Natural Inhibitors on Over-Activation of Microglia from Herbals

Bai, Zisong; Chen, Gang; Li, Wei; Hou, Yue; Li, Ning

doi:10.1248/cpb.c18-00926

Cited by 6 publications

(3 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Microglial inhibitors, including minocycline and natural products (e.g., apigenin, fisetin, and curcumin), show promise in the treatment of cognitive impairment associated with neuropsychiatric disorders, including schizophrenia 69 . Minocycline, a classical semi-synthetic tetracycline antibiotic with good brain infusion, is used most widely to inhibit microglial overactivation.…”

Section: Introductionmentioning

confidence: 99%

Microglia and cognitive impairment in schizophrenia: translating scientific progress into novel therapeutic interventions

et al. 2023

View full text Add to dashboard Cite

Cognitive impairment is a core clinical feature of schizophrenia, exerting profound adverse effects on social functioning and quality of life in a large proportion of patients with schizophrenia. However, the mechanisms underlying the pathogenesis of schizophrenia-related cognitive impairment are not well understood. Microglia, the primary resident macrophages in the brain, have been shown to play important roles in psychiatric disorders, including schizophrenia. Increasing evidence has revealed excessive microglial activation in cognitive deficits related to a broad range of diseases and medical conditions. Relative to that about age-related cognitive deficits, current knowledge about the roles of microglia in cognitive impairment in neuropsychiatric disorders, such as schizophrenia, is limited, and such research is in its infancy. Thus, we conducted this review of the scientific literature with a focus on the role of microglia in schizophrenia-associated cognitive impairment, aiming to gain insight into the roles of microglial activation in the onset and progression of such impairment and to consider how scientific advances could be translated to preventive and therapeutic interventions. Research has demonstrated that microglia, especially those in the gray matter of the brain, are activated in schizophrenia. Upon activation, microglia release key proinflammatory cytokines and free radicals, which are well-recognized neurotoxic factors contributing to cognitive decline. Thus, we propose that the inhibition of microglial activation holds potential for the prevention and treatment of cognitive deficits in patients with schizophrenia. This review identifies potential targets for the development of new treatment strategies and eventually the improvement of care for these patients. It might also help psychologists and clinical investigators in planning future research.

show abstract

Section: Introductionmentioning

confidence: 99%

Microglia and cognitive impairment in schizophrenia: translating scientific progress into novel therapeutic interventions

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Meanwhile, brain activity and multiple organ functions declined with aging [3]. Furthermore, cognitive deficiency and dementia related to brain elderly were identified as the directing sources of debility and dependency among worldwide elder people in the absence of effective therapeutic approaches [4]. 2.…”

Section: Introductionmentioning

confidence: 99%

Gero-protective Impact of Astaxanthin on Experimental Model of Brain Aging: Biochemical and Molecular Study

Baeissa,

Barqawi,

Tashkandi

et al. 2023

Egypt. J. Chem.

View full text Add to dashboard Cite

Brain activity and multiple organ functions declined with aging. Although the complexity of brain aging process, releasing free radicals and inflammation were strongly linked to the disorder. Astaxanthin is a dietary carotenoid which exerts antioxidant and anti-inflammatory activities. We intended to estimate the protective impact of Astaxanthin on aging caused by D-galactose. Forty male Wister rats were separated into 4 groups as follow: G1: (control) group:G2: (D-Gal) rats received D-Gal (300mg/kg,ip) ;G3 (D-Gal+Met) 4 h after D-Gal administration, rats received metformin (300 mg/kg, orally) , as reference drug group;G4 : (D-Gal+Asta) group: 4h after D-Gal treatment, rats received Astaxanthin (25 mg/kg , orally). Results showed that administering D-Gal caused brain aging manifested by significant (p<0.05) disturbance of antioxidant defense system, inflammatory biomarkers. Moreover, results of gene expression and histological assessment ensured biochemical findings. Astaxanthin supplementation promoted a remarkable significant (p<0.05) normalization in all parameters by triggering different brain mechanisms. In conclusion these results suggested that Astaxanthin modulates D-Gal induced brainabnormalities associated with aging.

show abstract

“…[15][16][17] Previous studies revealed that SE activated glial cells and intensified pro-inflammatory agents including TNF-α, and NO production, which are responsible for cell death and dysfunction in neuroinflammatory diseases. [18][19][20] Therefore, preventing the activation of TNF-α and NO pathways may control some neurological and peripheral effects.…”

mentioning

confidence: 99%

Dapsone Protects Against Lithium-Pilocarpine-Induced Status Epilepticus in Rats through Targeting Tumor Necrosis Factor-α and Nitrergic Pathway

Koohfar¹,

Eslami²,

Shayan³

et al. 2022

J Epilepsy Res

View full text Add to dashboard Cite

Background and Purpose: Status epilepticus (SE) results in permanent neuronal brain damage in the central nervous system. One of the complex etiologies underlying SE pathogenesis is neuroinflammation. Dapsone has been recently considered as a potential neuroprotective agent in neuroinflammatory conditions. Therefore, the present study aims to investigate effects of dapsone on lithium-pilocarpine-induced SE in rats and assess whether tumor necrosis factor-alpha (TNF-α) and nitric oxide (NO) pathway participate in this effect.Methods: SE was established by injecting lithium chloride (127 mg/kg, intraperitoneally [i.p.]) and pilocarpine (60 mg/kg, i.p.). The animals received pre-treatment dapsone (2, 5, 10, and 20 mg/kg, oral gavage) and post-treatment dapsone (10 mg/kg). Subsequently, seizure score and mortality rate were documented. To assess the underlying signaling pathway, L-Nω-Nitro-L-arginine methyl ester hydrochloride (a non-specific NO synthase [NOS] inhibitor), 7-nitroindazole (a specific neuronal NOS inhibitor), and aminoguanidine (a specific inducible NOS inhibitor) were administered 15 minutes before dapsone (10 mg/kg) pre- or post-treatment. Hippocampal tissue TNF-α and NO concentrations were quantified using the enzyme-linked immunosorbent assay method.Results: Dapsone (10 mg/kg) pre-and post-treatment significantly attenuated the increased seizure score and mortality rate due to lithium-pilocarpine-induced SE. The development of SE in animals was associated with higher TNF-α and NO metabolites levels, which notably decreased in the dapsone-treated rats. Moreover, co-administration of NOS inhibitors with dapsone markedly reversed the anti-epileptic effects of dapsone and caused an escalation in TNF-α level but a significant reduction in NO concentration level.Conclusions: It seems that dapsone may exert an anti-epileptic effect on lithium-pilocarpine-induced SE through TNF-α inhibition and modulation of the nitrergic pathway.

show abstract

Natural Inhibitors on Over-Activation of Microglia from Herbals

Cited by 6 publications

References 70 publications

Microglia and cognitive impairment in schizophrenia: translating scientific progress into novel therapeutic interventions

Microglia and cognitive impairment in schizophrenia: translating scientific progress into novel therapeutic interventions

Gero-protective Impact of Astaxanthin on Experimental Model of Brain Aging: Biochemical and Molecular Study

Dapsone Protects Against Lithium-Pilocarpine-Induced Status Epilepticus in Rats through Targeting Tumor Necrosis Factor-α and Nitrergic Pathway

Contact Info

Product

Resources

About