Tanshinone IIA Attenuates Sevoflurane Neurotoxicity in Neonatal Mice

Xia, Yanfei; Xu, Heng; Jia, Chenfei; Hu, Xiaodong; Kang, Yu; Yang, Xiaoxuan; Xue, Qingsheng; Tao, Guorong; Yu, Bo

doi:10.1213/ane.0000000000001942

Cited by 33 publications

(20 citation statements)

References 39 publications

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“…In recent years, anesthesia methods and the use of anesthetics have been suggested to be closely related to the occurrence of POCD [ 3 ]. Sevoflurane, as one of the most commonly used inhalation anesthetics in clinical practice, may induce mental retardation in children or trigger a higher incidence of POCD in elderly patients, when it inhaled in high concentrations or for many times [ 4 , 5 ]. Besides, previous evidence has published that the major neurotoxicity of sevoflurane included the accumulation of β-amyloid protein (Aβ) [ 6 ], neuroinflammation [ 7 ], and reduction of synaptic plasticity [ 8 ], which have been accepted as the physiological basis of POCD in certain patients.…”

Section: Introductionmentioning

confidence: 99%

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

Yang¹,

Yuan²

2018

BMC Anesthesiol

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BackgroundTo investigate the role of IL-17A in the neuroinflammation and cognitive function of aged rats anaesthetized with sevoflurane through NF-κB pathway.MethodThe aged and young adult rats were randomly divided into Control (inhale oxygen only), Sevoflurane (inhale oxygen and sevoflurane), Sevo (Sevoflurane) + anti-IL-17A (injected with IL-17A antibody, inhale oxygen and sevoflurane), and Sevo + NC groups (injected with IgG2a antibody, inhale oxygen and sevoflurane). Cognitive function was evaluated by Morris water maze and contextual fear conditioning tests. Tumor necrosis factor (TNF)-α, Interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein (MCP)-1 expressions in the hippocampus of rats were detected by ELISA (enzyme-linked immunosorbent assay) assay, and Nuclear factor (NF)-κB pathway-related proteins by Western blot.ResultsSevoflurane anaesthetized aged rats showed longer escape latency and swimming distance, fewer platform crossing times, shortened stay time in the platform quadrant compared to Control rats; In addition, increased levels in hippocampal expression of malondialdehyde (MDA), IL-17A, NF-κB p65, inducible nitric oxide synthase (iNOS) and COX-2, as well as a reduced level of superoxide dismutase (SOD) were also observed in these animals. However, the sevoflurane anesthetized aged rats treated with anti-IL-17A presented a completely opposite tendency concerning the above factors (all P < 0.05). Nevertheless, there was no significant difference in the acquisition of learning or memory, neuroinflammation and oxidative stress of young adult rats in all groups (all P > 0.05).ConclusionAnti-IL-17A may alleviate neuroinflammation and oxidative stress via inhibiting NF-κB pathway, thereby attenuating post-operative cognitive dysfunction (POCD) in aged rats anaesthetized with sevoflurane.

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Section: Introductionmentioning

confidence: 99%

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

Yang¹,

Yuan²

2018

BMC Anesthesiol

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“…Previous studies also found that a single exposure of neonatal mice to 3% sevoflurane for 2 h or 6 h did not increase the levels of IL-6 or/and TNF-α in the brain 23,24 . On the other hand, however, repeated exposure (3% sevoflurane, 2 h daily for 3 days), led to a notable increase in the levels of IL-6, IL-1β, and TNF-α, in the brains of neonatal mice immediately after anesthesia 23,25,26 . This discrepancy may be related to the different doses of anesthetics used, thus indicating that repeated episodes of anesthesia are far more neurotoxic and that the neurotoxicity of sevoflurane in neonatal mice is both dose-and time-dependent.…”

Section: Discussionmentioning

confidence: 97%

The differential effects of isoflurane and sevoflurane on neonatal mice

Zhao

Fan

et al. 2020

Sci Rep

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Previous research has shown that exposure to volatile anesthetics can induce acute neuroinflammation and neuroapoptopsis in neonatal rodents and that these events can lead to cognitive dysfunction at later stages. Isoflurane and sevoflurane are two of the most popular anesthetics used in the field of pediatrics. However, the relative impact of these two anesthetics on the developing brain at distinct time points after the induction of anesthesia has not been compared. In the present study, we exposed 7-day-old mice to clinically equivalent doses of isoflurane (1.5%) and sevoflurane (2.5%) for 4 h and then investigated consequential changes in the brains of these mice at six different time points. We analyzed the levels of proteins that are directly related to neuroapoptosis, neuroinflammation, synaptic function, and memory, in the brains of neonatal mice. Exposure of neonatal mice to isoflurane and sevoflurane resulted in acute neuronal apoptosis. Our analysis observed significant levels of neuroinflammation and changes in the expression levels of proteins associated with both synaptic transmission and memory in mice from the isoflurane group but not the sevoflurane group. Our results therefore indicate that isoflurane and sevoflurane induce differential effects in the brains of neonatal mice.

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“…These changes include neurodegenerative changes [3,4] , neural apoptosis or cell death, and impaired neurogenesis [5] . In addition, anaesthesia exposure in infancy has also been associated with memory impairment, behavioural disorders, and poor intellectual development persisting to early adulthood [6][7][8][9][10] . Repeated and prolonged exposure to general anaesthetics in the developing brain is still a high-risk factor for neuronal injury [6,11,12] .…”

Section: Introductionmentioning

confidence: 99%

WNK1 Antagonist Decreased Sevoflurane-induced Neurotoxicity in HT22 Hippocampal Neurons via the WNK1/NKCC1 Signalling Pathway

Bai

Zhang

et al. 2020

Preprint

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Background: . The GABAAR plays an important role in the neurotoxicity caused by sevoflurane, but the mechanism of its regulation in this context is unknown. The present study aimed to reveal the WNK1/NKCC1 pathway as a regulator of the neurotoxicity caused by sevoflurane on the HT22 hippocampal neuron cell line. Methods: HT22 cultured hippocampal neurons were divided into three groups: control group, 4.1% sevoflurane treatment group for 6h, WNK-463 (specific antagonist of WNK1, 1µmol) + sevoflurane treatment group. Cell viability and the optimum concentration of WNK-463 were measured by MTS method. Cell apoptosis was detected by Tunel method, and the content of cleaved caspase-3 protein apoptosis factor was detected by Western blot. Pathway protein detection including the expression of WNK1, NKCC1 were detected. Calcium imaging measures intracellular calcium ion concentration and verifies downstream targets.Results: The neurotoxic effects of sevoflurane on hippocampal neurons were observed. As setting the results of control group is “1”, compared with sevoflurane group, WNK-463 downregulated the protein expression of cleaved caspase-3 (1.96±0.49 vs 1.29±0.38), increased cell viability (0.68 vs 0.96) and decreased apoptosis (13.31±4.67/vision vs 7.05±3.82/vision, ***P < 0.001). Compared with the control group, sevoflurane treatment increased the expression of WNK1 kinase and NKCC1 protein, whereas WNK-463 reversed this increase without affecting the control HT22 cells (****P < 0.0001). Compared with the control group, sevoflurane exposure in HT22 cells increased intracellular Ca2+ concentrations, while WNK-463 reversed this change (1.0 vs 2.08±1.36 vs 1.26±0.77, **P < 0.01). Conclusion: This study demonstrated a neuroprotective role of the WNK1 antagonist WNK-463 in sevoflurane-induced neurotoxicity. WNK-463 promoted hippocampal neuron viability and reduced the apoptosis and intracellular calcium overload caused by sevoflurane on HT22 hippocampal neurons, possibly via the modulation of the WNK1/NKCC1 pathway.

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Tanshinone IIA Attenuates Sevoflurane Neurotoxicity in Neonatal Mice

Abstract: These results indicate that Tan IIA can alleviate sevoflurane-induced neurobehavioral abnormalities and may decrease neuroapoptosis and neuroinflammation.

Cited by 33 publications

References 39 publications

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

The differential effects of isoflurane and sevoflurane on neonatal mice

WNK1 Antagonist Decreased Sevoflurane-induced Neurotoxicity in HT22 Hippocampal Neurons via the WNK1/NKCC1 Signalling Pathway

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Tanshinone IIA Attenuates Sevoflurane Neurotoxicity in Neonatal Mice

Abstract: These results indicate that Tan IIA can alleviate sevoflurane-induced neurobehavioral abnormalities and may decrease neuroapoptosis and neuroinflammation.

Cited by 33 publications

References 39 publications

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

IL-17A promotes the neuroinflammation and cognitive function in sevoflurane anesthetized aged rats via activation of NF-κB signaling pathway

The differential effects of isoflurane and sevoflurane on neonatal mice

WNK1&nbsp;Antagonist Decreased Sevoflurane-induced Neurotoxicity in HT22 Hippocampal Neurons via the WNK1/NKCC1 Signalling Pathway

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WNK1 Antagonist Decreased Sevoflurane-induced Neurotoxicity in HT22 Hippocampal Neurons via the WNK1/NKCC1 Signalling Pathway