The white rose petal extract abrogates excitotoxic neuronal damage through antioxidative and anti-inflammatory activities

2021 ◽  
Vol 429 ◽  
pp. 119216
Author(s):  
Wang Cuicui
Keyword(s):  
Neuronal Damage ◽  
Rose Petal ◽  
Anti Inflammatory ◽  
White Rose

scholarly journals The Ethanol Fraction of White Rose Petal Extract Abrogates Excitotoxicity-Induced Neuronal Damage In Vivo and In Vitro through Inhibition of Oxidative Stress and Proinflammation

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1375 ◽  
Author(s):  
Jung-Min Yon ◽  
Yun-Bae Kim ◽  
Dongsun Park
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Radical Scavenging ◽  
Cresyl Violet ◽  
Anti Inflammatory ◽  
White Rose ◽  
The Brain

Since oxidative stress and inflammation are involved in seizure-related neurotoxicity, the neuroprotective effect of a white rose (Rosa hybrida) petal extract (WRPE) in mice that are challenged with kainic acid (KA) were examined using behavioral epileptiform seizures as well as biochemical and morphological parameters of oxidative stress and inflammation. WRPE (50–200 mg/kg) was orally administered to male ICR mice for 15 days, and intraperitoneally challenged with KA (30 mg/kg). Seizure activity, lipid peroxidation, inflammatory cytokines, and related enzymes were analyzed in the brain tissue, in addition to the morphological alterations in the hippocampal pyramidal neurons. Separately, antioxidant ingredients in WRPE were analyzed, and antioxidant, anti-inflammatory, and neuroprotective activities of WRPE were investigated in HB1.F3 human neural stem cells (NSCs) to elucidate underlying mechanisms. Total polyphenol and flavonoid contents in WRPE were 303.3 ± 15.3 mg gallic acid equivalent/g extract and 18.5 ± 2.2 mg catechin/g extract, respectively. WRPE exhibited strong radical-scavenging activities and inhibited lipid peroxidation in vitro, and protected glutamate-induced cytotoxicity in NSCs by suppressing inflammatory process. Treatment with WRPE attenuated epileptiform seizure scores to a half level in KA-challenged mice, and decreased hippocampal pyramidal neuronal injury and loss (cresyl violet and DAPI staining) as well as astrocyte activation (GFAP immunostaining). Lipid peroxidation was inhibited, and mRNA expression of antioxidant enzymes (GPx, PHGPx, SOD1, and SOD2) were recovered in the brain tissues. Inflammatory parameters (cytokines and enzymes) including NF-kB, IL-1β, TNF-α, IL-6, HMGB1, TGF-β, iNOS, COX2, and GFAP mRNAs and proteins were also down-regulated by WRPE treatment. Taken together, the results indicate that WRPE could attenuate KA-induced brain injury through antioxidative and anti-inflammatory activities.

scholarly journals Inflammatory Neuropsychiatric Disorders and COVID-19 Neuroinflammation

2021 ◽  
pp. 1-55
Author(s):  
Siu Wa Tang ◽  
Daiga Helmeste ◽  
Brian Leonard
Keyword(s):  
Immune Responses ◽  
Clinical Management ◽  
Neuronal Damage ◽  
Treatment Resistance ◽  
Neuropsychiatric Disorders ◽  
Acute Stage ◽  
Management Approach ◽  
Neuropsychiatric Diseases ◽  
Anti Inflammatory

Abstract Neuropsychiatric sequalae to COVID-19 infection are beginning to emerge, like previous Spanish influenza and SARS episodes. Streptococcal infection in pediatric patients causing OCD (PANDAS) is another recent example of an infection-based psychiatric disorder. Inflammation associated with neuropsychiatric disorders has been previously reported but there is no standard clinical management approach established. Part of the reason is that it is unclear what factors determine the specific neuronal vulnerability and the efficacy of anti-inflammatory treatment in neuroinflammation. The emerging COVID-19 data suggested that in the acute stage, wide-spread neuronal damage appears to be the result of abnormal and overactive immune responses and cytokine storm is associated with poor prognosis. It is still too early to know if there are long term specific neuronal or brain regional damages associated with COVID-19, resulting in distinct neuropsychiatric disorders. In several major psychiatric disorders where neuroinflammation is present, patients with abnormal inflammatory markers may also experience less than favorable response or treatment resistance when standard treatment is used alone. Evidence regarding the benefits of co-administered anti-inflammatory agents such as COX-2 inhibitor is encouraging in selected patients though may not benefit others. Disease modifying therapies are increasingly being applied to neuropsychiatric diseases characterized by abnormal or hyperreactive immune responses. Adjunct anti-inflammatory treatment may benefit selected patients and is definitely an important component of clinical management in the presence of neuroinflammation.

scholarly journals Dangguijakyak-San Protects against 1-Methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-Induced Neuronal Damage via Anti-Inflammatory Action

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Deok-Sang Hwang ◽  
Hyo Geun Kim ◽  
Jun-Bock Jang ◽  
Myung Sook Oh
Keyword(s):  
Neuronal Damage ◽  
Cell Damage ◽  
Substantia Nigra Pars Compacta ◽  
Inflammatory Factors ◽  
Dopaminergic Cell ◽  
Therapeutic Implications ◽  
Anti Inflammatory ◽  
Inflammatory Action

Dangguijakyak-san (DJS), a famous traditional Korean multiherbal medicine, has been used to treat gynecological and neuro-associated disease. Recent studies demonstrated that DJS has multiple bioactivities including neuroprotection. In the present study, we were to investigate the effect of DJS and its mechanism in anin vitroandin vivomodel of Parkinson’s disease (PD). In primary mesencephalic culture system, DJS attenuated the dopaminergic cell damage induced by 1-methyl-4-phenylpyridine toxicity, and it inhibited production of inflammatory factors such as tumor necrosis factorα(TNF-α), nitric oxide (NO), and activation of microglial cells. Then, we confirmed the effect of DJS in a mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In the pole test, DJS at 50 mg/kg/day for 5 days showed increase of motor activity showing shortened time to turn and locomotor activity compared with the MPTP only treated mice. In addition, DJS significantly protected nigrostriatal dopaminergic neuron from MPTP stress. Moreover, DJS showed inhibition of gliosis in the substantia nigra pars compacta. These results have therapeutic implications for DJS in the treatment of PD via anti-inflammatory effects.

Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in the microglia.

2020 ◽  
Author(s):  
Shao-Peng Lin ◽  
Jue-Xian Wei ◽  
Shan Ye ◽  
Jiasong Hu ◽  
Jingyi Bu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Inflammatory Cytokines ◽  
Nuclear Translocation ◽  
Neuronal Damage ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Neurocognitive Deficits ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Background and purpose: Artemisinin has been in use as an anti-malarial drug for almost half a century in the world. There is growing evidence that artemisinin also possesses potent anti-inflammatory and immunoregulatory properties. However, the efficacy of artemisinin treatment in neurocognitive deficits associated with sepsis remains unknown. Here, we evaluate the possible protective effects and explore the underlying mechanism of artemisinin on cognitive impairment resulting from sepsis.Methods: Male C57BL/6 mice were pretreated with either vehicle or artemisinin, and then injected with LPS to establish an animal model of sepsis. The cognitive function was then assessed using the Morris water maze. Neuronal damage and neuroinflammation in the hippocampus were evaluated by immunohistochemical and ELISA analysis. Additionally, the protective mechanism of artemisinin was determined in vitro.Results: The results showed that artemisinin preconditioning attenuated LPS-induced cognitive impairment, neural damage, and microglial activation in the mouse brain. The in vitro experiment revealed that artemisinin could reduce the production of pro-inflammatory cytokines and suppress the microglial migration in the BV2 microglia cells. Meanwhile, western blot demonstrated that artemisinin suppressed nuclear translocation of nuclear factor kappa-B and the expression of pro-inflammatory cytokines (i.e. tumor necrosis factor alpha, interleukin-6) by activating adenosine monophosphate-activated protein kinaseα1 (AMPKα1) pathway. Furthermore, knock-down of AMPKα1 markedly abolished the anti-inflammatory effects of artemisinin.Conclusion: Artemisinin is a potential therapeutic agent for sepsis-associated neuroinflammation and cognitive impairment, and its effect was probably mediated by the activation of AMPKα1 signalling pathway in microglia.

scholarly journals Ellagic acid produces neuroprotection against LPS-induced dopamine neurotoxicity via the inhibition of microglial NLRP3 inflammasome activation

2019 ◽  
Author(s):  
Xue-mei He ◽  
Qiu-yu Yang ◽  
Jing-yi He ◽  
Shuo Sheng ◽  
Jing-jie Li ◽  
...  
Keyword(s):  
Cell Line ◽  
Nlrp3 Inflammasome ◽  
Ellagic Acid ◽  
Neuronal Damage ◽  
Damage Model ◽  
Neuronal Loss ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
Anti Inflammatory ◽  
Signaling Activation

Abstract Background: Neuroinflammation plays a crucial role in the pathological process of Parkinson's disease (PD). Nod-like receptor protein 3 (NLRP3) inflammasome was highly located in microglia and involved in the process of neuroinflammation. Activation of NLRP3 inflammasome has been confirmed to contribute to the progression of PD. Thus, inhibition of NLRP3 inflammasomes activation could be an important breakthrough point in PD drug therapy. Ellagic acid (EA) is a natural polyphenol that has been widely found in soft fruits, nuts and other plant tissues with various anti-inflammatory and anti-oxidant properties. However, the mechanisms underlying EA-mediated anti-inflammatory and neuroprotection have not been fully elucidated. Methods: In this study, lipopolysaccharide (LPS)-induced rat dopamine (DA) neuronal damage model was performed to determine the effects of EA on the protection of DA neurons. Furthermore, DA neuron MN 9D cell line and microglia BV-2 cell line were employed to explore whether EA-mediated neuroprotection was through an NLRP3-dependent mechanism . Results: EA ameliorat ed LPS-induced DA neuronal loss in rat substantia nigra. Furtherly, inhibition of microglial NLRP3 inflammasome signaling activation was involved in EA-generated neuroprotection, as evidenced by the following observations. First, EA reduced NLRP3 inflammasome signaling activation in microglia and the subsequent pro-inflammatory cytokines excretion. In addition, EA-mediated anti-neuroinflammation and further DA neuroprotection from LPS-induced neurotoxicity was not shown upon microglial NLRP3 siRNA treatment. Conclusions: This study demonstrated EA has a profound effect on protecting DA neurons against LPS-induced neurotoxicity via the suppression of microglial NLRP3 inflammasome signaling activation.

Peripheral Immunosenescence and Central Neuroinflammation: A Dangerous Liaison - A Dietary Approach

2020 ◽  
Vol 20 (9) ◽  
pp. 1391-1411 ◽  
Author(s):  
Thea Magrone ◽  
Manrico Magrone ◽  
Matteo A. Russo ◽  
Emilio Jirillo
Keyword(s):  
Neurodegenerative Diseases ◽  
T Regulatory Cells ◽  
Neuronal Damage ◽  
Age Related ◽  
The Central Nervous System ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Neuro Inflammation ◽  
Inflammatory Profile ◽  
The Brain

Background & Objectives: In old people, both innate and adaptive immune responses are impaired, thus leading to a condition of systemic inflamm-ageing, even including the involvement of the central nervous system (CNS). Aims: Here, main mechanisms of the immune ageing and neuro-inflammation will be discussed along with the dietary approaches for the modulation of age related diseases. Discussion: Neuroinflammation is caused by the passage of inflammatory mediators through the brain blood barrier to CNS. Then, in the brain, antigenic stimulation of microglia and/or its activation by peripheral cytokines lead to a robust production of free radicals with another wave of proinflammatory cytokines which, in turn, causes massive neuronal damage. Also, infiltrating T cells [T helper (h) and T cytotoxic cells] contribute to neuronal damage. Additionally, a peripheral imbalance between inflammatory Th17 cells and anti-inflammatory T regulatory cells seems to be prevalent in the aged brain, thus leading to a proinflammatory profile. Alzheimer’s disease, Parkinson’s disease and multiple sclerosis will be described as typical neurodegenerative diseases. Finally, modulation of the immune response thanks to the anti-oxidant and anti-inflammatory effects exerted by dietary products and nutraceuticals in ageing will be discussed. Special emphasis will be placed on polyunsaturated fatty acids, polyphenols, micronutrients and pre-probiotics and synbiotics. Conclusion: Ageing is characterized by an imbalance subversion of the immune system with a condition of inflamm-ageing. Neuroinflammation and neurodegenerative diseases seem to be a central manifestation of a peripheral perturbation of the immune machinery. Dietary products and nutraceuticals may lead to a down-regulation of the oxidative and pro-inflammatory profile in ageing.

scholarly journals Skin anti-inflammatory activity of rose petal extract (Rosa gallica ) through reduction of MAPK signaling pathway

2018 ◽  
Vol 6 (8) ◽  
pp. 2560-2567 ◽  
Author(s):  
Myung-hee Lee ◽  
Tae Gyu Nam ◽  
Inil Lee ◽  
Eun Ju Shin ◽  
Ah-ram Han ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Inflammatory Activity ◽  
Rosa Gallica ◽  
Rose Petal ◽  
Anti Inflammatory

scholarly journals Palmitoylethanolamide Modulation of Microglia Activation: Characterization of Mechanisms of Action and Implication for Its Neuroprotective Effects

2021 ◽  
Vol 22 (6) ◽  
pp. 3054
Author(s):  
Alessia D’Aloia ◽  
Laura Molteni ◽  
Francesca Gullo ◽  
Elena Bresciani ◽  
Valentina Artusa ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Neuronal Damage ◽  
Electrode Array ◽  
Microglial Cells ◽  
Toll Like Receptor 4 ◽  
Neuroprotective Effects ◽  
M1 Polarization ◽  
Anti Inflammatory

Palmitoylethanolamide (PEA) is an endogenous lipid produced on demand by neurons and glial cells that displays neuroprotective properties. It is well known that inflammation and neuronal damage are strictly related processes and that microglia play a pivotal role in their regulation. The aim of the present work was to assess whether PEA could exert its neuroprotective and anti-inflammatory effects through the modulation of microglia reactive phenotypes. In N9 microglial cells, the pre-incubation with PEA blunted the increase of M1 pro-inflammatory markers induced by lipopolysaccharide (LPS), concomitantly increasing those M2 anti-inflammatory markers. Images of microglial cells were processed to obtain a set of morphological parameters that highlighted the ability of PEA to inhibit the LPS-induced M1 polarization and suggested that PEA might induce the anti-inflammatory M2a phenotype. Functionally, PEA prevented Ca2+ transients in both N9 cells and primary microglia and antagonized the neuronal hyperexcitability induced by LPS, as revealed by multi-electrode array (MEA) measurements on primary cortical cultures of neurons, microglia, and astrocyte. Finally, the investigation of the molecular pathway indicated that PEA effects are not mediated by toll-like receptor 4 (TLR4); on the contrary, a partial involvement of cannabinoid type 2 receptor (CB2R) was shown by using a selective receptor inverse agonist.

scholarly journals The role of prolactin in central nervous system inflammation

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Edgar Ramos-Martinez ◽  
Ivan Ramos-Martínez ◽  
Gladys Molina-Salinas ◽  
Wendy A. Zepeda-Ruiz ◽  
Marco Cerbon
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuronal Damage ◽  
Neurological Diseases ◽  
Neuroprotective Effect ◽  
General Information ◽  
Experimental Models ◽  
Neuroprotective Effects ◽  
Anti Inflammatory

Abstract Prolactin has been shown to favor both the activation and suppression of the microglia and astrocytes, as well as the release of inflammatory and anti-inflammatory cytokines. Prolactin has also been associated with neuronal damage in diseases such as multiple sclerosis, epilepsy, and in experimental models of these diseases. However, studies show that prolactin has neuroprotective effects in conditions of neuronal damage and inflammation and may be used as neuroprotector factor. In this review, we first discuss general information about prolactin, then we summarize recent findings of prolactin function in inflammatory and anti-inflammatory processes and factors involved in the possible dual role of prolactin are described. Finally, we review the function of prolactin specifically in the central nervous system and how it promotes a neuroprotective effect, or that of neuronal damage, particularly in experimental autoimmune encephalomyelitis and during excitotoxicity. The overall studies indicated that prolactin may be a promising molecule for the treatment of some neurological diseases.

scholarly journals Cholinergic blockade of neuroinflammation – from tissue to RNA regulators

2022 ◽  
Author(s):  
Tamara Zorbaz ◽  
Nimrod Madrer ◽  
Hermona Soreq
Keyword(s):  
Neuronal Damage ◽  
Neurological Diseases ◽  
Brain Inflammation ◽  
Aged Patients ◽  
Innate And Adaptive Immunity ◽  
Perivascular Macrophages ◽  
Inflammatory Stimuli ◽  
Inflammatory Processes ◽  
Rna Fragments ◽  
Anti Inflammatory

Inflammatory stimuli and consequent pro-inflammatory immune responses may facilitate neurodegeneration and threaten survival following pathogen infection or trauma, but potential controllers preventing these risks are incompletely understood. Here, we argue that small RNA regulators of acetylcholine (ACh) signaling, including microRNAs and transfer RNA fragments may tilt the balance between innate and adaptive immunity, avoid chronic inflammation and prevent the neuroinflammation-mediated exacerbation of many neurological diseases. While the restrictive permeability of the blood-brain barrier protects the brain from peripheral immune events, this barrier can be disrupted by inflammation and is weakened with age. The consequently dysregulated balance between pro- and anti-inflammatory processes may modify the immune activities of brain microglia, astrocytes, perivascular macrophages, oligodendrocytes and dendritic cells, leading to neuronal damage. Notably, the vagus nerve mediates the peripheral cholinergic anti-inflammatory reflex and underlines the consistent control of body-brain inflammation by pro-inflammatory cytokines, which affect cholinergic functions; therefore, the disruption of this reflex can exacerbate cognitive impairments such as attention deficits and delirium. RNA regulators can contribute to re-balancing the cholinergic network and avoiding its chronic deterioration, and their activities may differ between men and women and/or wear off with age. This can lead to hypersensitivity of aged patients to inflammation and higher risks of neuroinflammatory-driven cholinergic impairments such as delirium and dementia following COVID-19 infection. The age- and sex-driven differences in post-transcriptional RNA regulators of cholinergic elements may hence indicate new personalized therapeutic options for neuroinflammatory diseases.

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