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Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway

BACKGROUND: Cerebral ischemia/reperfusion injury (CI/RI) contributes to the process of autophagy. Huangqi-Honghua combination (HQ-HH) is a traditional Chinese medicine (TCM) combination that has been widely used in the treatment of cerebrovascular diseases in China. The role of autophagy in HQ-HH-me...

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Autores principales: Chen, Yue, Lei, Lu, Wang, Kai, Liang, Ruimin, Qiao, Yi, Feng, Zhijun, Zhang, Juanli, Bai, Min, Chen, Haixia, Zhao, Jiaxin, Xiong, Xingzhao, Cao, Jinyi, Shen, Xia, Yang, Zhifu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803436/
https://www.ncbi.nlm.nih.gov/pubmed/35111232
http://dx.doi.org/10.1155/2022/9496926
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author Chen, Yue
Lei, Lu
Wang, Kai
Liang, Ruimin
Qiao, Yi
Feng, Zhijun
Zhang, Juanli
Bai, Min
Chen, Haixia
Zhao, Jiaxin
Xiong, Xingzhao
Cao, Jinyi
Shen, Xia
Yang, Zhifu
author_facet Chen, Yue
Lei, Lu
Wang, Kai
Liang, Ruimin
Qiao, Yi
Feng, Zhijun
Zhang, Juanli
Bai, Min
Chen, Haixia
Zhao, Jiaxin
Xiong, Xingzhao
Cao, Jinyi
Shen, Xia
Yang, Zhifu
author_sort Chen, Yue
collection PubMed
description BACKGROUND: Cerebral ischemia/reperfusion injury (CI/RI) contributes to the process of autophagy. Huangqi-Honghua combination (HQ-HH) is a traditional Chinese medicine (TCM) combination that has been widely used in the treatment of cerebrovascular diseases in China. The role of autophagy in HQ-HH-mediated treatment of CI/RI is unclear. METHODS: Sprague-Dawley (SD) rats were used to establish the middle cerebral artery occlusion (MCAO) with QDBS syndrome model and evaluate the function of HQ-HH in protecting against CI/RI. RESULTS: HQ-HH significantly improved the neuronal pathology and reduced infarct volume, neurological deficits, and whole blood viscosity in rats with CI/RI. Western blot results showed that the expression of autophagy marker proteins LC3II/LC3I and Beclin1 in the HQ-HH group was significantly lower than that in the model group, while the expression of p62 was significantly higher in the HQ-HH group as compared with the model group. There were no significant differences in PI3K, Akt, and mTOR levels between the HQ-HH group and the model group; however, p-PI3K, p-Akt, and p-mTOR were significantly upregulated. In addition, HQ-HH also changed the composition and function of intestinal flora in MCAO + QDBS model rats. CONCLUSION: HQ-HH protects from CI/RI, and its underlying mechanism may involve the activation of the PI3K-Akt-mTOR signaling pathway, relating to the changes in the composition of intestinal flora.
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spelling pubmed-88034362022-02-01 Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway Chen, Yue Lei, Lu Wang, Kai Liang, Ruimin Qiao, Yi Feng, Zhijun Zhang, Juanli Bai, Min Chen, Haixia Zhao, Jiaxin Xiong, Xingzhao Cao, Jinyi Shen, Xia Yang, Zhifu Evid Based Complement Alternat Med Research Article BACKGROUND: Cerebral ischemia/reperfusion injury (CI/RI) contributes to the process of autophagy. Huangqi-Honghua combination (HQ-HH) is a traditional Chinese medicine (TCM) combination that has been widely used in the treatment of cerebrovascular diseases in China. The role of autophagy in HQ-HH-mediated treatment of CI/RI is unclear. METHODS: Sprague-Dawley (SD) rats were used to establish the middle cerebral artery occlusion (MCAO) with QDBS syndrome model and evaluate the function of HQ-HH in protecting against CI/RI. RESULTS: HQ-HH significantly improved the neuronal pathology and reduced infarct volume, neurological deficits, and whole blood viscosity in rats with CI/RI. Western blot results showed that the expression of autophagy marker proteins LC3II/LC3I and Beclin1 in the HQ-HH group was significantly lower than that in the model group, while the expression of p62 was significantly higher in the HQ-HH group as compared with the model group. There were no significant differences in PI3K, Akt, and mTOR levels between the HQ-HH group and the model group; however, p-PI3K, p-Akt, and p-mTOR were significantly upregulated. In addition, HQ-HH also changed the composition and function of intestinal flora in MCAO + QDBS model rats. CONCLUSION: HQ-HH protects from CI/RI, and its underlying mechanism may involve the activation of the PI3K-Akt-mTOR signaling pathway, relating to the changes in the composition of intestinal flora. Hindawi 2022-01-24 /pmc/articles/PMC8803436/ /pubmed/35111232 http://dx.doi.org/10.1155/2022/9496926 Text en Copyright © 2022 Yue Chen et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Chen, Yue
Lei, Lu
Wang, Kai
Liang, Ruimin
Qiao, Yi
Feng, Zhijun
Zhang, Juanli
Bai, Min
Chen, Haixia
Zhao, Jiaxin
Xiong, Xingzhao
Cao, Jinyi
Shen, Xia
Yang, Zhifu
Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title_full Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title_fullStr Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title_full_unstemmed Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title_short Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway
title_sort huangqi-honghua combination prevents cerebral infarction with qi deficiency and blood stasis syndrome in rats by the autophagy pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803436/
https://www.ncbi.nlm.nih.gov/pubmed/35111232
http://dx.doi.org/10.1155/2022/9496926
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