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Conference Paper: Nadph Oxidase Upregulated by AT1 Receptor Mediates Chronic Intermittent Hypoxia-Induced Oxidative Stress and Inflammation in Rat Adrenal Medulla

TitleNadph Oxidase Upregulated by AT1 Receptor Mediates Chronic Intermittent Hypoxia-Induced Oxidative Stress and Inflammation in Rat Adrenal Medulla
Authors
Issue Date2012
Citation
Hong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences (HKSN) & The Biophysical Society of Hong Kong (BPHK), The Chinese University of Hong Kong, Hong Kong, China, 14-15 June 2012, p. 53-54, abstract no. P18 How to Cite?
AbstractOur previous study found that chronic intermittent hypoxia (CIH) associated with recurrent apnea induced oxidative stress and inflammation in rat adrenal medulla. However, the underline mechanism was not clear. We hypothesized that, under CIH, the up-regulation of NADPH oxidase mediated by renin-angiotensin system (RAS) via an activation of angiotensin II receptor 1 (AT1) might take part in the oxidative stress and local inflammation in the adrenal medulla. Adult male SD rats were exposed to air (normoxic) control or CIH treatment (8 hours/day) which mimicked a severe recurrent sleep apneic condition for 14 days. Oral feeding of Telmisartan (10 mg/kg), a specific AT1 receptor blocker, or an intraperitoneal injection of apocynin (25 mg/kg i.p.), an inhibitor of NADPH oxidase, or vehicle was performed before the daily hypoxic treatment. The adrenal medulla was harvested for the measurement of markers for oxidative stress (MDA and NTR), macrophages infiltration (ED1), apoptosis, and inflammation (pro-inflammatory mediators) using TUNEL assay, real-time PCR, ELISA and Western blot. Levels of MDA and NTR were significantly increased in the hypoxic (CIH) group when compared with the normoxic control, but were normalized in the hypoxic groups treated with apocynin (AIH) or telmisartan (TIH). The expression levels of macrophage marker ED1-immunoreactivity and the pro-inflammatory mediators (TNFa, IL6) were also elevated in the CIH group, but were significantly ameliorated by the apocynin or telmisartan treatment. In addition, the amount of apoptotic cells in the CIH group was significantly higher than that of the AIH and TIH groups. Moreover, the mRNA levels of NADPH oxidase subunits (Nox2, Nox4) were increased significantly in the CIH group when compared with that of the AIH and TIH groups. Also, the protein expression of RAS components (AGT, AT1) was also increased in the CIH group. In conclusion, we showed that an up-regulation of NADPH oxidase via AT1 receptor activation mediates CIH-induced oxidative stress and inflammation in rat adrenal medulla.
DescriptionPoster presentation
Persistent Identifierhttp://hdl.handle.net/10722/165032

 

DC FieldValueLanguage
dc.contributor.authorLiu, Yen_US
dc.contributor.authorTipoe, GLen_US
dc.contributor.authorXiao, Jen_US
dc.contributor.authorHuang, Yen_US
dc.contributor.authorFung, MLen_US
dc.date.accessioned2012-09-20T08:13:45Z-
dc.date.available2012-09-20T08:13:45Z-
dc.date.issued2012en_US
dc.identifier.citationHong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences (HKSN) & The Biophysical Society of Hong Kong (BPHK), The Chinese University of Hong Kong, Hong Kong, China, 14-15 June 2012, p. 53-54, abstract no. P18en_US
dc.identifier.urihttp://hdl.handle.net/10722/165032-
dc.descriptionPoster presentation-
dc.description.abstractOur previous study found that chronic intermittent hypoxia (CIH) associated with recurrent apnea induced oxidative stress and inflammation in rat adrenal medulla. However, the underline mechanism was not clear. We hypothesized that, under CIH, the up-regulation of NADPH oxidase mediated by renin-angiotensin system (RAS) via an activation of angiotensin II receptor 1 (AT1) might take part in the oxidative stress and local inflammation in the adrenal medulla. Adult male SD rats were exposed to air (normoxic) control or CIH treatment (8 hours/day) which mimicked a severe recurrent sleep apneic condition for 14 days. Oral feeding of Telmisartan (10 mg/kg), a specific AT1 receptor blocker, or an intraperitoneal injection of apocynin (25 mg/kg i.p.), an inhibitor of NADPH oxidase, or vehicle was performed before the daily hypoxic treatment. The adrenal medulla was harvested for the measurement of markers for oxidative stress (MDA and NTR), macrophages infiltration (ED1), apoptosis, and inflammation (pro-inflammatory mediators) using TUNEL assay, real-time PCR, ELISA and Western blot. Levels of MDA and NTR were significantly increased in the hypoxic (CIH) group when compared with the normoxic control, but were normalized in the hypoxic groups treated with apocynin (AIH) or telmisartan (TIH). The expression levels of macrophage marker ED1-immunoreactivity and the pro-inflammatory mediators (TNFa, IL6) were also elevated in the CIH group, but were significantly ameliorated by the apocynin or telmisartan treatment. In addition, the amount of apoptotic cells in the CIH group was significantly higher than that of the AIH and TIH groups. Moreover, the mRNA levels of NADPH oxidase subunits (Nox2, Nox4) were increased significantly in the CIH group when compared with that of the AIH and TIH groups. Also, the protein expression of RAS components (AGT, AT1) was also increased in the CIH group. In conclusion, we showed that an up-regulation of NADPH oxidase via AT1 receptor activation mediates CIH-induced oxidative stress and inflammation in rat adrenal medulla.-
dc.languageengen_US
dc.relation.ispartofHong Kong-Taiwan Physiology Symposium and Joint Scientific Meeting of Hong Kong Society of Neurosciences & The Biophysical Society of Hong Kongen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleNadph Oxidase Upregulated by AT1 Receptor Mediates Chronic Intermittent Hypoxia-Induced Oxidative Stress and Inflammation in Rat Adrenal Medullaen_US
dc.typeConference_Paperen_US
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_US
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_US
dc.identifier.authorityTipoe, GL=rp00371en_US
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros209994en_US
dc.identifier.spage53, abstract no. P18-
dc.identifier.epage54, abstract no. P18-
dc.publisher.placeHong Kong, China-

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