Reduction of inflammatory responses by l-serine treatment leads to neuroprotection in mice after traumatic brain injury

Zhai, Peipei; Xu, Lihua; Yang, Juanjuan; Jiang, Zheng‐Lin; Zhao, Guang-Wei; Sun, Lixia; Wang, Guohua; Li, Xia

doi:10.1016/j.neuropharm.2015.02.026

Cited by 36 publications

(22 citation statements)

References 59 publications

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“…Furthermore, we observed maximal levels of TNF-α and IL-1β on the 3 rd and 1 st days, respectively, following TBI. These results are consistent with previous reports 10 22 . The increased levels of pro-inflammatory cytokines (e.g., TNF-α and IL-1β) that were released in the brain after TBI resulted in the expansion of secondary damage.…”

Section: Discussionsupporting

confidence: 94%

“…TNF-α is the central cytokine that initiates and regulates the inflammatory response 21 . IL-1β plays an important role in the development and progression of the cellular inflammatory cascade 22 . In addition, microglia/macrophages that are present in brain tissue after trauma are activated and persist as the M1 phenotype, which primarily produce pro-inflammatory cytokines (e.g., TNF-α and IL-1β) during the chronic phase 10 .…”

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confidence: 99%

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Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway

Xing

Xia

Peng

et al. 2016

Sci Rep

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Neuroinflammation is central to the pathology of traumatic brain injury (TBI). Xuefu Zhuyu decoction (XFZY) is an effective traditional Chinese medicine to treat TBI. To elucidate its potential molecular mechanism, this study aimed to demonstrate that XFZY functions as an anti-inflammatory agent by inhibiting the PI3K-AKT-mTOR pathway. Sprague-Dawley rats were exposed to controlled cortical impact to produce a neuroinflammatory response. The treatment groups received XFZY (9 g/kg and 18 g/kg), Vehicle group and Sham group were gavaged with equal volumes of saline. The modified neurologic severity score (mNSS) and the Morris water maze test were used to assess neurological deficits. Arachidonic acid (AA) levels in brain tissue were measured using tandem gas chromatography-mass spectrometry. TNF-α and IL-1β levels in injured ipsilateral brain tissue were detected by ELISA. AKT and mTOR expression were measured by western blot analysis. The results indicated that XFZY significantly enhanced spatial memory acquisition. XFZY (especially at a dose of 9 g/kg) markedly reduced the mNSS and levels of AA, TNF-α and IL-1β. Significant downregulation of AKT/mTOR/p70S6K proteins in brain tissues was observed after the administration of XFZY (especially at a dose of 9 g/kg). XFZY may be a promising therapeutic strategy for reducing inflammation in TBI.

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Section: Discussionsupporting

confidence: 94%

mentioning

confidence: 99%

Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway

Xing

Xia

Peng

et al. 2016

Sci Rep

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“…The sections (randomly chosen) were processed through different baths in the following order (and time): 100% ethanol (30 s), 95% ethanol (30 s), 70% ethanol (30 s), distilled water (30 s, three times), cresyl violet (56°C, 1 h), neutral differentiation solution (2 min), 100% ethanol (30 s), xylene (1 min); the samples were then mounted with neutral balata and covered with a coverslip (Zhai et al, 2015). The Nissl staining sections were visualized on a OLYMPUS SZX9 and BX51 microscope (Tokyo, Japan) with a digital camera.…”

Section: Methodsmentioning

confidence: 99%

Osthole Stimulated Neural Stem Cells Differentiation into Neurons in an Alzheimer's Disease Cell Model via Upregulation of MicroRNA-9 and Rescued the Functional Impairment of Hippocampal Neurons in APP/PS1 Transgenic Mice

Gao

Wang

et al. 2017

Front. Neurosci.

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Alzheimer's disease (AD) is the most serious neurodegenerative disease worldwide and is characterized by progressive cognitive impairment and multiple neurological changes, including neuronal loss in the brain. However, there are no available drugs to delay or cure this disease. Consequently, neuronal replacement therapy may be a strategy to treat AD. Osthole (Ost), a natural coumarin derivative, crosses the blood-brain barrier and exerts strong neuroprotective effects against AD in vitro and in vivo. Recently, microRNAs (miRNAs) have demonstrated a crucial role in pathological processes of AD, implying that targeting miRNAs could be a therapeutic approach to AD. In the present study, we investigated whether Ost could enhance cell viability and prevent cell death in amyloid precursor protein (APP)-expressing neural stem cells (NSCs) as well as promote APP-expressing NSCs differentiation into more neurons by upregulating microRNA (miR)-9 and inhibiting the Notch signaling pathway in vitro. In addition, Ost treatment in APP/PS1 double transgenic (Tg) mice markedly restored cognitive functions, reduced Aβ plague production and rescued functional impairment of hippocampal neurons. The results of the present study provides evidence of the neurogenesis effects and neurobiological mechanisms of Ost against AD, suggesting that Ost is a promising drug for treatment of AD or other neurodegenerative diseases.

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“…The release of inflammatory cytokines in cells after injury is a normal immune response, but the overexpression of some pro-inflammatory cytokines, such as IL-6 and TNF-a, are detrimental to wound recovery ( Zhai et al, 2015 ). A previous study by Zhang et al (2015) reports that ARC decreased lipopolysaccharide (LPS)-induced acute lung inflammation, infiltration of inflammatory cells into bronchoalveolar lavage fluid, and production of pro-inflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

“…However, some anti-inflammatory cytokines, such as IL-10, are beneficial to injury recovery ( Zhai et al, 2015 ). Thus, a drug that would increase favorable cytokines and reduce adverse cytokines is best for disease recovery.…”

Section: Introductionmentioning

confidence: 99%

Arctigenin Treatment Protects against Brain Damage through an Anti-Inflammatory and Anti-Apoptotic Mechanism after Needle Insertion

Song

Yang

et al. 2016

Front. Pharmacol.

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Convection enhanced delivery (CED) infuses drugs directly into brain tissue. Needle insertion is required and results in a stab wound injury (SWI). Subsequent secondary injury involves the release of inflammatory and apoptotic cytokines, which have dramatic consequences on the integrity of damaged tissue, leading to the evolution of a pericontusional-damaged area minutes to days after in the initial injury. The present study investigated the capacity for arctigenin (ARC) to prevent secondary brain injury and the determination of the underlying mechanism of action in a mouse model of SWI that mimics the process of CED. After CED, mice received a gavage of ARC from 30 min to 14 days. Neurological severity scores (NSS) and wound closure degree were assessed after the injury. Histological analysis and immunocytochemistry were used to evaluated the extent of brain damage and neuroinflammation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was used to detect universal apoptosis. Enzyme-linked immunosorbent assays (ELISA) was used to test the inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10) and lactate dehydrogenase (LDH) content. Gene levels of inflammation (TNF-α, IL-6, and IL-10) and apoptosis (Caspase-3, Bax and Bcl-2) were detected by reverse transcription-polymerase chain reaction (RT-PCR). Using these, we analyzed ARC’s efficacy and mechanism of action. Results: ARC treatment improved neurological function by reducing brain water content and hematoma and accelerating wound closure relative to untreated mice. ARC treatment reduced the levels of TNF-α and IL-6 and the number of allograft inflammatory factor (IBA)- and myeloperoxidase (MPO)-positive cells and increased the levels of IL-10. ARC-treated mice had fewer TUNEL+ apoptotic neurons and activated caspase-3-positive neurons surrounding the lesion than controls, indicating increased neuronal survival. Conclusions: ARC treatment confers neuroprotection of brain tissue through anti-inflammatory and anti-apoptotic effects in a mouse model of SWI. These results suggest a new strategy for promoting neuronal survival and function after CED to improve long-term patient outcome.

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Reduction of inflammatory responses by l-serine treatment leads to neuroprotection in mice after traumatic brain injury

Cited by 36 publications

References 59 publications

Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway

Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway

Osthole Stimulated Neural Stem Cells Differentiation into Neurons in an Alzheimer's Disease Cell Model via Upregulation of MicroRNA-9 and Rescued the Functional Impairment of Hippocampal Neurons in APP/PS1 Transgenic Mice

Arctigenin Treatment Protects against Brain Damage through an Anti-Inflammatory and Anti-Apoptotic Mechanism after Needle Insertion

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