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neuroprotection 5

cerebral ischemia 2

GABA 1

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acute ischemic stroke 1

antioxidant 1

chronic ocular hypertension 1

conditioned 1

fastigial neucleus 1

glaucoma 1

grape seed lignin 1

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Fastigial Nucleus Electrical Stimulation and Central Neurogenic Neuroprotection

Dong Weiwei

Strategic Study of CAE 2001, Volume 3, Issue 11,   Pages 32-38

Abstract: The first ome mediates a reflex neurogenic neuroprotection, which is associated with oxygen-sensitiveThe second is conditioned central neurogenic neuroprotection, which is represented in intrinsic neuronselectrical excitation of intrinsic neurons of fastigial nucleus and afford a persisting for almost two weeks neuroprotectionThis mode of neuroprotection is not restricted to focal ischmia,it also protects the brain against global

Keywords： neuroprotection     conditioned     fastigial neucleus     stimulation     cerebral ischemia    

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A modified chronic ocular hypertension rat model for retinal ganglion cell neuroprotection

Lichun Zhong

Frontiers of Medicine 2013, Volume 7, Issue 3,   Pages 367-377 doi: 10.1007/s11684-013-0266-2

Abstract:

This study aimed to modify a chronic ocular hypertension (OHT) rat model to screen for potential compounds to protect retinal ganglion cells (RGCs) from responding to increased intraocular pressure (IOP). A total of 266 rats were prepared and randomly grouped according to different time-points, namely, weeks 3, 8, 16, and 24. Rats were sedated and eye examination was performed to score as the corneal damage on a scale of 1 to 4. The OHT rat model was created via the injection of a hypertonic saline solution into the episcleral veins once weekly for two weeks. OHT was identified when the IOP at week 0 was≥6 mmHg than that at week -2 for the same eye. Viable RGCs were labeled by injecting 4% FluoroGold. Rats were sacrificed, and the eyes were enucleated and fixed. The fixed retinas were dissected to prepare flat whole-mounts. The viable RGCs were visualized and imaged. The IOP (meanβ±βSD) was calculated, and data were analyzed by the paired t-test and one-way ANOVA. The OHT model was created in 234 of 266 rats (87.97%), whereas 32 rats (12.03%) were removed from the study because of the absence of IOP elevation (11.28%) and/or corneal damage scores over 4 (0.75%). IOP was elevated by as much as 81.35% for 24 weeks. The average IOP was (16.68β±β0.98)βmmHg in non-OHT eyes (n = 234), but was (27.95±0.97)βmmHg in OHT eyes (n = 234). Viable RGCs in the OHT eyes were significantly decreased in a time-dependent manner by 29.41%, 38.24%, 55.32%, and 59.30% at weeks 3, 8, 16, and 24, respectively, as compared to viable RGCs in the non-OHT eyes (P<β0.05). The OHT model was successfully created in 88% of the rats. The IOP in the OHT eyes was elevated by approximately 81% for 24 weeks. The number of viable RGCs was decreased by 59% of the rats in a time-dependent manner. The modified OHT model may provide an effective and reliable method for screening drugs to protect RGCs from glaucoma.

Keywords： chronic ocular hypertension     intraocular pressure     retinal ganglion cells     neuroprotection     glaucoma    

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Leonurine protects ischemia-induced brain injury via modulating SOD, MDA and GABA levels

Shilei ZHENG, Jingru ZHU, Jiao LI, Shuang ZHANG, Yunfei MA

Frontiers of Agricultural Science and Engineering 2019, Volume 6, Issue 2,   Pages 197-205 doi: 10.15302/J-FASE-2018245

Abstract:

The present study was designed to investigate the protective effects of leonurine, a compound purified from that is active on ischemic rat behavior and cortical neurons, and explore the underlying mechanism. The general rat activity, cortical neuron morphology, superoxide dismutase (SOD), malondialdehyde (MDA), -aminobutyric acid (GABA) and glutamate decarboxylase 67 (GAD67) levels were measured. We found leonurine significantly improve the general activity of rats in an open-field test, which was associated with attenuated neuronal damage induced by ischemia. Moreover, serum SOD activity was significantly greater, MDA level lower in the leonurine group as compared with ischemia group. In addition, GABA content in the cerebral cortex was significantly greater in high-dose leonurine group. Correspondingly, GAD67 protein level coincided with the GABA level. Taken together, our results demonstrated that leonurine attenuated brain injury during ischemia via antioxidative and anti-excitotoxicity effects by targeting GABA and leonurine might become a useful adjuvant neuroprotective agent.

Keywords： cerebral ischemia     GABA     neuroprotection     leonurine     SOD    

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Protective effects of lignin fractions obtained from grape seeds against bisphenol AF neurotoxicity via antioxidative effects mediated by the Nrf2 pathway

Frontiers of Chemical Science and Engineering 2023, Volume 17, Issue 7,   Pages 976-989 doi: 10.1007/s11705-022-2237-0

Abstract: However, its neuroprotection capability has rarely been studied.

Keywords： grape seed lignin     structure     antioxidant     NE-4C cells     neuroprotection    

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Neuroprotective effects of Ginkgo biloba extract and Ginkgolide B against oxygen–glucose deprivation/reoxygenation and glucose injury in a new in vitro multicellular network model

Xiaohan Yang, Tiezheng Zheng, Hao Hong, Nan Cai, Xiaofeng Zhou, Changkai Sun, Liying Wu, Shuhong Liu, Yongqi Zhao, Lingling Zhu, Ming Fan, Xuezhong Zhou, Fengxie Jin

Frontiers of Medicine 2018, Volume 12, Issue 3,   Pages 307-318 doi: 10.1007/s11684-017-0547-2

Abstract:

Acute ischemic stroke (AIS), as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of extract (GBE) against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel rat cortical capillary endothelial cell-astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B (GB), against oxygen–glucose deprivation/reoxygenation and glucose (OGD/R) injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein (Na-F), and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury ; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.

Keywords： acute ischemic stroke     Ginkgo bilobaextract     Ginkgolide B     network model     neuroprotection    

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Title Author Date Type Operation

Fastigial Nucleus Electrical Stimulation and Central Neurogenic Neuroprotection

Dong Weiwei

Journal Article

A modified chronic ocular hypertension rat model for retinal ganglion cell neuroprotection

Lichun Zhong

Journal Article

Leonurine protects ischemia-induced brain injury via modulating SOD, MDA and GABA levels

Shilei ZHENG, Jingru ZHU, Jiao LI, Shuang ZHANG, Yunfei MA

Journal Article

Protective effects of lignin fractions obtained from grape seeds against bisphenol AF neurotoxicity via antioxidative effects mediated by the Nrf2 pathway

Journal Article

Neuroprotective effects of Ginkgo biloba extract and Ginkgolide B against oxygen–glucose deprivation/reoxygenation and glucose injury in a new in vitro multicellular network model

Xiaohan Yang, Tiezheng Zheng, Hao Hong, Nan Cai, Xiaofeng Zhou, Changkai Sun, Liying Wu, Shuhong Liu, Yongqi Zhao, Lingling Zhu, Ming Fan, Xuezhong Zhou, Fengxie Jin

Journal Article