Small interfering LncRNA-TUG1 (siTUG1) decreases ketamine-induced neurotoxicity in rat hippocampal neurons

Cao, Chunni; Zhang, Yanxiang; Zhang, Zuofu; Chen, Qi

doi:10.1080/00207454.2019.1594805

Cited by 12 publications

(8 citation statements)

References 40 publications

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“…Zhao et al (14) showed that ketamine (5 mM) administration caused neurotoxicity in embryonic stem cell-derived neuron culture. In another study, it has been indicated that ketamine (300 µM and 1000 µM) increased cell death at the 24th hour of administrations in rat hippocampal cells (15). It has also been demonstrated that ketamine (100 µM) administration induced apoptosis and decreased neuronal survival in rat cortical neuron culture (16).…”

Section: Discussionmentioning

confidence: 94%

Neuroprotective effects of thymoquinone against ketamine -and MK-801-induced neurotoxicity in SH-SY5Y cells: From the perspective of glutamatergic dysfunction in schizophrenia

Ünal

Erdoğan

2020

Clinical and Experimental Health Sciences

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Objective: Schizophrenia is a chronic disorder with approximately 1% prevalence and related to disrupted neurodevelopment process. It has been known that N-methyl D-Aspartate (NMDA) receptor antagonists such as ketamine and MK-801 mimic schizophrenia-like behaviors in rodents and cellular changes in cell culture. There are certain preliminary reports showing the beneficial effects of Nigella sativa L. extracts or its main active ingredient, thymoquinone, on psychiatric disorders. In our study, we aimed to investigate the neuroprotective effects of thymoquinone against ketamine -and MK-801 -induced neurotoxicites, which may be relevant to schizophrenia. Methods:The neurotoxic concentrations of ketamine and MK-801, and non-toxic concentrations of thymoquinone were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test at the 24th hour of administrations in SH-SY5Y cells. Seven different concentrations of thymoquinone (0.5 µM, 1 µM, 2.5 µM, 5 µM, 10 µM, 20 µM, 30 µM) were tested against two different concentrations of ketamine (250 µg/ml, 500 µg/ml) and one concentration of MK-801 (100 µM).Results: Ketamine (250 µg/ml and 500 µg/ml) and MK-801 (100 µM) decreased (P<0.05) the cellular viabilities at the 24 hour of administrations. Thymoquinone pretreatment prevented (P<0.05) the decrease of cell viabilities against ketamine (250 µg/ml) and ketamine (500 µg/ml) at 1 uM, 2.5 µM, 5 µM, 10 µM, 20 µM, and 2.5 µM concentrations, respectively. Thymoquinone pretreatment also increased (P<0.05) cell viability compared to MK-801. Conclusion:We suggested that thymoquinone had neuroprotective effects on the NMDA receptor antagonists induced neurotoxicity and encourage researchers for further in vivo studies for schizophrenia.

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Section: Discussionmentioning

confidence: 94%

Neuroprotective effects of thymoquinone against ketamine -and MK-801-induced neurotoxicity in SH-SY5Y cells: From the perspective of glutamatergic dysfunction in schizophrenia

Ünal

Erdoğan

2020

Clinical and Experimental Health Sciences

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“…An increasing number of studies have found that lncRNA can affect the biological behavior of hippocampal neurons, thereby regulating the progression of a variety of diseases [ 21 , 22 ] For example, the study of Wang et al confirmed that knocking out TUG1 can inhibit hippocampal neuronal apoptosis and reduce vascular cognitive impairment [ 23 ]. Cao et al found that silencing TUG1 can reduce the neurotoxicity of rat hippocampal neurons induced by ketamine [ 24 ]. In this study, we investigated the role of TUG1 in restoring hippocampal neuronal activity and preventing neuronal cell death.…”

Section: Discussionmentioning

confidence: 99%

Clinical value of lncRNA TUG1 in temporal lobe epilepsy and its role in the proliferation of hippocampus neuron via sponging miR-199a-3p

Zheng

et al. 2021

Bioengineered

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Temporal lobe epilepsy (TLE) often occurs in childhood and is the most common type of epilepsy. Studies have confirmed that long non-coding RNAs (lncRNAs) can affect the progression of neurological diseases. This study explored the expression level of lncRNA TUG1 in TLE children and its clinical significance and investigated its role in hippocampal neurons. 86 healthy individuals and 88 TLE children were recruited. The expressions of lncRNA TUG1 and miR-199a-3p in serum were detected by qRT-PCR. Hippocampal neurons were treated with non-Mg 2+ to establish TLE cell model. MTT assay and flow cytometry assay was used to detect the effect of lncRNA TUG1 on the proliferation and apoptosis of hippocampal neurons. A dual-luciferase reporter assay was done to confirm the target relationship. The expression of lncRNA TUG1 was increased in TLE children compared with the control group. The diagnostic potential was reflected by the receiver operator characteristic (ROC) curve, with the AUC of 0.915 at the cutoff value of 1.256. Elevated levels of TUG1 were detected in TLE cell models, and TUG1 knockout could enhance cell activity and inhibit cell apoptosis. MiR-199a-3p was the target of TUG1. Clinically, the serum miR-199a-3p levels showed a negative association with TUG1. LncRNA TUG1 may be a biomarker of TLE diagnosis in children, and can regulate hippocampal neuron cell activity and apoptosis via sponging miR-199a-3p.

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“…On the contrary, silencing of lncRNA TUG1 protected human nucleus pulposus cells from apoptosis and senescence evoked by TNF-α by diminishing caspase-3 expression [ 39 ]. Rat hippocampal neurons treated by si-TUG1 + Ketamine exhibited lower levels of TUG1 and c-caspase3 than those treated by Ketamine alone [ 40 ]. Considering the aforementioned findings, we concluded that lncRNA TUG1 is closely linked to death of cells.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 knockdown prevents neurons from death to alleviate acute spinal cord injury via the microRNA-338/BIK axis

Zhang

et al. 2021

Bioengineered

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Taurine up-regulated gene 1 (TUG1) is a cancer-associated long noncoding RNA (lncRNA) and engages in the development of spinal cord injury (SCI), a suffering neuropathological disorder. However, the regulatory role of TUG1 in acute SCI (ASCI) is still underdetermined. RT-qPCR and western blot analysis were applied to measure the expression of TUG1, microRNA-338 (miR-338), Bcl2-interacting killer (BIK), cleaved caspase 3 (c-caspase 3) and hypoxia-inducible factor-1 alpha (HIF-1α) in ASCI rats and hypoxic cells. Cell death was evaluated using flow cytometric analysis. The relationships among miR-338, TUG1 or BIK were confirmed by luciferase reporter assay, RNA immunoprecipitation and RNA pull-down. Accordingly, we monitored higher expression of TUG1 and BIK, but lower expression of miR-338 in ASCI rats and hypoxic cells. In vitro, hypoxia expedited cell death and c-caspase 3 levels. In vivo, ASCI rats were successfully developed as evidenced by diminished Basso-Beattie-Bresnahan (BBB) locomotor score and enhanced c-caspase 3 and HIF-1α expression. Nevertheless, TUG1 knockdown mitigated the cell death in ASCI rats and hypoxic cells. Mechanically, TUG1 interacted with miR-338 to regulate the BIK expression. Together, TUG1 silencing could alleviate the death in neurons and ASCI models via modulating the miR-338/BIK axis.

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Small interfering LncRNA-TUG1 (siTUG1) decreases ketamine-induced neurotoxicity in rat hippocampal neurons

Cited by 12 publications

References 40 publications

Neuroprotective effects of thymoquinone against ketamine -and MK-801-induced neurotoxicity in SH-SY5Y cells: From the perspective of glutamatergic dysfunction in schizophrenia

Neuroprotective effects of thymoquinone against ketamine -and MK-801-induced neurotoxicity in SH-SY5Y cells: From the perspective of glutamatergic dysfunction in schizophrenia

Clinical value of lncRNA TUG1 in temporal lobe epilepsy and its role in the proliferation of hippocampus neuron via sponging miR-199a-3p

Long non-coding RNA TUG1 knockdown prevents neurons from death to alleviate acute spinal cord injury via the microRNA-338/BIK axis

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