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DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses.

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Endothelial dysfunction, regarded as a key step in the pathophysiological course of diabetic vascular complications, is initiated and deteriorated by advanced glycation end products (AGEs). DL-3-n-butylphthalide (DL-NBP) has been proven to have protective effects on neurons and vascular endothelial

Dl-3-n-butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF-κB signalling.

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In this study, we examined the neuroprotective effects and anti-inflammatory properties of Dl-3-n-butylphthalide (NBP) in Sprague-Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro. Our results showed that

Inhibitory effects of chiral 3-n-butylphthalide on inflammation following focal ischemic brain injury in rats.

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OBJECTIVE To evaluate the degree of neutrophil infiltration into ischemic tissue after transient focal cerebral ischemia, and to examine the effects of chiral 3-n-butylphthalide (NBP) on this inflammatory process. METHODS After a 24-h reperfusion following transient cerebral ischemia, two different

Dl-3-n-butylphthalide Reduces Neurovascular Inflammation and Ischemic Brain Injury in Mice.

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Dl-3-n-butylphthalide (NBP) is a synthetic compound that has been approved for the treatment of ischemic stroke in China. The mechanisms underlying the treatment efficacy of NBP have been reported in multiple studies and remain controversial. Here, we show that NBP treatment attenuated ischemic

L-3-n-butylphthalide attenuates inflammation response and brain edema in rat intracerebral hemorrhage model

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L-3-n-butylphthalide(NBP), a compound found in Apium graveolens Linn seed extracts, has a therapeutic effect on acute ischemic stroke. The pathological inflammatory pathways and consequent brain edema in intracerebral hemorrhage (ICH) share some similar characteristics with ischemic stroke.

Dl-3-n-Butylphthalide Promotes Remyelination and Suppresses Inflammation by Regulating AMPK/SIRT1 and STAT3/NF-κB Signaling in Chronic Cerebral Hypoperfusion

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Demyelination in vascular dementia (VD) is partly attributable to inflammation induced by chronic cerebral hypoperfusion (CCH). Remyelination contributes to the recovery of cognitive impairment by inducing the proliferation and differentiation of oligodendrocyte progenitor cells. It was previously

3-N-butylphthalide (NBP) attenuates the amyloid-β-induced inflammatory responses in cultured astrocytes via the nuclear factor-κB signaling pathway.

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OBJECTIVE Activation of astrocytes is a common feature of Alzheimer's disease (AD). Proinflammatory molecules produced by activated astrocytes contribute to neuronal damage in AD. Moreover, dl-3-n-butylphthalide (NBP) has been reported to attenuate astroglial activation and exert neuroprotective

Multiple functional therapeutic effects of DL-3-n-butylphthalide in the cuprizone model of demyelination.

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Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). The disease mechanisms driving progressive MS remain unresolved. Without this information, current therapeutic strategies are unsatisfactory in preventing disease progression.

The Impact of Dl-3-n-butylphthalide on the Lipidomics of the Hippocampus in a Rat Model of Lipopolysaccharide-Induced Depression

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Elevated inflammation is commonly observed in depression, but whether this association is causal is not determined. Our previous basic research indicated that Dl-3-n-butylphthalide (NBP) possessed an anti-inflammatory effect. Additional recent evidence consistently suggests that depression is

UPLC-Q-TOF-MS profiling of the hippocampus reveals metabolite biomarkers for the impact of Dl-3-n-butylphthalide on the lipopolysaccharide-induced rat model of depression.

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An increasing body of evidence reveals that inflammation is involved in the pathological mechanisms of depression. Our previous basic research confirmed that Dl-3-n-butylphthalide (NBP) possess anti-inflammatory properties. However, studies investigating metabolite biomarkers for the

Butylphthalide has an Anti-Inflammatory Role in Spinal Cord Injury by Promoting Macrophage/Microglia M2 Polarization via p38 Phosphorylation.

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Experimental animal study of treatment of Spinal cord injury (SCI).This report aims to evaluate the in vivo effects of Butylphthalide NBP) on SCI biology and to explore its potential mechanism.Spinal cord injury (SCI) causes

Protective effects of DL‑3‑n‑butylphthalide in the lipopolysaccharide‑induced mouse model of Parkinson's disease.

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DL‑3‑n‑butylphthalide (NBP) is extracted from rapeseed and exhibits multiple neuroprotective effects, exerted by inhibiting the inflammatory process, including reducing oxidative stress, improving mitochondrial function and reducing neuronal apoptosis. The present study aimed to investigate the

DL-3-n-butylphthalide attenuates lipopolysaccharide-induced acute lung injury via SIRT1-dependent and -independent regulation of Nrf2.

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The acute respiratory distress syndrome (ARDS), a devastating clinical syndrome, is one of the most severe complications of acute lung injury (ALI). Despite of decades of clinical trials and supportive ventilation strategies, the incidence and mortality of ALI/ARDS remain high. DL-3-n-butylphthalide

N-Butylphthalide (NBP) ameliorated cerebral ischemia reperfusion-induced brain injury via HGF-regulated TLR4/NF-κB signaling pathway.

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N-Butylphthalide (NBP) has been known to have potential neuroprotective effects in Alzheimer's disease and stroke animal models. Hepatocyte-growth factor (HGF), with strong angiogenic properties, exerted protective role in brain injury. The present study was aimed to investigate the possible

L-3-n-Butylphthalide attenuates neuroinflammatory responses by downregulating JNK activation and upregulating Heme oxygenase-1 in lipopolysaccharide-treated mice.

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Microglia activation-induced neuroinflammation contributes to neuronal damage in neurodegenerative diseases. Inhibition of microglia activation and reduction of major neurotoxic cytokines have been becoming a therapeutic strategy for neurodegenerative diseases. L-3-n-Butylphthalide (L-NBP) has shown

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