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Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma

Currently, there is no effective therapy for traumatic brain injury (TBI). Therefore, this study was conducted to determine the protective effect of Lu Tong Ke Li (LTKL), a Chinese medicine, for TBI in experimental animals. The TBI rat model was induced using the modified Feeney's protocol. The...

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Autores principales: Chen, Jie, Li, Ting‐Ting, Chen, Ting‐Bao, Niu, Rui‐Ze, Chen, Ji‐Lin, Chen, Yong, Huang, Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10528765/
https://www.ncbi.nlm.nih.gov/pubmed/37786414
http://dx.doi.org/10.1002/ibra.12029
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author Chen, Jie
Li, Ting‐Ting
Chen, Ting‐Bao
Niu, Rui‐Ze
Chen, Ji‐Lin
Chen, Yong
Huang, Jin
author_facet Chen, Jie
Li, Ting‐Ting
Chen, Ting‐Bao
Niu, Rui‐Ze
Chen, Ji‐Lin
Chen, Yong
Huang, Jin
author_sort Chen, Jie
collection PubMed
description Currently, there is no effective therapy for traumatic brain injury (TBI). Therefore, this study was conducted to determine the protective effect of Lu Tong Ke Li (LTKL), a Chinese medicine, for TBI in experimental animals. The TBI rat model was induced using the modified Feeney's protocol. The rats were divided into four groups: Sham group, Control group, LTKL  lower‐dose group (LTL, 2 g/kg/day, p.o.), and LTKL higher‐dose group (LTH, 4 g/kg/day, p.o.). The Neurological Severity Score (NSS) was used to examine neurological function. Magnetic resonance imaging was performed to check the brain tissue lesions in rats. Cell apoptosis in the damaged area was evaluated using the Terminal deoxynucleotidyl transferase deoxy‐UTP‐nick end labeling assay. Reverse‐transcription polymerase chain reaction was used to investigate the expression of inflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), interleukin 1β (IL‐1β), and interleukin 10 (IL‐10). The TBI rat model was successfully constructed. Neurological function was enhanced at 14, 21, and 28 days post TBI in the LTH groups, indicated by gradually decreased NSS scores. Administration of LTH led to fewer brain defects in the damaged area, and the number of apoptosis cells in the brain injury area markedly decreased. LTKL treatment led to upregulation of IL‐10 expression and downregulation of TNF‐α and IL‐1β expressions at the molecular level. LTKL can improve the neurobehavior of TBI. The neuroprotective effect was probably related to regulation of inflammation cytokines. Our results provide crucial evidence of the potentially useful application of LTKL in the therapy of TBI in clinic practice in the future.
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spelling pubmed-105287652023-10-02 Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma Chen, Jie Li, Ting‐Ting Chen, Ting‐Bao Niu, Rui‐Ze Chen, Ji‐Lin Chen, Yong Huang, Jin Ibrain Original Articles Currently, there is no effective therapy for traumatic brain injury (TBI). Therefore, this study was conducted to determine the protective effect of Lu Tong Ke Li (LTKL), a Chinese medicine, for TBI in experimental animals. The TBI rat model was induced using the modified Feeney's protocol. The rats were divided into four groups: Sham group, Control group, LTKL  lower‐dose group (LTL, 2 g/kg/day, p.o.), and LTKL higher‐dose group (LTH, 4 g/kg/day, p.o.). The Neurological Severity Score (NSS) was used to examine neurological function. Magnetic resonance imaging was performed to check the brain tissue lesions in rats. Cell apoptosis in the damaged area was evaluated using the Terminal deoxynucleotidyl transferase deoxy‐UTP‐nick end labeling assay. Reverse‐transcription polymerase chain reaction was used to investigate the expression of inflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), interleukin 1β (IL‐1β), and interleukin 10 (IL‐10). The TBI rat model was successfully constructed. Neurological function was enhanced at 14, 21, and 28 days post TBI in the LTH groups, indicated by gradually decreased NSS scores. Administration of LTH led to fewer brain defects in the damaged area, and the number of apoptosis cells in the brain injury area markedly decreased. LTKL treatment led to upregulation of IL‐10 expression and downregulation of TNF‐α and IL‐1β expressions at the molecular level. LTKL can improve the neurobehavior of TBI. The neuroprotective effect was probably related to regulation of inflammation cytokines. Our results provide crucial evidence of the potentially useful application of LTKL in the therapy of TBI in clinic practice in the future. John Wiley and Sons Inc. 2022-03-11 /pmc/articles/PMC10528765/ /pubmed/37786414 http://dx.doi.org/10.1002/ibra.12029 Text en © 2022 The Authors. Ibrain published by Affiliated Hospital of Zunyi Medical University (AHZMU) and Wiley‐VCH GmbH. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Chen, Jie
Li, Ting‐Ting
Chen, Ting‐Bao
Niu, Rui‐Ze
Chen, Ji‐Lin
Chen, Yong
Huang, Jin
Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title_full Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title_fullStr Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title_full_unstemmed Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title_short Lu Tong Ke Li protects neurons from injury by regulating inflammation in rats with brain trauma
title_sort lu tong ke li protects neurons from injury by regulating inflammation in rats with brain trauma
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10528765/
https://www.ncbi.nlm.nih.gov/pubmed/37786414
http://dx.doi.org/10.1002/ibra.12029
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