Fucoidan attenuates angiotensin II-induced abdominal aortic aneurysms through the inhibition of c-Jun N-terminal kinase and nuclear factor κB activation

Tsai, Shih‐Hung; Wang, Jen-Chun; Liao, Wen‐I; Hsu, Yu‐Juei; Lin, Chih-Yuan; Liao, Min-Tser; Huang, Po‐Hsun; Lin, Shing‐Jong

doi:10.1016/j.jvs.2017.09.042

Cited by 22 publications

(14 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, we highlight 4-HNE and ROS production as a vicious cycle in heatstroke-induced ALI and the roles of ALDH2 in breaking the vicious cycle. Activation of NF-κB-induced NOXs activation and ROS production ( 34 , 49 , 50 ). Previous studies indicated that 4-HNE increased the production of ROS through NOX and 5-lipoxygenase (5-LO) ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Activation Of Aldehyde Dehydrogenase 2 Protects Against Heatstroke-Induced Acute Lung Injury by Modulating Oxidative Stress and Endothelial Dysfunction

Tsai

Hsu

et al. 2021

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

Heatstroke (HS) can cause acute lung injury (ALI). Heat stress induces inflammation and apoptosis via reactive oxygen species (ROS) and endogenous reactive aldehydes. Endothelial dysfunction also plays a crucial role in HS-induced ALI. Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme that detoxifies aldehydes such as 4-hydroxy-2-nonenal (4-HNE) protein adducts. A single point mutation in ALDH2 at E487K (ALDH2*2) intrinsically lowers the activity of ALDH2. Alda-1, an ALDH2 activator, attenuates the formation of 4-HNE protein adducts and ROS in several disease models. We hypothesized that ALDH2 can protect against heat stress-induced vascular inflammation and the accumulation of ROS and toxic aldehydes. Homozygous ALDH2*2 knock-in (KI) mice on a C57BL/6J background and C57BL/6J mice were used for the animal experiments. Human umbilical vein endothelial cells (HUVECs) were used for the in vitro experiment. The mice were directly subjected to whole-body heating (WBH, 42°C) for 1 h at 80% relative humidity. Alda-1 (16 mg/kg) was administered intraperitoneally prior to WBH. The severity of ALI was assessed by analyzing the protein levels and cell counts in the bronchoalveolar lavage fluid, the wet/dry ratio and histology. ALDH2*2 KI mice were susceptible to HS-induced ALI in vivo. Silencing ALDH2 induced 4-HNE and ROS accumulation in HUVECs subjected to heat stress. Alda-1 attenuated the heat stress-induced activation of inflammatory pathways, senescence and apoptosis in HUVECs. The lung homogenates of mice pretreated with Alda-1 exhibited significantly elevated ALDH2 activity and decreased ROS accumulation after WBH. Alda-1 significantly decreased the WBH-induced accumulation of 4-HNE and p65 and p38 activation. Here, we demonstrated the crucial roles of ALDH2 in protecting against heat stress-induced ROS production and vascular inflammation and preserving the viability of ECs. The activation of ALDH2 by Alda-1 attenuates WBH-induced ALI in vivo.

show abstract

Section: Discussionmentioning

confidence: 99%

Pharmacological Activation Of Aldehyde Dehydrogenase 2 Protects Against Heatstroke-Induced Acute Lung Injury by Modulating Oxidative Stress and Endothelial Dysfunction

Tsai

Hsu

et al. 2021

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…[ 20 ] Inflammatory factors, oxidative stress, and matrix metalloproteinases (MMPs) are enriched in the aneurysmal vascular wall. [ 23 , 24 ] High levels of alcohol have been shown to upregulate MMPs in the aorta and kidneys in rats. [ 25 , 26 ] The associations between alcohol consumption and doses and the incidence of AAA are still controversial.…”

Section: Discussionmentioning

confidence: 99%

Association between abdominal aortic aneurysms and alcohol-related diseases

Li¹,

Chien

Wang

et al. 2020

Medicine

Self Cite

View full text Add to dashboard Cite

Heterogeneous associations exist between alcohol consumption and the initial presentation of cardiovascular diseases (CVDs). Studies regarding the association between abdominal aortic aneurysms (AAAs) and alcohol consumption are still limited and controversial. We hypothesize that patients with alcohol-related diseases are susceptible to AAA formation due to the presence of overlapping epidemiological factors and molecular mechanisms. We aimed to use a nationwide population-based retrospective cohort study to evaluate the association between alcohol-related diseases and AAA. The data were extracted from the National Health Insurance Research Database (NHIRD) in Taiwan. The study outcome assessed was the cumulative incidence of AAA in patients with alcohol-related diseases during a 14-year follow-up period. Our study included 22,878 patients who had alcohol-related diseases; these patients with alcohol-related diseases had a significantly higher cumulative risk of developing AAA 5 years after the index date than did the 91,512 patients without alcohol-related diseases. Patients with alcohol-related diseases also exhibited a significantly increased incidence of AAA compared with the incidence among patients without alcohol-related diseases, according to Cox regression analysis and Fine & Gray's competing risk model (adjusted hazard ratio = 2.379, 95% confidence interval = 1.653 -3.424, P < .001). In addition, male gender, older age, and chronic kidney disease were also associated with an increased risk of developing AAA. An interaction model showed that males with alcohol-related diseases had a 10.4-fold higher risk of AAA than did females without alcohol-related diseases. We observed an association between alcohol-related diseases and AAA even after adjusting for several comorbidities and medications in a nationwide population database.

show abstract

“…AngII‐induced AAA formation in ApoE ‐/‐ mouse has become the most widely used animal model (Daugherty et al, ; Tsai et al, ). Hence, we evaluated the role of LA in AAA formation by using Ang II‐treated ApoE ‐/‐ mice.…”

Section: Resultsmentioning

confidence: 99%

“…Mice were randomly divided into four groups (n = 12 per/group): Control, AngII, AngII+LA5, and AngII+LA10. AAA models were established in the last three groups, as previously described (Tsai et al, 2017). Briefly, after anesthetizing with 50 mg/kg of pentobarbital sodium, the mice were given 1,000 ng/kg/min of AngII (Sigma-Aldrich, St. Louis, MO) via implantation with subcutaneous osmotic mini-pumps for 4 weeks.…”

mentioning

confidence: 99%

Licochalcone A attenuates abdominal aortic aneurysm induced by angiotensin II via regulating the miR‐181b/SIRT1/HO‐1 signaling

Hou

Yang

Zheng

2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Licochalcone A (LA), a chalcone derived from liquorice, exhibits multiple biological activities, including anti-oxidation and anti-inflammation. This study aimed to investigate the role and underlying mechanism of LA in the abdominal aortic aneurysm (AAA). AAA model was established by continuous infusion of 1000 ng/kg/min of angiotensin II (AngII) in ApoE -/mice for 4 weeks. At 7 days before AngII administration, 5 mg/kg/day or 10 mg/kg/day of LA was intraperitoneally administered to mice and continued for 4 weeks. The characteristics and quantification of AAAs were determined in situ. Real-time PCR or western blot was used to measure mRNA or protein levels of matrix metalloproteinase 2 and matrix metalloproteinase 9; pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6; apoptosis-related proteins Bax, Bcl-2, and active caspase-3; miR-181b; Sirtuin 1 (SIRT1); and heme oxygenase-1 (HO-1). Mouse-aorta-origin vascular smooth muscle (MOVAS) cells were used to confirm the involved pathways in vitro. We found LA administration dose-dependently reduced the incidence of AngII-induced AAA, aneurysm diameter enlargement, elastin degradation, matrix metalloproteinase production, pro-inflammatory cytokines and miR-181b expression, and vascular smooth muscle cell apoptosis. It elevated SIRT1 and HO-1 expression that was suppressed by AngII.AngII enhanced miR-181b but reduced SIRT1 and HO-1 expression in MOVAS cells. In AngII-stimulated MOVAS cells, downregulation of miR-181b significantly upregulated the expression of SIRT1 and HO-1, the effect of which was abrogated by SIRT1 siRNA.Collectively, LA could attenuate AngII-induced AAA by modulating the miR-181b/ SIRT1/HO-1 signaling. LA might be a potential medical therapy for small AAA. K E Y W O R D S abdominal aortic aneurysm (AAA), angiotensin II, licochalcone A (LA), miR-181b, SIRT1/HO-1

show abstract

Fucoidan attenuates angiotensin II-induced abdominal aortic aneurysms through the inhibition of c-Jun N-terminal kinase and nuclear factor κB activation

Abstract: Fucoidan inhibits the progression of experimental AAA growth through the attenuation of proinflammatory nuclear factor κB and c-Jun N-terminal kinase activation. Fucoidan could be a potential medical adjunctive therapy for small AAAs.

Cited by 22 publications

References 61 publications

Pharmacological Activation Of Aldehyde Dehydrogenase 2 Protects Against Heatstroke-Induced Acute Lung Injury by Modulating Oxidative Stress and Endothelial Dysfunction

Pharmacological Activation Of Aldehyde Dehydrogenase 2 Protects Against Heatstroke-Induced Acute Lung Injury by Modulating Oxidative Stress and Endothelial Dysfunction

Association between abdominal aortic aneurysms and alcohol-related diseases

Licochalcone A attenuates abdominal aortic aneurysm induced by angiotensin II via regulating the miR‐181b/SIRT1/HO‐1 signaling

Contact Info

Product

Resources

About