mouse neuron ht22 line  (iCell Bioscience Inc)

Journal: IBRO Neuroscience Reports

Article Title: Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions

doi: 10.1016/j.ibneur.2025.05.007

Figure Lengend Snippet: In vitro toxicity safety window determination of GCK and evaluation of its neuroprotective effects in Aβ pathology models. (A, B) Cytotoxicity analysis of GCK on HT22 and BV2 cells. Cell viability was measured using the CCK-8 assay after 24-h treatment with varying GCK concentrations (0, 2, 4, 6, 8, and 10 μM). Results showed that 8 μM GCK significantly inhibited HT22 cell viability (p < 0.05), while no significant toxicity was observed at 6 μM or lower concentrations. For BV2 cells, viability remained relatively high at 8 μM but significantly decreased at 10 μM (p < 0.05). (C, D) Construction of an Aβ1–42 oligomer-induced Alzheimer's disease in vitro pathology model. After 24-h treatment with Aβ1–42 oligomers (0, 2, 4, 8, 16, and 32 nM), cell viability in both HT22 and BV2 cells decreased significantly with increasing Aβ concentrations (p < 0.001). The 32 nM concentration was selected as optimal for modeling pathology, reducing survival rates to 81.03 ± 5.50 % in HT22 and 78.58 ± 4.37 % in BV2 cells. (E, F) Neuroprotective effects of GCK against Aβ1–42 oligomer-induced cellular damage. Pretreatment with GCK (2, 4, 6, and 8 μM) for 2 h followed by 24-h co-treatment with 32 nM Aβ1–42 oligomers revealed that 4 μM GCK provided the most significant protection (p < 0.05), restoring cell viability to levels comparable to the control group. Note: Data presented as mean ± SD (n = 6); *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: The HT22 mouse hippocampal neuron cell line and BV2 microglial cell line were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China; official website: www.procell.com.cn ).

Techniques: In Vitro, CCK-8 Assay, Concentration Assay, Control

Journal: IBRO Neuroscience Reports

Article Title: Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions

doi: 10.1016/j.ibneur.2025.05.007

Figure Lengend Snippet: GCK counteracts Aβ1–42 oligomer-induced neurotoxicity through direct and indirect mechanisms. (A) Schematic workflow for conditioned medium preparation. Top panel: BV2 cells were treated with Aβ1–42 oligomers (32 nM) for 12 h, followed by medium replacement and additional 12 h incubation. The supernatant was collected and centrifuged to prepare Conditioned Medium 1 (CM1). Bottom panel: BV2 cells were pretreated with GCK (4 μM) for 2 h before Aβ1–42 oligomer treatment. Conditioned Medium 2 (CM2) was prepared using the same protocol. (B) Evaluation of GCK's direct protective effects. Compared to the control group, Aβ1–42 oligomer treatment significantly reduced HT22 cell viability (70.51 ± 4.75 %, ***p < 0.0001). GCK pretreatment markedly improved cell viability (84.49 ± 5.82 %, **p < 0.01 vs. Aβ group). (C) Evaluation of GCK's indirect protective effects. Both Aβ1–42 oligomers and CM1 treatment significantly decreased HT22 cell viability compared to controls (77.34 ± 5.21 % and 81.28 ± 6.14 %, respectively; **p < 0.01). In contrast, CM2 treatment significantly enhanced cell viability (88.69 ± 6.97 %, **p < 0.01 vs. CM1 group). Note: Data are expressed as mean ± standard deviation (n = 6). *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: C-K, Ginsenoside Compound K; CM1, Conditioned Medium 1; CM2, Conditioned Medium 2.

Article Snippet: The HT22 mouse hippocampal neuron cell line and BV2 microglial cell line were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China; official website: www.procell.com.cn ).

Techniques: Incubation, Control, Standard Deviation

Journal: Neuroscience Bulletin

Article Title: Pseudogene Lamr1-ps1 Aggravates Early Spatial Learning Memory Deficits in Alzheimer’s Disease Model Mice

doi: 10.1007/s12264-024-01336-6

Figure Lengend Snippet: Lamr1-ps1 is mainly expressed in neuronal cells. A Representative images showing the expression of Lamr1-ps1 (green) and NeuN (the neuronal marker, red) in the hippocampus of APP/PS1 mice. The stained images in the CA1, CA3, and DG areas are plotted from upper to lower (scale bars, 100 μm), and the merged enlarged images show co-staining of neurons and Lamr1-ps1 (right column, scale bars, 20 μm). B , C The relative expression of Lamr-ps1 in the N2a (B) and HT22 (C) cells treated with 0, 5, and 10 μmol/L Aβ 1-42 . Data are the mean ± SEM ( n = 6 per group, in the N2a cell group, F = 10.49, Con vs 5 μmol/L ** P = 0.0065, Con vs 10 μmol/L ** P = 0.0012; in the HT22 cell group, F = 3.850, Con vs 10 μmol/L * P = 0.041; one-way ANOVA followed by Bonferroni multiple comparisons). D Representative images showing the expression of Lamr1-ps1 (green) and GFAP (a marker of astrocytes, red) in the hippocampus of APP/PS1 mice; the merged images show that astrocytes are not co-stained with Lamr1-ps1 (scale bar, 100 μm).

Article Snippet: The mouse brain neuroma cell line Neuro-2a (N2a) (CL-0168, Procell, China), and the mouse hippocampal neuronal line, HT22 cells (CL-0697, Procell, China) were cultured in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% fetal bovine serum and 1% penicillin and streptomycin.

Techniques: Expressing, Marker, Staining