Effects of Propofol on Excitatory and Inhibitory Amino Acid Neurotransmitter Balance in Rats with Neurogenic Pulmonary Edema Induced by Subarachnoid Hemorrhage

Zhang, Lili; Jin, Jin; Yao, Jiaquan; Yue, Ziyong; Wei, Yuting; Yang, Wanchao; Fu, Songbin

doi:10.1007/s12028-015-0206-x

Cited by 16 publications

(5 citation statements)

References 48 publications

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“…The most crucial cytokines in brain ischemic inflammatory response are IL-1, TNF-α, IL-6, IL-10, and transforming growth factor-β (TGF-β). In CIRI, excessive pro-inflammatory cytokines such as IL-6 and TNF-α are released and they suppress the production of anti-inflammatory cytokines such as IL-10, thus aggravating brain injury (Zhang et al, 2016). Reportedly, FPA represses IL-1β and TNF-α levels in a rat model of CIRI (Wu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Flurbiprofen axetil protects against cerebral ischemia/reperfusion injury via regulating miR‐30c‐5p and SOX9

et al. 2021

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The modulatory mechanism of flurbiprofen axetil (FPA) by which it relieves cerebral ischemia/reperfusion (I/R) injury (CIRI) is still obscure. In the present work, adult male Sprague-Dawley (SD) rats were pre-treated with FPA before the construction of a rat model of CIRI. Longa's scoring method and dry-wet method were employed to examine the neurological function and brain water content of the rats. MiR-30c-5p, SOX9, AQP4, SOX9, NF-κB, and p-NF-κB expression levels in the brain tissues of the rats were examined by qRT-PCR or Western blot.ELISA was executed to evaluate the IL-10, IL-6, and TNF-α levels in the serum of rat. SOD and MDA levels in rat brain homogenates were also examined to indicate the oxidative stress. Hematoxylin-eosin (HE) staining was used to examine the pathological changes of the brain tissues. Dual-luciferase reporter gene experiment was implemented to validate the binding relationship between miR-30c-5p and SOX9. In the present work, compared with the rats with CIRI, FPA pre-treatment attenuated neurological injury, cerebral edema, oxidative stress, inflammatory response, and cerebral pathological changes in the rat model with CIRI. FPA up-modulated miR-30c-5p expression. SOX9 was a downstream target of miR-30c-5p. In conclusion, FPA ameliorates CIRI through up-modulating miR-30c-5p expression and reducing SOX9 expression.

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Section: Discussionmentioning

confidence: 99%

Flurbiprofen axetil protects against cerebral ischemia/reperfusion injury via regulating miR‐30c‐5p and SOX9

et al. 2021

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“…Neurotransmitters such as glutamate, norepinephrine (NE) (a marker of sympathetic activity), and gamma-aminobutyric acid (GABA) in the PVN are known to be involved in the pathogenesis of hypertension 11 12 . Glutamate and NE in the PVN are the neurotransmitters that excite the sympathetic outflow 13 , and GABA in the PVN is an important neurotransmitter that inhibits sympathetic activity 14 . Evidences showed that NE and GABA in the PVN contribute to the pathogenesis of hypertension 15 16 17 , Moreover, the hypertensive responses are due to increases of excitatory adrenergic and glutamatergic activities and a decrease of GABAergic activity in the PVN 18 .…”

mentioning

confidence: 99%

PVN Blockade of p44/42 MAPK Pathway Attenuates Salt-induced Hypertension through Modulating Neurotransmitters and Attenuating Oxidative Stress

Gao

Liu

et al. 2017

Sci Rep

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The imbalance of neurotransmitters and excessive oxidative stress responses contribute to the pathogenesis of hypertension. In this study, we determined whether blockade of p44/42 MAPK pathway in the hypothalamic paraventricular nucleus (PVN) ameliorates the development of hypertension through modulating neurotransmitters and attenuating oxidative stress. Dahl salt-sensitive (S) rats received a high-salt diet (HS, 8% NaCl) or a normal-salt diet (NS, 0.3% NaCl) for 6 weeks and were treated with bilateral PVN infusion of PD-98059 (0.025 μg/h), a p44/42 MAPK inhibitor, or vehicle via osmotic minipump. HS resulted in higher mean arterial pressure (MAP) and Fra-like (Fra-LI) activity, and plasma and PVN levels of norepinephrine (NE), tyrosine hydroxylase (TH), NOX2 and NOX4, lower PVN levels of gamma-aminobutyric acid (GABA), copper/zinc superoxide dismutase (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67), as compared with NS group. PD-98059 infusion reduced NE, TH, NOX2 and NOX4 in the PVN, and induced Cu/Zn-SOD and GAD67 in the PVN. It suggests that PVN blockade of p44/42 MAPK attenuates hypertension through modulating neurotransmitters and attenuating oxidative stress.

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“…Our findings demonstrated that propofol increased GABA concentration, consistent with the view that general anesthesia inhibits excitatory synaptic transmission and enhances inhibitory synaptic transmission ( Wang et al, 2016 ; Yang et al, 2019 ). Notably, our study also showed that the concentrations of DA, Glu, NE, and ACh increased under propofol anesthesia, challenging prevailing perspectives ( Gamou et al, 2010 ; Shirasaka et al, 2011 ; Zhang et al, 2016 ). To unravel this unexpected phenomenon, we explored previous studies highlighting the potential of propofol to amplify neurotransmitter levels by inhibiting reuptake mechanisms ( Pain et al, 2002 ; Zhao & Sun, 2008 ; Zhu et al, 2023 ).…”

Section: Discussionmentioning

confidence: 51%

<i>In vivo</i> imaging reveals a synchronized correlation among neurotransmitter dynamics during propofol and sevoflurane anesthesia

Qiu,

Peng,

Wang

et al. 2024

Zoological Research

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General anesthesia is widely applied in clinical practice. However, the precise mechanism of loss of consciousness induced by general anesthetics remains unknown. Here, we measured the dynamics of five neurotransmitters, including γ-aminobutyric acid, glutamate, norepinephrine, acetylcholine, and dopamine, in the medial prefrontal cortex and primary visual cortex of C57BL/6 mice through in vivo fiber photometry and genetically encoded neurotransmitter sensors under anesthesia to reveal the mechanism of general anesthesia from a neurotransmitter perspective. Results revealed that the concentrations of γ-aminobutyric acid, glutamate, norepinephrine, and acetylcholine increased in the cortex during propofol-induced loss of consciousness. Dopamine levels did not change following the hypnotic dose of propofol but increased significantly following surgical doses of propofol anesthesia. Notably, the concentrations of the five neurotransmitters generally decreased during sevoflurane-induced loss of consciousness. Furthermore, the neurotransmitter dynamic networks were not synchronized in the non-anesthesia groups but were highly synchronized in the anesthetic groups. These findings suggest that neurotransmitter dynamic network synchronization may cause anesthetic-induced loss of consciousness.

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Effects of Propofol on Excitatory and Inhibitory Amino Acid Neurotransmitter Balance in Rats with Neurogenic Pulmonary Edema Induced by Subarachnoid Hemorrhage

Abstract: The current findings suggest that propofol improves NPE likely via IAA accumulation and the regulation of EAA and IAA balance, which may represent an effective treatment for NPE.

Cited by 16 publications

References 48 publications

Flurbiprofen axetil protects against cerebral ischemia/reperfusion injury via regulating miR‐30c‐5p and SOX9

Flurbiprofen axetil protects against cerebral ischemia/reperfusion injury via regulating miR‐30c‐5p and SOX9

PVN Blockade of p44/42 MAPK Pathway Attenuates Salt-induced Hypertension through Modulating Neurotransmitters and Attenuating Oxidative Stress

<i>In vivo</i> imaging reveals a synchronized correlation among neurotransmitter dynamics during propofol and sevoflurane anesthesia

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