Lotus Seedpod Proanthocyanidins Protect Against Light-Induced Retinal Damage via Antioxidative Stress, Anti-Apoptosis, and Neuroprotective Effects

In the present study, the replicative lifespan assay of yeast was used to guide the isolation of antiaging substance from Gentiana rigescens Franch, a traditional Chinese medicine. A compound with antiaging effect was isolated, and the chemical structure of this molecule as amarogentin was identified by spectral analysis and compared with the reported data. It significantly extended the replicative lifespan of K6001 yeast at doses of 1, 3, and 10 μM. Furthermore, amarogentin improved the survival rate of yeast under oxidative stress by increasing the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and these enzymes’ gene expression. In addition, this compound did not extend the replicative lifespan of sod1, sod2, uth1, and skn7 mutants with K6001 background. These results suggested that amarogentin exhibited antiaging effect on yeast via increase of SOD2, CAT, GPx gene expression, enzyme activity, and antioxidative stress. Moreover, we evaluated antioxidant activity of this natural products using PC12 cell system, a useful model for studying the nervous system at the cellular level. Amarogentin significantly improved the survival rate of PC12 cells under H2O2-induced oxidative stress and increased the activities of SOD and SOD2, and gene expression of SOD2, CAT, GPx, Nrf2, and Bcl-x1. Meanwhile, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) of PC12 cells were significantly reduced after treatment of the amarogentin. These results indicated that antioxidative stress play an important role for antiaging and neuroprotection of amarogentin. Interestingly, amarogentin exhibited neuritogenic activity in PC12 cells. Therefore, the natural products, amarogentin from G. rigescens with antioxidant activity could be a good candidate molecule to develop drug for treating neurodegenerative diseases.

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Brazilian Green Propolis Protects against Retinal Damage In Vitro and In Vivo

Evidence-based Complementary and Alternative Medicine ◽

10.1093/ecam/nek005 ◽

2006 ◽

Vol 3 (1) ◽

pp. 71-77 ◽

Cited By ~ 41

Author(s):

Yuta Inokuchi ◽

Masamitsu Shimazawa ◽

Yoshimi Nakajima ◽

Shinsuke Suemori ◽

Satoshi Mishima ◽

...

Keyword(s):

Oxidative Stress ◽

Retinal Ganglion Cells ◽

Ganglion Cells ◽

Water Soluble ◽

Retinal Damage ◽

Retinal Ganglion ◽

Neuroprotective Effects ◽

Brazilian Green Propolis

Propolis, a honeybee product, has gained popularity as a food and alternative medicine. Its constituents have been shown to exert pharmacological (anticancer, antimicrobial and anti-inflammatory) effects. We investigated whether Brazilian green propolis exerts neuroprotective effects in the retinain vitroand/orin vivo.In vitro, retinal damage was induced by 24 h hydrogen peroxide (H2O2) exposure, and cell viability was measured by Hoechst 33342 and YO-PRO-1 staining or by a resazurin–reduction assay. Propolis inhibited the neurotoxicity and apoptosis induced in cultured retinal ganglion cells (RGC-5, a rat ganglion cell line transformed using E1A virus) by 24 h H2O2 exposure. Propolis also inhibited the neurotoxicity induced in RGC-5 cultures by staurosporine. Regarding the possible underlying mechanism, in pig retina homogenates propolis protected against oxidative stress (lipid peroxidation), as also did trolox (water-soluble vitamin E). In micein vivo, propolis (100 mg kg−1; intraperitoneally administered four times) reduced the retinal damage (decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitrealin vivo N-methyl-d-aspartate injection. These findings indicate that Brazilian green propolis has neuroprotective effects against retinal damage bothin vitroandin vivo, and that a propolis-induced inhibition of oxidative stress may be partly responsible for these neuroprotective effects.

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Neuroprotective effects of interleukin-6 on NMDA-induced rat retinal damage

Biochemical and Biophysical Research Communications ◽

10.1016/s0006-291x(03)00127-x ◽

2003 ◽

Vol 302 (2) ◽

pp. 226-232 ◽

Cited By ~ 26

Author(s):

Yasuya Inomata ◽

Akira Hirata ◽

Naoko Yonemura ◽

Takahisa Koga ◽

Noriaki Kido ◽

...

Keyword(s):

Interleukin 6 ◽

Retinal Damage ◽

Neuroprotective Effects

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Cytoprotective Effects of Citicoline and Homotaurine against Glutamate and High Glucose Neurotoxicity in Primary Cultured Retinal Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/2825703 ◽

2017 ◽

Vol 2017 ◽

pp. 1-7 ◽

Cited By ~ 15

Author(s):

Sergio Davinelli ◽

Flavia Chiosi ◽

Roberto Di Marco ◽

Ciro Costagliola ◽

Giovanni Scapagnini

Keyword(s):

High Glucose ◽

Molecular Mechanisms ◽

Primary Cultures ◽

Retinal Damage ◽

Experimental Conditions ◽

Neuroprotective Effects ◽

Fetal Rats ◽

Retinal Neurodegeneration ◽

Insight Into ◽

Retinal Cultures

Citicoline and homotaurine are renowned compounds that exhibit potent neuroprotective activities through distinct molecular mechanisms. The present study was undertaken to demonstrate whether cotreatment with citicoline and homotaurine affects cell survival in primary retinal cultures under experimental conditions simulating retinal neurodegeneration. Primary cultures were obtained from the retina of fetal rats and exposed to citicoline plus homotaurine (100 μM). Subsequently, neurotoxicity was induced using excitotoxic levels of glutamate and high glucose concentrations. The effects on retinal cultures were assessed by cell viability and immunodetection of apoptotic oligonucleosomes. The results showed that a combination of citicoline and homotaurine synergistically decreases proapoptotic effects associated with glutamate- and high glucose-treated retinal cultures. This study provides an insight into the potential application of citicoline and homotaurine as a valuable tool to exert neuroprotective effects against retinal damage.

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Human Umbilical Cord-Mesenchymal Stem Cells Survive and Migrate within the Vitreous Cavity and Ameliorate Retinal Damage in a Novel Rat Model of Chronic Glaucoma

Stem Cells International ◽

10.1155/2021/8852517 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Yao Wang ◽

Jiexuan Lv ◽

Changquan Huang ◽

Xiaohong Li ◽

Yongxiong Chen ◽

...

Keyword(s):

Umbilical Cord ◽

Rat Model ◽

Fluorescent Protein ◽

Ganglion Cells ◽

Therapeutic Option ◽

Vitreous Cavity ◽

Human Umbilical Cord ◽

Retinal Damage ◽

Neuroprotective Effects ◽

Chronic Glaucoma

Glaucoma is the leading cause of irreversible blindness worldwide, and pathologically elevated intraocular pressure (IOP) is the major risk factor. Neuroprotection is one of the potential therapies for glaucomatous retinal damage. Intravitreal mesenchymal stem cell (MSC) transplantation provides a viable therapeutic option, and human umbilical cord- (hUC-) MSCs are attractive candidates for cell-based neuroprotection. Here, we investigated the ability of transplanted hUC-MSCs to survive and migrate within the vitreous cavity and their neuroprotective effects on chronic glaucomatous retina. For this, we developed a chronic ocular hypertension (COH) rat model through the intracameral injection of allogeneic Tenon’s fibroblasts. Green fluorescent protein-transduced hUC-MSCs were then injected into the vitreous cavity one week after COH induction. Results showed that a moderate IOP elevation lasted for two months. Transplanted hUC-MSCs migrated toward the area of damaged retina, but did not penetrate into the retina. The hUC-MSCs survived for at least eight weeks in the vitreous cavity. Moreover, the hUC-MSCs were efficient at decreasing the loss of retinal ganglion cells; retinal damage was attenuated through the inhibition of apoptosis. In this study, we have developed a novel COH rat model and demonstrated the prolonged neuroprotective potential of intravitreal hUC-MSCs in chronic glaucoma.

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Neuroprotective effects of exogenous erythropoietin in Wistar rats by downregulating apoptotic factors to attenuate N-methyl-D-aspartate-mediated retinal ganglion cells death

10.1101/773754 ◽

2019 ◽

Author(s):

Wen-Sheng Cheng ◽

I-Hung Lin ◽

Kathy Ming Feng ◽

Zhi-Yang Chang ◽

Yu Chuan Huang ◽

...

Keyword(s):

Retinal Ganglion Cells ◽

Wistar Rats ◽

Ganglion Cells ◽

Immunohistochemical Method ◽

Inner Plexiform Layer ◽

Retinal Damage ◽

Retinal Ganglion ◽

Caspase 9 ◽

Neuroprotective Effects ◽

Apoptotic Factors

AbstractThe aim of this study was to investigate whether exogenous erythropoietin (EPO) administration attenuates N-methyl-D-aspartate (NMDA)-mediated excitotoxic retinal damage in Wistar rats. The survival rate of retinal ganglion cells (RGCs) were investigated by flat mount analysis and flow cytometry. A group of male Wistar rats were randomly assigned to five groups: negative control, NMDA80 (i.e., 80 nmoles NDMA intravitreally injected), NMDA80 + 10ng EPO, NMDA80 + 50ng EPO, and NMDA80 + 250ng EPO. The NMDA80 + 50ng EPO treatment group was used to evaluate various administrated points (pre-/co-/post-administration of NMDA80). Meanwhile, the transferase dUTP Nick-End Labeling (TUNEL) assay of RGCs, the inner plexiform layer (IPL) thickness and the apoptotic signal transduction pathways of μ-calpain, Bax, and caspase 9 were assessed simultaneously using an immunohistochemical method (IHC). When EPO was co-administered with NMDA, attenuated cell death occurred through the downregulation of the apoptotic indicators: μ-calpain was activated first (peak at ∼18hrs), followed by Bax and caspase 9 (peak at ∼40hrs). Furthermore, the morphology of RGCs has clearly demonstrated the visual recovery of IPL thickness at 40 hours after injection. Exogenous EPO successfully protected RGCs by downregulating apoptotic factors to attenuate NMDA-mediated excitotoxic retinal damage.

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Neuroprotective effects of lotus seedpod procyanidins on extremely low frequency electromagnetic field-induced neurotoxicity in primary cultured hippocampal neurons

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2016.05.032 ◽

2016 ◽

Vol 82 ◽

pp. 628-639 ◽

Cited By ~ 9

Author(s):

Chunchun Yin ◽

Xiaoping Luo ◽

Yuqing Duan ◽

Wenyi Duan ◽

Haihui Zhang ◽

...

Keyword(s):

Electromagnetic Field ◽

Hippocampal Neurons ◽

Low Frequency ◽

Neuroprotective Effects ◽

Extremely Low Frequency ◽

Lotus Seedpod ◽

Cultured Hippocampal Neurons

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Preparation and Neuroprotective Activity of Glucuronomannan Oligosaccharides in an MPTP-Induced Parkinson’s Model

Marine Drugs ◽

10.3390/md18090438 ◽

2020 ◽

Vol 18 (9) ◽

pp. 438

Author(s):

Yingjuan Liu ◽

Weihua Jin ◽

Zhenzhen Deng ◽

Jing Wang ◽

Quanbin Zhang

Keyword(s):

Dopaminergic Neurons ◽

Complex Structure ◽

Saccharina Japonica ◽

Neuroprotective Activity ◽

Dopamine Depletion ◽

Neuron Degeneration ◽

Neuroprotective Effects ◽

Behavioral Deficits ◽

Antioxidative Stress ◽

Global Population

Parkinson’s disease (PD), characterized by dopaminergic neuron degeneration in the substantia nigra and dopamine depletion in the striatum, affects up to 1% of the global population over 50 years of age. Our previous study found that a heteropolysaccharide from Saccharina japonica exhibits neuroprotective effects through antioxidative stress. In view of its high molecular weight and complex structure, we degraded the polysaccharide and subsequently obtained four oligosaccharides. In this study, we aimed to further detect the neuroprotective mechanism of the oligosaccharides. We applied MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to induce PD, and glucuronomannan oligosaccharides (GMn) was subsequently administered. Results showed that GMn ameliorated behavioral deficits in Parkinsonism mice. Furthermore, we observed that glucuronomannan oligosaccharides contributed to down-regulating the apoptotic signaling pathway through enhancing the expression of tyrosine hydroxylase (TH) in dopaminergic neurons. These results suggest that glucuronomannan oligosaccharides protect dopaminergic neurons from apoptosis in PD mice.

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Activity Engagement in Cognitive Aging: A Review of the Evidence

Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders ◽

10.1044/nnsld23.1.35 ◽

2013 ◽

Vol 23 (1) ◽

pp. 1-12 ◽

Cited By ~ 2

Author(s):

Yvonne Rogalski ◽

Muriel Quintana

Keyword(s):

Older Adults ◽

Cognitive Decline ◽

Cognitive Aging ◽

Social Activity ◽

Current Evidence ◽

Omega 3 ◽

Neuroprotective Effects ◽

Activity Engagement ◽

Age Related ◽

Age Related Cognitive Decline

The population of older adults is rapidly increasing, as is the number and type of products and interventions proposed to prevent or reduce the risk of age-related cognitive decline. Advocacy and prevention are part of the American Speech-Language-Hearing Association’s (ASHA’s) scope of practice documents, and speech-language pathologists must have basic awareness of the evidence contributing to healthy cognitive aging. In this article, we provide a brief overview outlining the evidence on activity engagement and its effects on cognition in older adults. We explore the current evidence around the activities of eating and drinking with a discussion on the potential benefits of omega-3 fatty acids, polyphenols, alcohol, and coffee. We investigate the evidence on the hypothesized neuroprotective effects of social activity, the evidence on computerized cognitive training, and the emerging behavioral and neuroimaging evidence on physical activity. We conclude that actively aging using a combination of several strategies may be our best line of defense against cognitive decline.

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