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Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway.
Med Sci Monit. 2020 Mar 01; 26:e919600.MS

Abstract

BACKGROUND

Compound porcine cerebroside and ganglioside injection (CPCGI) has been widely applied in clinical practice in China to treat functional confusion caused by brain diseases. Sevoflurane, a frequently-used inhalational anesthetic, was discovered to have neurotoxicity that can cause neurological damage in patients. The present study was performed to investigate the protective effect of CPCGI on sevoflurane-induced nerve damage and to reveal the neuroprotective mechanisms of CPCGI. MATERIAL AND

METHODS

Firstly, the hippocampal neurons were separated from Sprague-Dawley embryonic rats, and were stimulated by 3% sevoflurane for different times (0, 2, 4, and 6 h). Then, cell viability and cell apoptosis were assessed by thiazolyl blue tetrazolium bromide (MTT) and flow cytometry (FCM), respectively. Western blot analysis was used to determine the apoptosis-related protein expression levels.

RESULTS

The results demonstrated that 3% sevoflurane significantly inhibited cell viability but induced cell apoptosis in neurons in a time-dependent manner. Treatment with 3% sevoflurane also promoted the Bax (B cell leukemia/lymphoma 2​ (Bcl2)-associated X protein) and cleaved caspase3 protein expressions, and suppressed Bcl-2 and pro-caspase3 expressions in hippocampal neurons. In addition, phosphorylated (p)-p38 and p-p65 expression and the ratio of p-p38/p38 and p-p65/p65 were upregulated in a time-dependent manner after 3% sevoflurane treatment. Further analysis indicated that all the effects of 3% sevoflurane on hippocampal neurons were reversed by CPCGI pre-treatment.

CONCLUSIONS

We demonstrated the neuroprotective role of CPCGI in sevoflurane-stimulated neuronal cell damage via regulation of the MAPK/NF-kappaB signaling pathway.

Authors+Show Affiliations

Department of Anesthesiology, Xianyang Hospital of Yan'an University, Xianyang, Shaanxi, China (mainland).Department of First Anesthesiology and Surgery, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, Shaanxi, China (mainland).Department of First Anesthesiology and Surgery, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, Shaanxi, China (mainland).Department of First Anesthesiology and Surgery, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, Shaanxi, China (mainland).Department of Anesthesiology, The Fifth Medical Center of PLA General Hospital, Beijing, China (mainland).

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32114591

Citation

Song, Haigang, et al. "Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury By Regulating the Phosphorylation of P38 MAP Kinase (p38MAPK)/Nuclear Factor Kappa B (NF-κB) Pathway." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 26, 2020, pp. e919600.
Song H, Xun S, He H, et al. Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway. Med Sci Monit. 2020;26:e919600.
Song, H., Xun, S., He, H., Duan, C., & Li, Q. (2020). Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 26, e919600. https://doi.org/10.12659/MSM.919600
Song H, et al. Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury By Regulating the Phosphorylation of P38 MAP Kinase (p38MAPK)/Nuclear Factor Kappa B (NF-κB) Pathway. Med Sci Monit. 2020 Mar 1;26:e919600. PubMed PMID: 32114591.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway. AU - Song,Haigang, AU - Xun,Shining, AU - He,Huali, AU - Duan,Chongzhen, AU - Li,Qiang, Y1 - 2020/03/01/ PY - 2020/3/2/entrez PY - 2020/3/3/pubmed PY - 2020/12/22/medline SP - e919600 EP - e919600 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med Sci Monit VL - 26 N2 - BACKGROUND Compound porcine cerebroside and ganglioside injection (CPCGI) has been widely applied in clinical practice in China to treat functional confusion caused by brain diseases. Sevoflurane, a frequently-used inhalational anesthetic, was discovered to have neurotoxicity that can cause neurological damage in patients. The present study was performed to investigate the protective effect of CPCGI on sevoflurane-induced nerve damage and to reveal the neuroprotective mechanisms of CPCGI. MATERIAL AND METHODS Firstly, the hippocampal neurons were separated from Sprague-Dawley embryonic rats, and were stimulated by 3% sevoflurane for different times (0, 2, 4, and 6 h). Then, cell viability and cell apoptosis were assessed by thiazolyl blue tetrazolium bromide (MTT) and flow cytometry (FCM), respectively. Western blot analysis was used to determine the apoptosis-related protein expression levels. RESULTS The results demonstrated that 3% sevoflurane significantly inhibited cell viability but induced cell apoptosis in neurons in a time-dependent manner. Treatment with 3% sevoflurane also promoted the Bax (B cell leukemia/lymphoma 2​ (Bcl2)-associated X protein) and cleaved caspase3 protein expressions, and suppressed Bcl-2 and pro-caspase3 expressions in hippocampal neurons. In addition, phosphorylated (p)-p38 and p-p65 expression and the ratio of p-p38/p38 and p-p65/p65 were upregulated in a time-dependent manner after 3% sevoflurane treatment. Further analysis indicated that all the effects of 3% sevoflurane on hippocampal neurons were reversed by CPCGI pre-treatment. CONCLUSIONS We demonstrated the neuroprotective role of CPCGI in sevoflurane-stimulated neuronal cell damage via regulation of the MAPK/NF-kappaB signaling pathway. SN - 1643-3750 UR - https://www.unboundmedicine.com/medline/citation/32114591/Compound_Porcine_Cerebroside_and_Ganglioside_Injection__CPCGI__Attenuates_Sevoflurane_Induced_Nerve_Cell_Injury_by_Regulating_the_Phosphorylation_of_p38_MAP_Kinase__p38MAPK_/Nuclear_Factor_kappa_B__NF_κB__Pathway_ L2 - https://www.medscimonit.com/download/index/idArt/919600 DB - PRIME DP - Unbound Medicine ER -