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Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation by Regulating p38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons.
Med Sci Monit. 2020 Jul 07; 26:e926441.MS

Abstract

BACKGROUND

Hyperbilirubinemia is associated with central nervous system damage in preterm neonates due to the neurotoxicity of bilirubin. This study explored the possible mechanisms of bilirubin's neurotoxicity, and the protective effect of baicalin (BAI) was also investigated. MATERIAL AND

METHODS

Isolated neonatal rat hippocampal neurons were exposed to free bilirubin (Bf). BAI was used to treat these neurons. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate the cell viability. Terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay was used to detect apoptosis. Contents of inflammatory cytokines were determined by enzyme-linked immunosorbent assay (ELISA). Protein expression and phosphorylation levels were assessed by Western blotting. Nuclear translocation was observed by immunofluorescent staining.

RESULTS

Bf incubation significantly induced apoptosis and decreased viabilities of neurons. The phosphorylation levels of MAP kinase kinase (MKK)3, MKK6, p38 mitogen- activated protein kinases (MAPK), nuclear translocation level of p65, and the expression levels of cleaved caspase3 and tumor necrosis factor (TNF)alpha were found to be dramatically higher in Bf-incubated neurons. BAI pre-treatment, however, increased cell viability by reducing cell apoptosis. BAI pre-treatment also reduced phosphorylation levels of MKK3, MKK6, p38 MAPK, and nuclear translocation level of p65, as well as the expression levels of cleaved caspase3 and TNFalpha, in Bf- incubated neurons.

CONCLUSIONS

BAI suppressed bilirubin-induced neuron apoptosis and inflammation by deactivating p38 MAPK signaling.

Authors+Show Affiliations

Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).Department of Medicine, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32633271

Citation

Shi, Shuang, et al. "Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation By Regulating P38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 26, 2020, pp. e926441.
Shi S, Cui Q, Xu J, et al. Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation by Regulating p38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons. Med Sci Monit. 2020;26:e926441.
Shi, S., Cui, Q., Xu, J., Tang, Z., Shi, B., & Liu, Z. (2020). Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation by Regulating p38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 26, e926441. https://doi.org/10.12659/MSM.926441
Shi S, et al. Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation By Regulating P38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons. Med Sci Monit. 2020 Jul 7;26:e926441. PubMed PMID: 32633271.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Baicalin Suppresses Bilirubin-Induced Apoptosis and Inflammation by Regulating p38 Mitogen-Activated Protein Kinases (MAPK) Signaling in Neonatal Neurons. AU - Shi,Shuang, AU - Cui,Qianwei, AU - Xu,Jing, AU - Tang,Zhiguo, AU - Shi,Binya, AU - Liu,Zhongwei, Y1 - 2020/07/07/ PY - 2020/7/8/entrez PY - 2020/7/8/pubmed PY - 2020/7/8/medline SP - e926441 EP - e926441 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med. Sci. Monit. VL - 26 N2 - BACKGROUND Hyperbilirubinemia is associated with central nervous system damage in preterm neonates due to the neurotoxicity of bilirubin. This study explored the possible mechanisms of bilirubin's neurotoxicity, and the protective effect of baicalin (BAI) was also investigated. MATERIAL AND METHODS Isolated neonatal rat hippocampal neurons were exposed to free bilirubin (Bf). BAI was used to treat these neurons. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate the cell viability. Terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay was used to detect apoptosis. Contents of inflammatory cytokines were determined by enzyme-linked immunosorbent assay (ELISA). Protein expression and phosphorylation levels were assessed by Western blotting. Nuclear translocation was observed by immunofluorescent staining. RESULTS Bf incubation significantly induced apoptosis and decreased viabilities of neurons. The phosphorylation levels of MAP kinase kinase (MKK)3, MKK6, p38 mitogen- activated protein kinases (MAPK), nuclear translocation level of p65, and the expression levels of cleaved caspase3 and tumor necrosis factor (TNF)alpha were found to be dramatically higher in Bf-incubated neurons. BAI pre-treatment, however, increased cell viability by reducing cell apoptosis. BAI pre-treatment also reduced phosphorylation levels of MKK3, MKK6, p38 MAPK, and nuclear translocation level of p65, as well as the expression levels of cleaved caspase3 and TNFalpha, in Bf- incubated neurons. CONCLUSIONS BAI suppressed bilirubin-induced neuron apoptosis and inflammation by deactivating p38 MAPK signaling. SN - 1643-3750 UR - https://www.unboundmedicine.com/medline/citation/32633271/Baicalin_Suppresses_Bilirubin-Induced_Apoptosis_and_Inflammation_by_Regulating_p38_Mitogen-Activated_Protein_Kinases_(MAPK)_Signaling_in_Neonatal_Neurons L2 - https://www.medscimonit.com/download/index/idArt/926441 DB - PRIME DP - Unbound Medicine ER -
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