MicroRNA‑489‑3p plays a significant role in congenital hypothyroidism through regulating neuronal cell apoptosis via targeting translationally controlled tumor protein 1

ABSTRACTThis study aimed to explore the mechanism of perfluorooctylbromide (PFOB) nanoparticles (NPs) combined with ulinastatin (UTI) on early brain injury (EBI) caused by carbon monoxide poisoning (CMP). Firstly, PFOB NPs were prepared by high-speed dispersion and high-speed homogenization. The physicochemical characteristics of the particle size distribution and Zeta potential distribution of the NPs were analyzed using a laser particle size analyzer. The thermal and photoinduced phase transition characteristics of the NPs were analyzed under heating and laser irradiation conditions. Then, 50 Sprague Dawley (SD) rats were deemed as the research objects to establish the CMP rat models using hyperbaric oxygen chambers. According to different treatment methods, they were rolled into a healthy control group, a carbon monoxide (CO) model group, a PTOB treatment group, an UTI treatment group, and a PTOB + UTI treatment group. The brain tissues of each group of rats were collected 3 days after treatment. The neuronal cell apoptosis, expression of Caspase-3, messenger ribonucleic acid (mRNA) of inflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rat brain tissue were detected through immunohistochemical staining, in situ cell apoptosis detection, Reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting, so did the relative expression of target proteins B-cell lymphoma-2 (Bcl-2), Bcl2-Associated X (Bax) and myelin basic protein (MBP). As a result, the average particle size and the average Zeta potential of the prepared PFOB NPs was 103±31 nm and −23 ± 15 mV, respectively. When the PFOB NPs were heated to 80 °C, the particle size increased greatly and cracks appeared. The particle size of PFOB NPs also increased obviously after laser irradiation, and the PFOB inside the particles changed into gas phase. Compared to CO group, expression of Caspase-3, neuronal cell apoptosis rate, mRNA expression of IL-1β and TNF-α, and protein expression of Bax and Bcl-2 in the brain tissue of PTOB group, UTI group, and PFOB + UTI group were notably decreased (P < 0.05), while the MBP protein expression increased considerably (P < 0.05). Changes in PFOB + UTI group were more obvious than those in PTOB group and UTI group, and those indicators weren’t considerably different from the controls. In summary, PFOB NPs were successfully prepared with favorable phase transition characteristics. Moreover, PFOB NPs combined with UTI could reduce the apoptosis of brain neurons after CMP, improve the inflammatory response, and play a protective effect on EBI of CMP.

Download Full-text

Dehydroepiandrosterone, as Endogenous Inhibitor of Neuronal Cell Apoptosis: Potential Therapeutic Implications in Neurodegenerative Diseases

Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders ◽

10.1007/978-1-4020-6854-6_11 ◽

2008 ◽

pp. 217-225

Author(s):

Ioannis Charalampopoulos ◽

Christos Tsatsanis ◽

Andrew N. Margioris ◽

Elias Castanas ◽

Achille Gravanis

Keyword(s):

Neurodegenerative Diseases ◽

Cell Apoptosis ◽

Neuronal Cell ◽

Endogenous Inhibitor ◽

Therapeutic Implications

Download Full-text

MicroRNA-27a-3p Downregulation Inhibits Inflammatory Response and Hippocampal Neuronal Cell Apoptosis by Upregulating Mitogen-Activated Protein Kinase 4 (MAP2K4) Expression in Epilepsy: In Vivo and In Vitro Studies

Medical Science Monitor ◽

10.12659/msm.916458 ◽

2019 ◽

Vol 25 ◽

pp. 8499-8508 ◽

Cited By ~ 3

Author(s):

Jun Lu ◽

Nina Zhou ◽

Ping Yang ◽

Lanqiuzi Deng ◽

Ganzhe Liu

Keyword(s):

Protein Kinase ◽

Inflammatory Response ◽

Cell Apoptosis ◽

Neuronal Cell ◽

In Vitro Studies ◽

Mitogen Activated Protein Kinase ◽

Mitogen Activated Protein

Download Full-text

Haloperidol and Risperidone Induce Apoptosis Neuronal Cell : Invivo Study

Scientia Psychiatrica ◽

10.37275/scipsy.v1i1.5 ◽

2020 ◽

Vol 1 (1) ◽

Author(s):

Ester G Panserga ◽

Cecep S Kristanto ◽

Budi Pratiti ◽

Patricia Wulandari

Keyword(s):

Cell Apoptosis ◽

Wistar Rats ◽

Caspase 3 ◽

Neuronal Cells ◽

Neuronal Cell ◽

Total Percentage ◽

White Rats ◽

Male Wistar Rats ◽

Group B

Abstract Introduction Antipsychotics are drugs that are widely prescribed for mental disorders, such as schizophrenia and psychosis. Recent in vitro studies show antipsychotics play a role in the initiation of neuronal cell apoptosis. This study aims to determine the effect of haloperidol and risperidone on neuronal cell apoptosis in Wistar white rats. Methods Male wistar rats aged 8 weeks (n = 30) were used in this study. Wistar rats were randomized into 6 groups. Group A: 5 wistar rats as a control without induced schizophrenia, aquades and drugs. Group B: 5 Wistar-induced psychotic mice (using 30 mg / kgBB ketamine, intraperitoneal injection for 5 days) and aquadest. Group C: 5 rats were induced psychotic and were given haloperidol or 0.05 mg / kgBB orally, for 28 days. Group D: 5 mice were induced psychotic and were given haloperidol 0.1 mg / kg orally, for 28 days. Group E: 5 mice were induced psychotic and were given risperidone 0.05 mg / kgBB orally, for 28 days. Group F: 5 mice were induced psychotic and given risperidone 0.1 mg / kgBB orally, for 28 days. Apoptosis of neuronal cells in the ventral tegmental area was assessed by caspase-3 immunohistochemistry. The colored area will be calculated as a total percentage using the imageJ program. Results Risperidone and haloperidol increase caspase-3 activity, but haloperidol increases caspase-3 activity more than risperidone. Conclussion Risperidone and haloperidol induce apoptosis of neuronal cells and tardive dyskinesia in Wistar rats with psychotic models.

Download Full-text

Regulation of the p75 Neurotrophin Receptor Attenuates Neuroinflammation and Stimulates Hippocampal Neurogenesis in Experimental Streptococcus Pneumoniae Meningitis

10.21203/rs.3.rs-586130/v1 ◽

2021 ◽

Author(s):

Dandan Zhang ◽

Shengnan Zhao ◽

Zhijie Zhang ◽

Danfeng Xu ◽

Di Lian ◽

...

Keyword(s):

Transcription Factors ◽

Streptococcus Pneumoniae ◽

Cell Apoptosis ◽

Neuronal Cell ◽

Hippocampal Neurogenesis ◽

Clinical Severity ◽

Neurotrophin Receptor ◽

Double Labeling

Abstract Background: Streptococcus pneumoniae meningitis is a destructive central nervous system (CNS) infection with acute and long-term neurological disorders. Compelling evidence provided by previous studies suggests that p75NTR signaling influences cell survival, apoptosis, and proliferation in brain-injured conditions. However, the role of p75NTR signaling in regulating pneumococcal meningitis (PM)-induced neuroinflammation and altered neurogenesis remains largely to be elucidated.Methods: p75NTR signaling activation in the pathological process of PM was assessed. During acute PM, a small-molecule p75NTR modulator LM11A-31 or vehicle was intranasally administered for 3 days prior to S.pneumoniae exposure. At 24h post-infection, clinical severity, histopathology, astrocytes/microglia activation, neuronal cell apoptosis and death, inflammation-related transcription factors and inflammatory factors were evaluated. Additionally, p75NTR was knocked down by the adenovirus-mediated short-hairpin RNA (shRNA) to ascertain the role of p75NTR in PM. During long-term PM, the intranasal administration of LM11A-31 or vehicle was continued for 7 days after successfully establishing the PM model. Hippocampal neurogenesis was evaluated by double-labeling immunofluorescence with EdU, DCX and NeuN. Results: Our results revealed that both 24h (acute) and 7,14,28day (long-term) groups of infected rats demonstrated increased p75NTR expression in the brain. During acute PM, modulation of p75NTR through pretreatment of PM model with LM11A-31 significantly alleviated S.pneumoniae-induced clinical severity, histopathological injury and the activation of astrocytes and microglia. LM11A-31 pretreatment also significantly ameliorated neuronal cell apoptosis and death. Moreover, we found that blocking p75NTR with LM11A-31 decreased the expression of inflammation-related transcription factors (NF-κBp65, C/EBPβ) and proinflammatory cytokine (IL-1β, TNF-α, IL-6 and iNOS) in the cortex and hippocampus. Furthermore, p75NTR knockdown induced significant changes in histopathology and inflammation-related transcription factors expression. Importantly, combined LM11A-31 adjuvant therapy significantly improved hippocampal neurogenesis.Conclusion: Our findings suggest that the p75NTR signaling plays an essential role in the pathogenesis of PM. Targeting p75NTR has benefit effects on PM rats by alleviating neuroinflammation and promoting hippocampal neurogenesis. Thus, the p75NTR signaling may be a potential therapeutic target to improve the outcome of PM.

Download Full-text