Abstract：
:Atherosclerosis is a complex chronic inflammatory disease that remains one of the leading causes of death and disability worldwide. A previous study reported that glaucocalyxin A (GLA), a natural ent-Kaurane diterpenoid triptolide, exhibits anti-atherosclerotic activity. However, the underlying molecular mechanism has not yet been explored. In the present study, we evaluated the anti-atherosclerotic effect of GLA and the underlying mechanism in vitro. Human coronary artery smooth muscle cells (HCASMCs) were stimulated by hydrogen peroxide (H2 O2 ) to induce oxidative stress and inflammation. The results showed that GLA pretreatment improved the viability of H2 O2 -induced HCASMCs. The increased reactive oxygen species production and decreased superoxide dismutase and glutathione peroxidase activities in H2 O2 -induced HCASMCs were reversed by GLA pretreatment. In addition, GLA treatment suppressed the H2 O2 -induced expression of inducible nitric oxide synthase, NADPH oxidase (NOX) 2, and NOX4 in HCASMCs. Moreover, treatment with GLA reduced the production of several inflammatory cytokines, including tumour necrosis factor-alpha, interleukin (IL)-6, and IL-1β in H2 O2 -induced HCASMCs. Furthermore, GLA treatment suppressed the phosphorylation of p38, as well as inactivating the NF-κB signalling pathway. These findings suggested that GLA protected against H2 O2 -induced oxidative stress and inflammation via inhibition of p38 phosphorylation and NF-κB activation in HCASMCs.
journal_name
Clin Exp Pharmacol Physioljournal_title
Clinical and experimental pharmacology & physiologyauthors
Zhu S,Zhang J,Lv Ydoi
10.1111/1440-1681.13253subject
Has Abstractpub_date
2020-05-01 00:00:00pages
765-770issue
5eissn
0305-1870issn
1440-1681journal_volume
47pub_type
杂志文章abstract：:1. In an isolated right atrial preparation, an increase in right atrial pressure (RAP) produces an increase in atrial rate. This rate response is larger and occurs faster when there is background vagal or muscarinic stimulation. 2. We hypothesized that in the latter situation, an increase in RAP antagonizes the effect...
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journal_title：Clinical and experimental pharmacology & physiology
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doi：10.1111/j.1440-1681.1980.tb00117.x
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更新日期：2008-07-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1440-1681.1985.tb00885.x
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更新日期：2010-02-01 00:00:00
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pub_type： 杂志文章,随机对照试验
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更新日期：2015-01-01 00:00:00
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journal_title：Clinical and experimental pharmacology & physiology
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doi：10.1111/j.1440-1681.1989.tb01605.x
更新日期：1989-07-01 00:00:00
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更新日期：2007-01-01 00:00:00
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更新日期：2003-04-01 00:00:00
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更新日期：2017-08-01 00:00:00
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更新日期：2011-05-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1440-1681.1986.tb00337.x
更新日期：1986-03-01 00:00:00
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journal_title：Clinical and experimental pharmacology & physiology
pub_type： 杂志文章,评审
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更新日期：2007-05-01 00:00:00
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journal_title：Clinical and experimental pharmacology & physiology
pub_type： 杂志文章
doi：10.1046/j.1440-1681.2002.03671.x
更新日期：2002-05-01 00:00:00
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journal_title：Clinical and experimental pharmacology & physiology
pub_type： 杂志文章
doi：10.1111/j.1440-1681.1991.tb01429.x
更新日期：1991-03-01 00:00:00
