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Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

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Neural Regeneration Research 2014年第3期9卷 252-259页

作者： Lining Ke Wei Guo Jianwen Xu Guodong Zhang Wei Wang Wenhua Huang department of Human anatomy Histology and Embryology Southern Medical University department of Human anatomy Histology and Embryology Fujian Medical University

The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral isch- emia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb 1, an active component of ginseng, and cortical neurons. Ginsenoside Rb l protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rbl inhibited levels of tumor necrosis factor-a in a co-culture system containing activated N9 microglial cells. Ginse-noside Rbl also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rbl attenuates damage to cerebral cortex neu-rons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-a expression in hypoxia-activated microglia.

关键词： nerve regeneration traditional Chinese medicine ischemia/hypoxia microglia neurons apoptosis ginsenoside Rb l nerve inflammation factor NSFC grant neural regeneration

The mutual interaction between the host spinal cord and grafted undifferentiated stem cells fosters the production of a lesion-induced secretome

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Neural Regeneration Research 2020年第10期15卷 1844-1845页

作者： Krisztián Pajer Tamás Bellák Antal Nógrádi department of anatomy Histology and Embryology Faculty of Medicine University of Szeged

Pathophysiology of spinal cord injury:Injury to the spinal cord results in loss of gray and white matter i.e.,it produces a segmental spinal cord lesion and,as a consequence leads to a fatal loss of motor,sensory and autonomic functions.Spinal cord injuries in humans and other mammals are not followed by the replacement of lost neurons and oligodendrocytes and regrowth of injured axons,instead they lead to permanent,fatal and incurable functional deficits.The primary physical injury is followed by a cascade of tissue-decaying events,called secondary injury,which leads to ischemia,vascular disruption,neuroinflammation,excitotoxicity,demyelination and death of neurons and glial cells(Silva et al.,2014;Figure 1A).The direct mechanical disruption of the vasculature results in the increased permeability of the blood-spinal cord barrier.Due to the leakiness of blood-spinal cord barrier and production of cytokines by activated microglia,a number of various immune cells(T lymphocytes,neutrophils and monocytes)invade the injury site.The macrophages generate a set of inflammatory cytokines such as tumor necrosis factor-α,interleukin(IL)-1α,IL-1β,and IL-6,which may further augment the secondary events(Ahuja et al.,2017).In addition,a number of other disruptive processes contribute to the heterogeneous and time-sensitive pathophysiology of spinal cord injury.

关键词： mutual Figure injuries

Cell-based therapy in Alzheimer's disease: can human fetal cholinergic neurons “untangle the skein”?

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Neural Regeneration Research 2018年第12期13卷 2105-2107页

作者： Giulia Guarnieri Erica Sarchielli Gabriella B.Vannelli Annamaria Morelli anatomy and histology Unit Department of Clinical and Experimental Medicine University of Florence

Alzheimer＇s disease（AD）is a devastating neurodegenerative disorder and the most common form of old-age dementia.The disease is characterized by a progressive decline in cognitive functions,gradual loss of memory an... 详细信息

关键词： untangle the skein can human fetal cholinergic neurons Cell-based therapy in Alzheimer’s disease

Thrombin in peripheral nerves:friend or foe?

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Neural Regeneration Research 2021年第6期16卷 1223-1224页

作者： Elena Pompili Cinzia Fabrizi department of anatomy HistologyForensic Medicine and OrthopedicsSapienza UniversityRomeItaly

Differently from the central nervous system(CNS),the peripheral nervous system(PNS)exhibits a high regenerative capacity.This ability is related to the remarkable plasticity of Schwann cells(SCs)which after nerve injury convert to a repair-promoting phenotype to a large extent.Nerve injury is accompanied by a rapid rise of thrombin levels(Bushi et al.,2016;Gera et al.,2016).Thrombin is the key effector protease of the coagulation cascade which elicits hormonelike actions by the activation of G-protein coupled receptors known as proteaseactivated receptors(PARs).Inflammation and coagulation are two complex and interconnected pathways whose mutual interactions have been only partially elucidated.

关键词： mutual injury convert

The seeming paradox of adenosine receptors as targets for the treatment of Alzheimer's disease: agonists or antagonists?

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Neural Regeneration Research 2015年第2期10卷 205-207页

作者： Rubina Marzagalli Alessandro Castorina department of Biomedical Sciences and Biotechnologies Section of Human Anatomy and Histology University of Catania

Alzheimer＇s disease （AD） is the most common neurodegenerative disorder, and its incidence is relatively high among elderly people, affecting about 1-2% of the population between 60-65 years old and rising dramatically （about 30%） in people aged 80 years or older （Selkoe, 2002）. Nowadays, considering the increasing mean lifespan of populations in developed countries, the disease is becoming more and more a health concern, and the search for an effective cure has turned into＂a real need＂.

关键词： The seeming paradox of adenosine receptors as targets for the treatment of Alzheimer’s disease agonists or antagonists

Intentional and unintentional impacts of anaesthesia： insights from experiments in pain and injury

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Neural Regeneration Research 2017年第12期12卷 1985-1986页

作者： James W.M.Kang Department of Anatomy and Histology School of Medical SciencesUniversity of Sydney Sydney NSW Australia

The study of brain function in the presence of pain and injury is a rapidly expanding field of experimental research.Clinically,the presence of pain and injury is often accompanied by reports of behavioural change and altered cognition.Even in a highly controlled environment such as the surgical operating theatre postoperative behavioural changes including posttraumatic stress disorder,depression,chronic fatigue,

关键词： Intentional unintentional impacts anaesthesia insights from experiments pain and injury

Hemodynamic changes in hepatic sinusoids of hepatic steatosis mice

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World Journal of Gastroenterology 2019年第11期25卷 1355-1365页

作者： Jing Fan Chong-Jiu Chen Yu-Chen Wang Wei Quan Jian-Wei Wang Wei-Guang Zhang department of anatomy Histology and EmbryologySchool of Basic Medical SciencesPeking University Health Science Center

BACKGROUND Fatty liver(FL) is now a worldwide disease. For decades, researchers have been kept trying to elucidate the mechanism of FL at the molecular level, but rarely involve the study of morphology and medical physics. Traditionally, it was believed that hemodynamic changes occur only when fibrosis occurs, but it has been proved that these changes already show in steatosis stage, which may help to reveal the pathogenesis and its progress. Because the pseudolobules are not formed during the steatosis stage, this phenomenon may be caused by the compression of the liver microcirculation and changes in the hemodynamics.AIM To understand the pathogenesis of hepatic steatosis and to study the hemodynamic changes associated with hepatic steatosis.METHODS Eight-week-old male C57 BL/6 mice were divided into three groups randomly(control group, 2-wk group, and 4-wk group), with 16 mice per group. A hepatic steatosis model was established by subcutaneous injection of carbon tetrachloride in mice. After establishing the model, liver tissue from mice was stained with hematoxylin and eosin(HE), and oil red O stains. Blood was collected from the angular vein, and hemorheological parameters were estimated. A two-photon fluorescence microscope was used to examine the flow properties of red blood cells in the hepatic sinusoids.RESULTS Oil red O staining indicated lipid accumulation in the liver after CCl_4 treatment.HE staining indicated narrowing of the hepatic sinusoidal vessels. No significant difference was observed between the 2-wk and 4-wk groups of mice onmorphological examination. Hemorheological tests included whole blood viscosity(mPas, γ = 10 s-1/γ = 100 s-1)(8.83 ± 2.22/4.69 ± 1.16, 7.73 ± 2.46/4.22 ±1.32, and 8.06 ± 2.88/4.22 ± 1.50), red blood cell volume(%)(51.00 ± 4.00, 42.00 ±5.00, and 40.00 ± 3.00), the content of plasma fibrinase(g/L)(3.80 ± 0.50, 2.90 ±0.80, and 2.30 ± 0.70), erythrocyte deformation index(%)(44.49 ± 5.81, 48.00 ±15.29, and 44.36 ± 15.01), erythrocyte electrophoresis rate(mm/s per V/m)(0.55

关键词： Hepatic steatosis Hemodynamics Hepatic sinusoids Two-photon fluorescence microscopy Carbon tetrachloride

Loss of the ubiquitin-conjugating enzyme Rad6B disturbs mitochondrial function and cellular homeostasis in mouse skin

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BIOCELL 2021年第3期45卷 761-772页

作者： LINGHUI YU RONG SHEN YANAN GUO YANXUAN GUO CHEN LI YANFENG SONG DEGUI WANG Department of Anatomy and Histology School of Basic Medical SciencesLanzhou UniversityLanzhou730000China

Various factors can induce cell degeneration by altering the phenotype and metabolism of cells.Mitochondria play an essential role in cellular homeostasis and function,rendering aging processes highly associated with mitochondrial function and status.Herein,we describe an aging-prone phenotype of murine skin cells caused by depletion of Rad6B(Ube2b),an E2 ubiquitin-conjugating enzyme.In this study,using Masson’s trichrome,we showed that loss of Rad6B causes physiological structure changes in mouse skin with age.In addition,a combination of western blotting experiments,transmission electron microscopy and employment of immunofluorescence staining revealed that depletion of Rad6B was characterized by an abnormal mitochondrial metabolic profile,including decreased mitochondrial biosynthesis and mitochondrial complex activities,increased ROS production and suppressed mitophagy resulting in metabolic disorders.Taken together,these results highlight an important relationship between Rad6B and skin senescence,suggesting that Rad6B plays an indispensable role in maintaining a healthy mitochondrial network and intracellular homeostasis.

关键词： Rad6B Skin Mitochondria Respiratory chain Senescence

Mesenchymal stem cells-based therapy as a potential treatment in neurodegenerative disorders: is the escape from senescence an answer?

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Neural Regeneration Research 2015年第6期10卷 850-858页

作者： Alessandro Castorina Marta Anna Szychlinska Rubina Marzagalli Giuseppe Musumeci department of Biomedical and Biotechnological Science Section of Human Anatomy and HistologySchool of MedicineUniversity of Catania

Aging is the most prominent risk factor contributing to the development of neurodegenerative disorders. In the United States, over 35 million of elderly people suffer from age-related diseases. Aging impairs the self-repair ability of neuronal cells, which undergo progressive deterioration. Once initiated, this process hampers the already limited regenerative power of the central nervous system, making the search for new therapeutic strategies particularly difficult in elderly affected patients. So far, mesenchymal stem cells have proven to be a viable option to ameliorate certain aspects of neurodegeneration, as they possess high proliferative rate and differentiate in vitro into multiple lineages. However, accumulating data have demonstrated that during longterm culture, mesenchymal stem cells undergo spontaneous transformation. Transformed mesenchymal stem cells show typical features of senescence, including the progressive shortening of telomers, which results in cell loss and, as a consequence, hampered regenerative potential. These evidences, in line with those observed in mesenchymal stem cells isolated from old donors, suggest that senescence may represent a limit to mesenchymal stem cells exploitation in therapy, prompting scholars to either find alternative sources of pluripotent cells or to arrest the age-re- lated transformation. In the present review, we summarize findings from recent literature, and critically discuss some of the major hurdles encountered in the search of appropriate sources of mesenchymal stem cells, as well as benefits arising from their use in neurodegenerative diseases. Finally, we provide some insights that may aid in the development of strategies to arrest or, at least, delay the aging of mesenchymal stem cells to improve their therapeutic potential.

关键词： aging neurodegenerative disorders telomere shortening MSCs cellular therapy