Transferrin-Conjugated Melittin-Loaded L-Arginine-Coated Iron Oxide Nanoparticles for Mitigating Beta-Amyloid Pathology of the 5XFAD Mouse Brain DOI Open Access
Moonseok Choi, Jung-Hwa Ryu, Huy Duc Vu

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(19), С. 14954 - 14954

Опубликована: Окт. 6, 2023

Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases and a major contributor to dementia. Although cause this condition has been identified long ago as aberrant aggregations amyloid tau proteins, effective therapies for it remain elusive. The complexities drug development AD treatment are often compounded by impermeable blood-brain barrier low-yield brain delivery. In addition, use high concentrations overcome challenge may entail side effects. To address these challenges enhance precision delivery into regions affected aggregation, we proposed transferrin-conjugated nanoparticle-based system. melittin-loaded L-arginine-coated iron oxide nanoparticles (Tf-MeLioNs) developed in study successfully mitigated melittin-induced cytotoxicity hemolysis cell culture 5XFAD mouse brain, Tf-MeLioNs remarkably reduced plaque accumulation, particularly hippocampus. This suggested Tf-LioNs potential platform candidate therapeutic targeting plaques AD. These findings provide foundation further exploration advancement therapeutics.

Язык: Английский

Unveiling the Protective Roles of Melatonin on Glial Cells in the Battle Against Alzheimer’s Disease—Insights from In Vivo and In Vitro Studies DOI

Nopdanai Sirimaharaj,

Kitti Thiankhaw,

Nipon Chattipakorn

и другие.

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 10, 2025

Язык: Английский

Процитировано

0

Transcriptome Analysis Unveils That Exosomes Derived from M1-Polarized Microglia Induce Ferroptosis of Neuronal Cells DOI Creative Commons
Sheng Gao,

Shu Jia,

Luyue Bai

и другие.

Cells, Год журнала: 2022, Номер 11(24), С. 3956 - 3956

Опубликована: Дек. 7, 2022

Microglia play a vital role in neurodegenerative diseases. However, the effects of microglia-derived exosomes on neuronal cells are poorly understood. This study aimed to explore M1-polarized microglia by transcriptome analysis. Exosomes isolated from resting M0-phenotype BV2 (M0-BV2) and (M1-BV2) were analyzed using high-throughput sequencing transcriptome. Differentially expressed genes (DEGs) between two types identified analyzing data. The biological functions pathways regulated DEGs then bioinformatics analyses. Finally, we evaluated coculturing M0-BV2 M1-BV2 with primary cells. Enrichment analyses revealed that significantly enriched ferroptosis pathway (p = 0.0137). had no distinct cells, whereas reduced suppressor proteins (GPX4, SLC7A11, FTH1) elevated levels intracellular mitochondrial ferrous iron lipid peroxidation Polarized can induce thereby aggravating damage. Taken together, these findings enhance knowledge pathogenesis neurological disorders suggest potential therapeutic targets against

Язык: Английский

Процитировано

17

Artemisia annua Extract Improves the Cognitive Deficits and Reverses the Pathological Changes of Alzheimer’s Disease via Regulating YAP Signaling DOI Open Access
Wenshu Zhou, Bingxi Lei, Chao Yang

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(6), С. 5259 - 5259

Опубликована: Март 9, 2023

Alzheimer's disease (AD) is a chronic neurodegenerative characterized by the occurrence of cognitive deficits. With no effective treatments available, search for new therapies has become major focus interest. In present study, we describe potential therapeutic effect Artemisia annua (A. annua) extract on AD. Nine-month-old female 3xTg AD mice were treated with A. three months via oral administration. Animals assigned to WT and model groups administrated an equal volume water same period. Treated significantly improved deficits exhibited reduced Aβ accumulation, hyper-phosphorylation tau, inflammatory factor release apoptosis when compared untreated mice. Moreover, promoted survival proliferation neural progenitor cells (NPS) increased expression synaptic proteins. Further assessment implicated mechanisms revealed that regulates YAP signaling pathway in studies comprised incubation PC12 Aβ1-42 at concentration 8 μM or without different concentrations 24 h. Obtained ROS levels, mitochondrial membrane potential, caspase-3 activity, neuronal cell pathways involved was performed using western blot immunofluorescence staining. The obtained results showed reversed Aβ1-42-induced increase activity vitro. either inhibition pathway, specific inhibitor CRISPR cas9 knockout gene, neuroprotective extract. These findings suggest may be multi-target anti-AD drug use prevention treatment

Язык: Английский

Процитировано

7

Activation of α7nAChR by PNU282987 improves cognitive impairment through inhibiting oxidative stress and neuroinflammation in D-galactose induced aging via regulating α7nAChR/Nrf2/HO-1 signaling pathway DOI Creative Commons
Yawen Zhang, Rui Ma, Wencheng Wang

и другие.

Experimental Gerontology, Год журнала: 2023, Номер 175, С. 112139 - 112139

Опубликована: Март 10, 2023

Aging is an important risk factor for neurodegenerative diseases. The activation of α7 nicotinic acetylcholine receptor (α7nAChR) involved in inflammation and cognition, but the specific role it plays aging remains unknown. This study aimed to investigate anti-aging effect α7nAChR on rats BV2 cells induced by D-galactose, as well its potential mechanism. D-galactose increase SA-β-Gal positive cells, expression p16 p21 vivo vitro. selective agonist PNU282987 decreased levels pro-inflammatory factors, MDA, Aβ, enhanced SOD activity anti-inflammatory (IL10) vivo. Arg1, iNOS, IL1β TNFα upregulated α7nAChR, Nrf2 HO-1 results Morris water maze novel object recognition tests showed that improved cognitive impairment rats. Furthermore, inhibitor methyllycaconitine (MLA) were opposite with PNU282987. improves through inhibiting oxidative stress neuroinflammation via regulating α7nAChR/Nrf2/HO-1 signaling pathway. Therefore, targeting may be a viable therapeutic approach anti-inflammaging

Язык: Английский

Процитировано

7

Transferrin-Conjugated Melittin-Loaded L-Arginine-Coated Iron Oxide Nanoparticles for Mitigating Beta-Amyloid Pathology of the 5XFAD Mouse Brain DOI Open Access
Moonseok Choi, Jung-Hwa Ryu, Huy Duc Vu

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(19), С. 14954 - 14954

Опубликована: Окт. 6, 2023

Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases and a major contributor to dementia. Although cause this condition has been identified long ago as aberrant aggregations amyloid tau proteins, effective therapies for it remain elusive. The complexities drug development AD treatment are often compounded by impermeable blood-brain barrier low-yield brain delivery. In addition, use high concentrations overcome challenge may entail side effects. To address these challenges enhance precision delivery into regions affected aggregation, we proposed transferrin-conjugated nanoparticle-based system. melittin-loaded L-arginine-coated iron oxide nanoparticles (Tf-MeLioNs) developed in study successfully mitigated melittin-induced cytotoxicity hemolysis cell culture 5XFAD mouse brain, Tf-MeLioNs remarkably reduced plaque accumulation, particularly hippocampus. This suggested Tf-LioNs potential platform candidate therapeutic targeting plaques AD. These findings provide foundation further exploration advancement therapeutics.

Язык: Английский

Процитировано

7