Figure 4 - available via license: Creative Commons Attribution 4.0 International
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Photomicrograph of H&E-stained hippocampus, cerebellum, and brain cortex sections of AD-induced rats treated with GeO2NPs (AD + GeO2NPs), treated with CeO2NPs (AD + CeO2NPs), left untreated (AD) and healthy rats (Control). Arrows depicted degeneration and necrosis of neurons and arrows in the brain section of AD group depicted diffused neurofibrillary tangles. The star in the cerebellum section of CeO2NPs + AD group depicts where the cells of granular area had gliosis, degeneration, and clumps together. Magnification was 400× in all samples except in the sections of the control where it was 40×.
Source publication
Alzheimer’s disease (AD) is a neurodegenerative disorder that jeopardizes the lives of diagnosed patients at late stages. This study aimed to assess, for the first time, the efficiency of germanium dioxide nanoparticles (GeO2NPs) in mitigating AD at the in vivo level compared to cerium dioxide nanoparticles (CeO2NPs). Nanoparticles were synthesized...
Contexts in source publication
Context 1
... the four groups, the hippocampus, cerebellum, and brain cortex were investigated. The (Figure 4). The AD group treated with GeO 2 NPs was the only one showing a normal feature of pyramidal cells and neurons of the hippocampus whereas the AD treated group with CeO 2 NPs showed advanced degeneration and necrosis of neurons and pyramidal cells. ...
Context 2
... real-time PCR, we assessed the expression of these nine miRNAs in brain tissue from treated and non-treated AD groups ( Figure 5). There was no significant difference in microRNAs expression Figure 4. Photomicrograph of H&E-stained hippocampus, cerebellum, and brain cortex sections of AD-induced rats treated with GeO 2 NPs (AD + GeO 2 NPs), treated with CeO 2 NPs (AD + CeO 2 NPs), left untreated (AD) and healthy rats (Control). ...
Citations
... In both in vitro and in vivo, miRNA-21 has been linked to the control of Aβ oligomer-induced toxicity (Xie et al., 2019). Down-regulation of miRNA-181 has been demonstrated in the cerebrospinal fluid of individuals diagnosed with AD (Abdel Gaber et al., 2023). Notably, miRNA-181 demonstrates an inverse correlation with the levels of IL-6 and TNF-a but demonstrates a positive association with antiinflammatory cytokines like TGF-b and IL-10. ...
Background
Taurine, an amino acid abundantly found in the brain and other tissues, has potential neuroprotective properties. Alzheimer’s disease (AD) is a commonly occurring type of dementia, which becomes more prevalent as people age. This experiment aimed to assess the neuroprotective effects of taurine on SH-SY5Y cells by examining its impact on Dihydrotestosterone (DHT), Dihydroprogesterone (DHP), as well as the expression of miRNA-21 and miRNA-181.
Methods
The effects of various taurine concentrations (0.25, and 0.75 mg/mL), and LPS (0.1, and 12 mg/mL) on the SH-SY5Y cell line were assessed using the MTT assay. The levels of DHT and DHP were quantified using an ELISA kit. Additionally, the expression levels of miRNA-181 and miRNA-21 genes were examined through Real-Time PCR analysis.
Results
The results of the MTT assay showed that treatment with taurine at concentrations of 0.25, and 0.75 mg/mL reduces the toxicity of LPS in SH-SY5Y cells. ELISA results indicated that taurine at a concentration of 0.25, and 0.75 mg/mL significantly elevated DHT and DHP hormones in the SH-SY5Y cell line compared to the untreated group ( p < 0.01). The expression levels of IL-1β and IL-6 were decreased under the influence of LPS in SH-SY5Y cells after taurine treatment (p < 0.01). Gene expression analysis revealed that increasing taurine concentration resulted in heightened expression of miRNA-181 and miRNA-21, with the most significant increase observed at a concentration of 0.75 mg/mL ( p < 0.001).
Conclusion
Our study findings revealed that the expression of miRNA-181 and miRNA-21 can be enhanced by taurine. Consequently, exploring the targeting of taurine, miRNA-181, and miRNA-21 or considering hormone therapy may offer potential therapeutic approaches for treating AD or alleviating severe symptoms. Nonetheless, in order to fully comprehend the precise mechanisms involved, additional research is required.
