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Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ 1-40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus.
Mediators Inflamm. 2018; 2018:3802324.MI

Abstract

Objective

This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event.

Methods

Thirty-two rats were randomly divided into four groups of normal saline (NS) + O2, NS + sevoflurane (sevo), amyloid-β peptide (Aβ) + O2, and Aβ + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or Aβ. The treated hippocampus was harvested after inhaling 30% O2 or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an Aβ 1-42 level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR.

Results

Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of Aβ 1-42 of the brain in the Aβ-treated group. Sevoflurane inhalation but not O2 significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in Aβ-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled O2 and sevoflurane in Aβ-treated groups (all P < 0.05). Interleukin- (IL-) 1β, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) mRNA expression increased after the rats inhaled sevoflurane in the Aβ-treated group (both P < 0.01). There were no significant differences in the change of GFAP, IBA1, Bcl-xL, caspase-9, RAGE, BDNF, IL-1β, NF-κB, and iNOS in the NS + O2 and NS + sevo group (all P > 0.05).

Conclusion

Sevoflurane exacerbates cognitive impairment induced by Aβ 1-40 in rats through initiating neurotoxicity, neuroinflammation, and neuronal apoptosis in rat hippocampus.

Authors+Show Affiliations

Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.Department of Laboratory Animal Science, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.Department of Pharmacy, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Herping District, Shenyang, Liaoning 110004, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30402039

Citation

Tian, Yue, et al. "Sevoflurane Exacerbates Cognitive Impairment Induced By Aβ 1-40 in Rats Through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus." Mediators of Inflammation, vol. 2018, 2018, p. 3802324.
Tian Y, Chen KY, Liu LD, et al. Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ 1-40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus. Mediators Inflamm. 2018;2018:3802324.
Tian, Y., Chen, K. Y., Liu, L. D., Dong, Y. X., Zhao, P., & Guo, S. B. (2018). Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ 1-40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus. Mediators of Inflammation, 2018, 3802324. https://doi.org/10.1155/2018/3802324
Tian Y, et al. Sevoflurane Exacerbates Cognitive Impairment Induced By Aβ 1-40 in Rats Through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus. Mediators Inflamm. 2018;2018:3802324. PubMed PMID: 30402039.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ 1-40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus. AU - Tian,Yue, AU - Chen,Ke-Yan, AU - Liu,Li-Dan, AU - Dong,Yun-Xia, AU - Zhao,Ping, AU - Guo,Shan-Bin, Y1 - 2018/10/09/ PY - 2018/02/26/received PY - 2018/07/25/accepted PY - 2018/11/8/entrez PY - 2018/11/8/pubmed PY - 2019/1/23/medline SP - 3802324 EP - 3802324 JF - Mediators of inflammation JO - Mediators Inflamm. VL - 2018 N2 - Objective: This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event. Methods: Thirty-two rats were randomly divided into four groups of normal saline (NS) + O2, NS + sevoflurane (sevo), amyloid-β peptide (Aβ) + O2, and Aβ + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or Aβ. The treated hippocampus was harvested after inhaling 30% O2 or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an Aβ 1-42 level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR. Results: Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of Aβ 1-42 of the brain in the Aβ-treated group. Sevoflurane inhalation but not O2 significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in Aβ-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled O2 and sevoflurane in Aβ-treated groups (all P < 0.05). Interleukin- (IL-) 1β, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) mRNA expression increased after the rats inhaled sevoflurane in the Aβ-treated group (both P < 0.01). There were no significant differences in the change of GFAP, IBA1, Bcl-xL, caspase-9, RAGE, BDNF, IL-1β, NF-κB, and iNOS in the NS + O2 and NS + sevo group (all P > 0.05). Conclusion: Sevoflurane exacerbates cognitive impairment induced by Aβ 1-40 in rats through initiating neurotoxicity, neuroinflammation, and neuronal apoptosis in rat hippocampus. SN - 1466-1861 UR - https://www.unboundmedicine.com/medline/citation/30402039/Sevoflurane_Exacerbates_Cognitive_Impairment_Induced_by_Aβ_1_40_in_Rats_through_Initiating_Neurotoxicity_Neuroinflammation_and_Neuronal_Apoptosis_in_Rat_Hippocampus_ L2 - https://dx.doi.org/10.1155/2018/3802324 DB - PRIME DP - Unbound Medicine ER -