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阳和平喘颗粒减轻支气管哮喘大鼠模型的氧化应激和炎症:IKK/IκB/NF-κB信号通路的作用

Yanghe Pingchuan granules mitigates oxidative stress and inflammation in a bronchial asthma rat model: role of the IKK/IκB/NF-κB signalling pathway.

作者信息

Pan Lingyu, Gong Chunxia, Chen Yan, Jiang Yeke, Sun Yehong, He Bangfu, Duan Xianchun, Han Yanquan, Wang Yongzhong

机构信息

The First Affiliated Hospital of Anhui University of Chinese Medicine.

Anhui University of Chinese Medicine, Hefei 230012, Anhui, China.

出版信息

Ann Med Surg (Lond). 2023 Nov 27;86(1):212-218. doi: 10.1097/MS9.0000000000001553. eCollection 2024 Jan.

DOI:10.1097/MS9.0000000000001553
PMID:38222706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10783385/
Abstract

BACKGROUND

Bronchial asthma (BA) is a chronic inflammatory airway disease. Previous research has shown that Yanghe Pingchuan granules (YPG), among the granules formulated by the First Affiliated Hospital of the Anhui University of Chinese Medicine, exerts a precise therapeutic effect on BA. We previously showed that YPG improves airway inflammation in BA rats. Other studies have shown that the inhibitor of kappa-B kinase (IKK)/inhibitor of NF-κB (IκB)/nuclear factor kappa-B (NF-κB) signalling pathway plays a key role in inflammation mediation. Therefore, this study explored whether YPG could intervene in BA through the IKK/IκB/NF-κB signalling pathway.

METHODS

Ovalbumin-induced method was used to established BA rat model. After successful modelling, the authors used YPG to intervene the rats in BA rats. Hematoxylin-eosin (HE) staining was used to detect the bronchial pathological changes in BA rats, enzyme-linked immunosorbent assay (ELISA) was used to detect the changes of inflammatory factors (IL-1β and IL-6) and oxidative stress indexes malondialdehyde (MDA), superoxide dismutase (SOD) and nitrogen monoxide (NO), Quantitative real-time polymerase chain reactionCR and western blot were used to detect the expression of IKK/IκB/NF-κB signalling pathway.

RESULTS

In BA model rats, YPG significantly improved the inflammatory response in bronchial tissues, reduced inflammatory factors IL-1β and IL-6, alleviated oxidative stress, reduced MDA and NO, and increased SOD. Quantitative real-time polymerase chain reaction and western blot results showed that YPG could block the IKK/IκB/NF-κB signalling pathway.

CONCLUSION

These findings showed that YPG had a definite therapeutic effect on BA, which may be related to blocking the IKK/IκB/NF-κB signalling pathway and improving inflammation and oxidative stress.

摘要

背景

支气管哮喘(BA)是一种慢性炎症性气道疾病。先前的研究表明,安徽中医药大学第一附属医院配制的颗粒剂中,阳和平喘颗粒(YPG)对BA具有确切的治疗效果。我们之前表明YPG可改善BA大鼠的气道炎症。其他研究表明,κB激酶(IKK)/核因子κB抑制蛋白(IκB)/核因子κB(NF-κB)信号通路抑制剂在炎症介导中起关键作用。因此,本研究探讨YPG是否可通过IKK/IκB/NF-κB信号通路干预BA。

方法

采用卵清蛋白诱导法建立BA大鼠模型。建模成功后,作者用YPG干预BA大鼠。苏木精-伊红(HE)染色用于检测BA大鼠的支气管病理变化,酶联免疫吸附测定(ELISA)用于检测炎症因子(IL-1β和IL-6)及氧化应激指标丙二醛(MDA)、超氧化物歧化酶(SOD)和一氧化氮(NO)的变化,实时定量聚合酶链反应(qRT-PCR)和蛋白质免疫印迹法用于检测IKK/IκB/NF-κB信号通路的表达。

结果

在BA模型大鼠中,YPG显著改善支气管组织的炎症反应,降低炎症因子IL-1β和IL-6,减轻氧化应激,降低MDA和NO,并增加SOD。qRT-PCR和蛋白质免疫印迹结果表明,YPG可阻断IKK/IκB/NF-κB信号通路。

结论

这些结果表明,YPG对BA具有确切的治疗作用,这可能与阻断IKK/IκB/NF-κB信号通路及改善炎症和氧化应激有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/b47e9af4b989/ms9-86-212-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/1bef3a1c3b33/ms9-86-212-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/ea4ef3942772/ms9-86-212-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/5c4d6a7513fb/ms9-86-212-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/c5a4996f2071/ms9-86-212-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/6c4763652e5c/ms9-86-212-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/b47e9af4b989/ms9-86-212-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/1bef3a1c3b33/ms9-86-212-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/ea4ef3942772/ms9-86-212-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/5c4d6a7513fb/ms9-86-212-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/c5a4996f2071/ms9-86-212-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/6c4763652e5c/ms9-86-212-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeab/10783385/b47e9af4b989/ms9-86-212-g006.jpg

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