L‐3‐n‐butylphthalide Promotes Neurogenesis and Neuroplasticity in Cerebral Ischemic Rats

Yang, Lichao; Li, Jiang; Xu, Shixiao; Cai, Jie; Lei, Hui; Li, Dongmei; Zhang, Man; Rong, Xianfang; Cui, Dandan; Wang, Ling; Peng, Ying; Wang, Xiaoliang

doi:10.1111/cns.12438

Cited by 67 publications

(60 citation statements)

References 32 publications

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“…It has been hypothesized that there is a possibility of migration of newborn precursor cells to the damage areas prior to maturation. However, the downfall is that newly generated cells hardly survive [29]. A recent study stated that dl-NBP stimulates the angiogenic process and protects the brain microvascular endothelial cells (BMECs) against oxygen glucose deprivation (OGD), by means of an increase of HIF-1 α and Bcl-2 expressions [24].…”

Section: Nbp and Ischemic Strokementioning

confidence: 99%

“…A recent study stated that dl-NBP stimulates the angiogenic process and protects the brain microvascular endothelial cells (BMECs) against oxygen glucose deprivation (OGD), by means of an increase of HIF-1 α and Bcl-2 expressions [24]. Additionally, studies on newborn neural cells showed that l-NBP improves their proliferation, survival, and differentiation [29]. The underlying process has been described as through an increase of 5-bromo-2′-deoxyuridine- (BRdU-) positive cells in the dentate gyrus of damaged areas.…”

Section: Nbp and Ischemic Strokementioning

confidence: 99%

“…The underlying process has been described as through an increase of 5-bromo-2′-deoxyuridine- (BRdU-) positive cells in the dentate gyrus of damaged areas. Furthermore, an increase in growth-associated protein-43 (GAP-43) expression, cAMP response element-binding protein (CREB) activity, and synaptophysin was also observed, indicating the possibility of a positive effect of l-NBP on neurogenesis, newborn neurons survival, and neuroplasticity [29]. Recent studies have been more focused on the effects of NBP on tandem-pore-domain potassium channels.…”

Section: Nbp and Ischemic Strokementioning

confidence: 99%

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A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

Abdoulaye

Guo

2016

BioMed Research International

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The research of alternative treatment for ischemic stroke and degenerative diseases has always been a priority in neurology. 3-N-Butylphthalide (NBP), a family of compounds initially isolated from the seeds of Apium graveolens Linn., has shown significant neuroprotective effects. Previous extensive studies have demonstrated that NBP promotes a better poststroke outcome and exerts a multitargeted action on several mechanisms, from oxidative stress to mitochondrial dysfunction to apoptosis to inflammation. Additionally, recent findings on several neurological disorders have shown that NBP's beneficial effects extend beyond the management of stroke. However, despite the increasing number of studies toward a better understanding and the rapid advances made in therapeutic options, to date, dl-3-N-butylphthalide, a synthetic variation of l-3-N-butylphthalide, remains the only clinically approved anti-ischemic agent in China, stressing the difficulties for a viable and effective transition from experimental to clinical practice. Events indicate that NBP, due to its multitargeted effect and the adaptability of its basic structure, can be an important game changer and a precursor to a whole new therapeutic approach to several neurological conditions. The present review discusses recent advances pertaining to the neuroprotective mechanisms of NBP-derived compounds and the possibility of their clinical implementation in the management of various neurological conditions.

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Section: Nbp and Ischemic Strokementioning

confidence: 99%

Section: Nbp and Ischemic Strokementioning

confidence: 99%

Section: Nbp and Ischemic Strokementioning

confidence: 99%

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A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

Abdoulaye

Guo

2016

BioMed Research International

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“…N -butylphthalide (NBP), a new drug extracted from celery seeds (see Figure 1 ), was approved by China Food and Drug Administration in 2002. To date, many experiments confirm that NBP treatment could significantly reduce oxidative damage, regulate energy metabolism, and alleviate cerebral edema in acute focal cerebral ischemia rats, protecting mitochondria function from brain damage directly through BBB in patients with acute and chronic cerebral ischemia and dementia (Yang et al, 2015). Meanwhile, NBP had also positive effects in stabilizing the NVUs and improving the neurological deficits through its primary target vascular endothelium (Li et al, 2007; Thored et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

N-Butylphthalide Alleviates Blood–Brain Barrier Impairment in Rats Exposed to Carbon Monoxide

Zhang

Guo

et al. 2016

Front. Pharmacol.

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Carbon monoxide (CO) poisoning is one of the most important health concerns and may result in neuropathologic changes and neurologic sequelae. However, few studies have addressed the correlation between CO poisoning and blood–brain barrier (BBB) impairment. In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. The results indicated that the brain water content was obviously increased, and the tight junctions between endothelial cells were disrupted, resulting in significant cerebral edema and BBB dysfunction in a rat model of CO poisoning. Meanwhile, the ultrastructure of endothelial cells and pericytes was seriously damaged, and the expressions of ZO-1 and claudin-5 were decreased at an early stage (<7 days). NBP treatment could efficiently maintain the ultrastructural and functional integrity of BBB, alleviate cerebral edema. Besides, NBP could also markedly increase the levels of both ZO-1 and claudin-5 proteins compared with those in rats exposed to CO (P < 0.05), whereas NBP had no apparent regulatory effect on AQP-4 expression. Taken together, this study highlights the importance of ZO-1 and claudin-5 proteins in maintaining BBB ultrastructure and function after CO poisoning. NBP, as a novel treatment approach, may effectively inhibit the down-regulation of ZO-1 and claudin-5 proteins (but not AQP-4), thereby preserving the barrier function and reducing cerebral edema after CO poisoning.

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“…The treatment mechanisms of butylphthalide include mobilization of circulating endothelial progenitor cells [12] and promoting neurogenesis and neuroplasticity in the brain. [13] In addition, previous study has shown that butylphthalide has a neuroprotective effect in rats after acute CO poisoning. [14] We speculated that a combined therapy of MSC transplantation and butylphthalide might have a promising treatment outcome for DEACMP.…”

Section: Introductionmentioning

confidence: 99%

Combination of butylphthalide with umbilical mesenchymal stem cells for the treatment of delayed encephalopathy after carbon monoxide poisoning

Wang¹,

Li²,

Wu³

et al. 2016

Medicine

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Delayed encephalopathy after carbon monoxide (CO) poisoning (DEACMP) is still a clinical challenge. This study aimed to investigate the efficacy of combined therapy of mesenchymal stem cell (MSC) transplantation and butylphthalide in DEACMP patients.Forty-two DEACMP patients were treated with 1 of the 3 therapies: combined therapy of MSC transplantation and butylphthalide; MSC transplantation alone; or hyperbaric oxygen therapy. The MSCs were alternatively injected into the subarachnoid space and the carotid artery using a self-made high-pressure injector. The Mini-Mental State Examination and the Barthel index of activities of daily living were administered before the treatment, and at 1 month, 3 months, and 6 months after the treatment. Computed tomography and magnetic resonance imaging results before and after the treatment were compared.At 1 month, 3 months, and 6 months after the treatment, the Mini-Mental State Examination scores and the Barthl scores were significantly higher in patients with the combined therapy of MSC transplantation and butylphthalide than those in patients with MSC transplantation alone or hyperbaric oxygen therapy (all P < 0.0001). No significant adverse events occurred.The combination of MSC transplantation and butylphthalide is safe and effective in treating DEACMP.

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L‐3‐n‐butylphthalide Promotes Neurogenesis and Neuroplasticity in Cerebral Ischemic Rats

Abstract: It first demonstrates that l-NBP may improve the behavioral outcome of cerebral ischemia by promoting neurogenesis and neuroplasticity. Activation of CREB and Akt and inhibition of STAT3 signaling might be involved in.

Cited by 67 publications

References 32 publications

A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

N-Butylphthalide Alleviates Blood–Brain Barrier Impairment in Rats Exposed to Carbon Monoxide

Combination of butylphthalide with umbilical mesenchymal stem cells for the treatment of delayed encephalopathy after carbon monoxide poisoning

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