Induction of neural stem cell proliferation by iron oxide nanoparticles and magnetic field and <i>Ki67 </i>gene expression in rat hippocampus after ischemia/reperfusion

Hosseini, Farnaz; Koohpar, Zeinab Khazaei; Falahati, Mojtaba

doi:10.34172/jsums.2019.11

Cited by 2 publications

(1 citation statement)

References 23 publications

(25 reference statements)

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“…After treatment, all mice were injected with 5-Bromo-2′-deoxyuridine at a concentration of 50 mg/kg (BrdU, Sigma-Aldrich, St. Louis, MO, USA) by intraperitoneal injections administered twice a day for 4 days [ 69 ]. All mice were then euthanized using chloral hydrate (0.25 mg/mL) and the brains were dissected and fixed in 4% paraformaldehyde (4% PFA) for 48 h at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Artemisia annua Extract Improves the Cognitive Deficits and Reverses the Pathological Changes of Alzheimer’s Disease via Regulating YAP Signaling

Zhou¹,

Lei²,

Yang³

et al. 2023

IJMS

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

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Section: Methodsmentioning

confidence: 99%