Dexmedetomidine improves propofol-induced neuronal injury in rat hippocampus with the involvement of miR-34a and the PI3K/Akt signaling pathway

Xing, Na; Xing, Fei; Li, Yanna; Pingle, Li; Zhang, Jianwen; Wang, Dongmei; Zhang, Wei; Yang, Jianjun

doi:10.1016/j.lfs.2020.117359

Cited by 30 publications

(26 citation statements)

References 42 publications

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“…Specifically, the following findings from cell culture models showed that miR-15a-5p [53], MicroRNA-582-5p [54] and miR-34a [55] were involved in propofol-induced neuron and astrocyte death, respectively; miR-21 was involved in propofol-induced inhibition of proliferation and epithelial-mesenchymal transition in breast cancer cells [56]; miR-495 was involved in propofol-induced inhibition of proliferation and metastasis in JEG-3 choriocarcinoma cells [57]. In this study, propofol treatment decreased cell migration followed by miR-34a and E-cadherin upregulation in the PANC-1 cells.…”

Section: Discussionmentioning

confidence: 99%

“…miR-34 has been shown to regulate pancreatic cancer cell growth, invasion and metastasis in vitro and in vivo by targeting members of key signaling pathways [28][29][30]. Recent studies have demonstrated that propofol upregulated miR-34a expression and induced cell apoptosis in SH-SY5Y cells in vitro, and targeting miR-34 protected the SH-SY5Y cells from propofol-induced apoptosis [31,32].…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

Wang¹,

Jiao²,

Jiang³

et al. 2020

Bioengineered

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Propofol has exhibited potent antitumor activity in pancreatic cancer cells in vitro and in vivo. The study aimed to investigate the anti-tumor mechanisms of propofol on pancreatic cancer PANC-1 cells in vitro. PANC-1 cells were exposure to concentration 20 μg/ml of propofol for 72 h. Long non-coding RNA LOC285194 siRNA LOC285194 siRNA, E-cadherin siRNA and microRNA-34a (miR-34a) inhibitor were used to investigate the effect of propofol on PANC-1 cells. miR-34a and LOC285194 were analyzed by quantitative real-time PCR (qRT-PCR). Pro-apoptotic protein bax, cleaved-caspase-3 and anti-apoptotic protein bcl-2 were analyzed by Western blot. Cell viability and cell apoptosis were detected by MTT and TUNEL staining, respectively. Cell migration was detected by wound-healing assay. The results showed that propofol upregulated miR-34a expression, which, in turn, upregulated LOC285194 expression, resulting in PANC-1 cell apoptosis and growth inhibition. In addition, propofol upregulated miR-34a expression, which, in turn, upregulated E-cadherin expression, resulting in cell migration inhibition. Our research confirmed that propofol-induced cell apoptosis and inhibited cell migration in PANC-1 cells in vitro via promoting miR-34a-dependent LOC285194 and E-cadherin upregulation, respectively.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

Wang¹,

Jiao²,

Jiang³

et al. 2020

Bioengineered

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“…Similarly, post-conditioning of DEX has already been found to confer therapeutic impacts on CIRI by decreasing infarction area [ 26 , 27 ]. Besides, it has also been observed that DEX relieves neuronal injury in the rat hippocampus through reduction of neuronal cell apoptosis [ 28 ]. These references further substantiated our results that DEX has the potency to alleviate CIRI.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of dexmedetomidine on cerebral ischemia/reperfusion injury via the microRNA-214/ROCK1/NF-κB axis

et al. 2021

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Background Cerebral ischemia/reperfusion injury (CIRI) is a complication of surgical procedure associated with high mortality. The protective effect of dexmedetomidine (DEX) on CIRI has been explored in previous works, yet the underlying molecular mechanism remains unclear. Our study explored the protective effect of DEX and its regulatory mechanism on CIRI. Methods A CIRI rat model was established using middle cerebral artery occlusion (MCAO). Neurological deficit scores for rats received MCAO modeling or DEX treatment were measured. Cerebral infarction area of rats was detected by TTC staining, while damage of neurons in hippocampal regions of rats was determined by hematoxylin-eosin (HE) staining. Apoptosis rate of neurons in hippocampal regions was examined by TUNEL staining. The dual-luciferase assay was performed to detect the binding of microRNA-214 (miR-214) to Rho-associated kinase 1 (ROCK1). Results DEX treatment significantly reduced infarction area of MCAO rats and elevated miR-214 expression. Injection of miR-214 inhibitor attenuated the effect of DEX in MCAO rats by increasing the area of cerebral infarction in rats and apoptosis rate of hippocampal neurons. ROCK1 was targeted and negatively regulated by miR-214. The overexpression of ROCK1 led to activation of NF-κB to aggravate CIRI. Conclusion Therapeutic effects of DEX on CIRI was elicited by overexpressing miR-214 and impairing ROCK1 expression and NF-κB activation. Our finding might provide novel insights into the molecular mechanism of DEX in rats with CIRI.

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“…The mechanisms of anesthetic neurotoxicity include excessive and abnormal activation of the N-methyl-D-aspartate (NMDA) and GABA-A receptors, 26 generation of free radicals, 27 activation of P75 growth factor, 28 inflammation, and excessive increase of Ca 2, 29 We considered using edaravone as a free radical scavenger to reduce anesthetic neurotoxicity. In cell proliferation, nestin is an intermediate neurofilament protein that can be used as a marker of neural stem cells for immunolocalization, indicating that neural stem cells are actively proliferating based on the incorporation of ki67.…”

Section: Discussionmentioning

confidence: 99%

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Yang¹,

Yi²,

Pan³

et al. 2021

DDDT

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Background: To investigate the neuroprotective effect of edaravone on excessive-dose propofol-induced neurotoxicity in the hippocampus of newborn rats and HT22 cells.Methods: Cell proliferation was investigated by assessing ki67 expression in the neural stem of the hippocampus of newborn rats and by cell counting kit-8 (CCK8) assay in HT22 cells. Cell apoptosis was assessed in vivo by caspase 3 detection in Western blots and measurement of apoptosis in neurons and glial cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Apoptosis was analyzed by flow cytometry in HT22 cells. The Morris water maze was used to evaluate the long-term learning and memory ability of rats. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). The expression of mBDNF/TrkB/PI3K pathway-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction (q-RT PCR). Results: In neonatal rat hippocampus and HT22 cells, edaravone increased cell proliferation and decreased cell apoptosis after excessive propofol-induced neurotoxicity. In addition, the levels of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α were reduced by edaravone pretreatment. The use of the tropomyosin receptor kinase B (TrkB) antagonist ANA-12 and TrkB agonist 7,8DHF with propofol groups showed that edaravone mitigated excessive propofol-induced neurotoxicity through the mature brain-derived neurotrophic factor (mBDNF)/TrkB/phosphoinositide 3-kinase (PI3K) pathway. However, the current dose of propofol did not significantly affect long-term learning and memory in rats. Conclusion: Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.

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Dexmedetomidine improves propofol-induced neuronal injury in rat hippocampus with the involvement of miR-34a and the PI3K/Akt signaling pathway

Cited by 30 publications

References 42 publications

RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

RETRACTED ARTICLE: Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals

Protective effects of dexmedetomidine on cerebral ischemia/reperfusion injury via the microRNA-214/ROCK1/NF-κB axis

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

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