanisms remain unclear. This study was carried out to explore the role of SIN on SAH-induced EBI and its effects on the microglial inflammatory response following SAH. In this study, a model of SAH in rats was established. Modified neurological severity scores (mNSS), encephaledema, and Nissl staining were employed to determine the effects of SIN. Western blot and immunofluorescence analysis were performed to evaluate nuclear factor erythroid 2-related factor 2 (Nrf2) expression. Nrf2-related downstream proteins, including heme oxygenase-1 (HO-1) and quinine oxidoreductase-1 (NQO-1), were detected with immunohistochemistry analyses and Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR). Microglia activation and associated inflammatory factors, factor-kappa B (NF-κB), interleukin-1β (IL-1β), and interleukin-6 (IL-6), were assessed after SAH. The results showed that SIN administration improved neurobehavior function, and attenuated neural apoptosis and brain edema after SAH. In addition, SIN inhibited microglial action and the subsequent inflammatory response after SAH through the upregulated expression of HO-1 and NQO-1 via activation of the Nrf2 pathway. These results demonstrated that SIN supplementation provided protection against SAH-induced neuronal apoptosis by microglial inflammatory response regulation and possible involvement of the Nrf2 pathway.
Insights
Sinomenine (SIN) protects against early brain injury after subarachnoid hemorrhage (SAH) by reducing inflammation. It achieves this by activating the Nrf2 pathway, upregulating protective proteins, and inhibiting microglial activation.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Early brain injury (EBI) following subarachnoid hemorrhage (SAH) involves microglial activation and sustained inflammation.
- Sinomenine (SIN) shows neuroprotective effects in traumatic brain injury (TBI) models, but its role in SAH-induced EBI is unclear.
Purpose of the Study:
- To investigate the protective role of SIN in SAH-induced EBI.
- To elucidate the effects of SIN on microglial inflammatory responses and the underlying mechanisms.
Main Methods:
- SAH model in rats.
- Assessment of neurological function (mNSS), brain edema, and neuronal apoptosis (Nissl staining).
- Evaluation of Nrf2 pathway activation (Western blot, immunofluorescence), downstream proteins (HO-1, NQO-1 via IHC, RT-qPCR), and inflammatory markers (NF-κB, IL-1β, IL-6).
Main Results:
- SIN administration improved neurobehavioral scores, reduced brain edema, and attenuated neuronal apoptosis post-SAH.
- SIN inhibited microglial activation and inflammatory responses.
- SIN upregulated HO-1 and NQO-1 expression, indicating Nrf2 pathway activation.
Conclusions:
- SIN exerts neuroprotection against SAH-induced EBI.
- SIN mitigates neuronal apoptosis by regulating microglial inflammatory responses, potentially via the Nrf2 pathway.
