Neuroscience Letters, Год журнала: 2022, Номер 793, С. 136997 - 136997
Опубликована: Дек. 2, 2022
Язык: Английский
Neuroscience Letters, Год журнала: 2022, Номер 793, С. 136997 - 136997
Опубликована: Дек. 2, 2022
Язык: Английский
Heliyon, Год журнала: 2024, Номер 10(5), С. e26909 - e26909
Опубликована: Фев. 25, 2024
BackgroundEarly brain injury (EBI) caused by inflammatory responses in acute phase of Intracerebral hemorrhage (ICH) plays a vital role the pathological progression ICH. Increasing evidences demonstrate A1 reactive astrocytes are associated with severity EBI. G-protein coupled estrogen receptor 1 (GPER1) has been proved mediating neuroprotective effects central nervous system (CNS) disease. However, whether GPER1 protective effect on ICH and activation is not well studied.MethodsICH model was established infused autologous whole blood into right basal ganglia wild type knockout mice. specific agonist G1 antagonist G15 were administered intraperitoneal injection at h or 0.5 after Neurological function detected day 3 open field test corner turn following Besides, determined immunofluorescence staining 3. To further identify possible mechanism mediated effect, Western blot assays performed 3.ResultsAfter ICH, treatment alleviated mice neurobehavior deficits Meanwhile, also significantly reduced GFAP positive C3 cells Interestingly, reversed expression GFAP+C3+ GPER1. Mechanistic studies indicated TLR4 NF-κB GPER1.ConclusionGenerally, EBI through inhibiting via TLR4/NF-κB pathway Additionally, GPER1may be promising target for treatment.
Язык: Английский
Процитировано
2Biomolecules, Год журнала: 2022, Номер 12(12), С. 1745 - 1745
Опубликована: Ноя. 24, 2022
Parkinson’s disease (PD) is an incurable neurodegenerative of high prevalence, characterized by the prominent death dopaminergic neurons in substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal cell autonomous pathology, damage vulnerable responsible for disease, growing evidence strongly suggests that astrocytes might have active role neurodegeneration observed. In present review, we discuss several studies evidencing astrocyte implications PD, highlighting consequences both loss normal homeostatic functions and gain toxic wellbeing neurons. The revised information provides significant allows be positioned crucial players etiology, factor needs taken into account when considering therapeutic targets treatment disease.
Язык: Английский
Процитировано
11Cells, Год журнала: 2024, Номер 13(14), С. 1188 - 1188
Опубликована: Июль 12, 2024
Astrocytes specifically synthesize and release endozepines, a family of regulatory peptides including octadecaneuropeptide (ODN). We have previously reported that ODN rescues neurons astrocytes from 6-OHDA-induced oxidative stress cell death. The purpose this study was to examine the potential implication miR-34b, miR-29a, miR-21 in protective activity on death cultured rat astrocytes. Flow cytometry analysis showed 6-OHDA increased number early apoptotic dead cells while treatment with subnanomolar dose significantly reduced induced by 6-OHDA. 6-OHDA-treated exhibited over-expression (+118%) associated knockdown miR-34b (−61%) miR-29a (−49%). Co-treatment blocked 6-OHDA-stimulated production ROS NO stimulation Bax caspase-3 gene transcription. Concomitantly, down-regulated expression rescued 6-OHDA-associated miR21, indicating regulates their during Transfection miR-21-3p inhibitor prevented effect against In conclusion, our indicated (i) miRNAs is modified under injury (ii) prevents deregulation induce its neuroprotective action. present identified as an emerging candidate promising pharmacological target opens new therapeutic strategies neurodegenerative diseases, especially Parkinson’s disease.
Язык: Английский
Процитировано
2Brain Research, Год журнала: 2023, Номер 1822, С. 148603 - 148603
Опубликована: Сен. 23, 2023
Язык: Английский
Процитировано
5Neuroscience Letters, Год журнала: 2022, Номер 793, С. 136997 - 136997
Опубликована: Дек. 2, 2022
Язык: Английский
Процитировано
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