Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury

Epidemiological studies have shown that the elevated concentration of particulate matter with aerodynamic diameter less than 10 µm (PM10) is closely related to the increased risk of heart and lung diseases in the population. Natural isoflavone compound biochanin A (BCA) has anti-inflammatory and ant...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Shihao Li, Junyu Wang, Yue Yu, Bowen Zheng, Juan Ma, Xiaohong Kou, Zhaohui Xue
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Biochanin A PM10 Acute pulmonary cell injury PI3K/Akt Environmental pollution TD172-193.5 Environmental sciences GE1-350
Acceso en línea:	https://doaj.org/article/86a952fa32f74264b20081a383bff325
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:86a952fa32f74264b20081a383bff325
record_format	dspace
spelling	oai:doaj.org-article:86a952fa32f74264b20081a383bff3252021-11-04T04:25:50ZInvestigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury0147-651310.1016/j.ecoenv.2021.112953https://doaj.org/article/86a952fa32f74264b20081a383bff3252021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321010654https://doaj.org/toc/0147-6513Epidemiological studies have shown that the elevated concentration of particulate matter with aerodynamic diameter less than 10 µm (PM10) is closely related to the increased risk of heart and lung diseases in the population. Natural isoflavone compound biochanin A (BCA) has anti-inflammatory and antioxidant activities, and has efficacy in alleviating lung injury. The objective of this study was to investigate the inhibitory effect of BCA on PM10 induced acute human bronchial epithelial cells injury. The results showed that PM10 decreased intracellular catalase level to 1.19 ± 0.01 nmol/min/mg prot and induce a surge of reactive oxygen species (ROS). It also increased lactate dehydrogenase (LDH) activity by 428.89% and caused the lipid peroxidation phenomenon. PM10 exposure also upregulates the expression of inflammatory cytokines and mediators. However, BCA could interfere with the above changes caused by PM10, inhibit the LDH level to 8.22 ± 0.03 u/mL, and show anti-inflammatory and antioxidant activities. In addition, the phosphatidylinositol 3-kimase (PI3K) /protein kinase B (PKB/Akt) is a key signal pathway in response to PM10 exposure. In this study, PI3K/Akt signaling pathway is seriously affected by PM10 exposure. PI3K/Akt signaling pathway, PI3K, AKT, tensin homolog deleted on chromosome 10 (PTEN), mechanistic target of rapamycin (mTOR) and p53 protein were all inhibited by PM10 exposure, and PI3K/Akt signaling pathway was inactivated. BCA exert anti-damage function by regulating the activation process of PI3K protein, intervening the regulation process of PI3K/Akt by PTEN, and intervening the expression and phosphorylation of downstream Akt protein.Shihao LiJunyu WangYue YuBowen ZhengJuan MaXiaohong KouZhaohui XueElsevierarticleBiochanin APM10Acute pulmonary cell injuryPI3K/AktEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 112953- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biochanin A PM10 Acute pulmonary cell injury PI3K/Akt Environmental pollution TD172-193.5 Environmental sciences GE1-350
spellingShingle	Biochanin A PM10 Acute pulmonary cell injury PI3K/Akt Environmental pollution TD172-193.5 Environmental sciences GE1-350 Shihao Li Junyu Wang Yue Yu Bowen Zheng Juan Ma Xiaohong Kou Zhaohui Xue Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
description	Epidemiological studies have shown that the elevated concentration of particulate matter with aerodynamic diameter less than 10 µm (PM10) is closely related to the increased risk of heart and lung diseases in the population. Natural isoflavone compound biochanin A (BCA) has anti-inflammatory and antioxidant activities, and has efficacy in alleviating lung injury. The objective of this study was to investigate the inhibitory effect of BCA on PM10 induced acute human bronchial epithelial cells injury. The results showed that PM10 decreased intracellular catalase level to 1.19 ± 0.01 nmol/min/mg prot and induce a surge of reactive oxygen species (ROS). It also increased lactate dehydrogenase (LDH) activity by 428.89% and caused the lipid peroxidation phenomenon. PM10 exposure also upregulates the expression of inflammatory cytokines and mediators. However, BCA could interfere with the above changes caused by PM10, inhibit the LDH level to 8.22 ± 0.03 u/mL, and show anti-inflammatory and antioxidant activities. In addition, the phosphatidylinositol 3-kimase (PI3K) /protein kinase B (PKB/Akt) is a key signal pathway in response to PM10 exposure. In this study, PI3K/Akt signaling pathway is seriously affected by PM10 exposure. PI3K/Akt signaling pathway, PI3K, AKT, tensin homolog deleted on chromosome 10 (PTEN), mechanistic target of rapamycin (mTOR) and p53 protein were all inhibited by PM10 exposure, and PI3K/Akt signaling pathway was inactivated. BCA exert anti-damage function by regulating the activation process of PI3K protein, intervening the regulation process of PI3K/Akt by PTEN, and intervening the expression and phosphorylation of downstream Akt protein.
format	article
author	Shihao Li Junyu Wang Yue Yu Bowen Zheng Juan Ma Xiaohong Kou Zhaohui Xue
author_facet	Shihao Li Junyu Wang Yue Yu Bowen Zheng Juan Ma Xiaohong Kou Zhaohui Xue
author_sort	Shihao Li
title	Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
title_short	Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
title_full	Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
title_fullStr	Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
title_full_unstemmed	Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury
title_sort	investigation on the mechanisms of biochanin a alleviate pm10-induced acute pulmonary cell injury
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/86a952fa32f74264b20081a383bff325
work_keys_str_mv	AT shihaoli investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT junyuwang investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT yueyu investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT bowenzheng investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT juanma investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT xiaohongkou investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury AT zhaohuixue investigationonthemechanismsofbiochaninaalleviatepm10inducedacutepulmonarycellinjury
_version_	1718445285548490752

Investigation on the mechanisms of biochanin A alleviate PM10-induced acute pulmonary cell injury

Ejemplares similares