Arctiin protects against cardiac hypertrophy through inhibiting MAPKs and AKT signaling pathways

Li, Jing; Yao, Yuan; Xu, Si-Chi; Zhang, Ning; Xu, Chunru; Chen, Wan; Ren, Jie; Zeng, Xiaofeng; Tang, Qi‐Zhu

doi:10.1016/j.jphs.2017.05.012

Cited by 29 publications

(27 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the effects of galangin on cardiac remodeling and the potential signaling mechanisms have not yet been elucidated. et al, 2006;J. Li et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways

Wang

Huang

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

Cardiac remodeling is associated with inflammation and apoptosis. Galangin, as a natural flavonol, has the potent function of regulating inflammation and apoptosis, which are factors related to cardiac remodeling. Beginning 3 days after aortic banding (AB) or Sham surgery, mice were treated with galangin for 4 weeks. Cardiac remodeling was assessed according to echocardiographic parameters, histological analyses, and hypertrophy and fibrosis markers. Our results showed that galangin administration attenuated cardiac hypertrophy, dysfunction, and fibrosis response in AB mice and angiotensin II‐treated H9c2 cells. The inhibitory action of galangin in cardiac remodeling was mediated by MEK1/2–extracellular‐regulated protein kinases 1/2 (ERK1/2)–GATA4 and phosphoinositide 3‐kinase (PI3K)–protein kinase B (AKT)–glycogen synthase kinase 3β (GSK3β) activation. Furthermore, we found that galangin inhibited inflammatory response and apoptosis. Our findings suggest that galangin protects against cardiac remodeling through decreasing inflammatory responses and apoptosis, which are associated with inhibition of the MEK1/2–ERK1/2–GATA4 and PI3K–AKT–GSK3β signals.

show abstract

“…However, the effects of galangin on cardiac remodeling and the potential signaling mechanisms have not yet been elucidated. et al, 2006;J. Li et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…AKT mainly regulates cell survival and apoptosis. Recent studies have shown that PI3K-AKT signaling pathways play a considerable role in the process and pathogenesis of cardiac remodeling (J Li et al, 2017)…”

mentioning

confidence: 99%

Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways

Wang

Huang

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…Recent studies have emphasized the protective effect of arctiin in several disease models including has also been found to exert functions in protecting against endothelial cell damage, anti-Alzheimer' disease and antiaging, the antihair loss, and so on, and these bioactivities are closely related to the antioxidative stress effect of arctiin. Arctiin also protected against cardiac hypertrophy, and LPS induced acute lung injury via the inhibition of MAPKs/AKT and PI3K/AKT signaling pathways, respectively [ 39 , 40 ]. Although several researches have demonstrated that arctiin could play a vital role in strong response to oxidative stress, however, there are no reported studies on the protective effect of arctiin through the study in Nrf2 pathway, an important pathway of oxidative stress, have not been reported.…”

Section: Discussionmentioning

confidence: 99%

Arctiin Antagonizes Triptolide‐Induced Hepatotoxicity via Activation of Nrf2 Pathway

Zhou

Yao

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Triptolide (TP) is the most effective ingredient found in the traditional Chinese herbal Tripterygium wilfordii Hook F, and it is widely used in therapies of autoimmune and inflammatory disorders. However, the hepatotoxicity induced by TP has restricted its use in clinical trials. Arctiin is known as a protective agent against oxidative stress, and it exerts liver-protecting effect. This study was aimed at investigating the protective role of arctiin against TP-induced hepatotoxicity using in vitro and in vivo models. The results indicated that TP not only obviously induced liver injury in mice but also significantly inhibited the growth of HepG2 cells and increased the level of intracellular reactive oxygen. Furthermore, TP obviously decreased the expressions of proteins of Nrf2 pathway including HO-1, NQO1, and Nrf2 associated with oxidative stress pathway. However, the above experimental indexes were reversed by the treatment of arctiin. Our results suggested that arctiin could alleviate TP-induced hepatotoxicity, and the molecular mechanism is likely related to its capacity against oxidative stress.

show abstract

“…Neonatal rat ventricular myocytes (NRVMs) were isolated from Sprague‐Dawley rats within 3 days of birth and cultured as previously described . Briefly, the hearts were quickly removed a; then, they were washed with phosphate‐buffered saline (PBS) three times, and incubated with 0.125% trypsin‐EDTA (Gibco, 2520‐072) for 15 minutes at 34°C for a total of five times.…”

Section: Methodsmentioning

confidence: 99%

Cordycepin ameliorates cardiac hypertrophy via activating the AMPKα pathway

Wang

Duan

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Increase of myocardial oxidative stress is closely related to the occurrence and development of cardiac hypertrophy. Cordycepin, also known as 3'‐deoxyadenosine, is a natural bioactive substance extracted from Cordyceps militaris (which is widely cultivated for commercial use in functional foods and medicine). Since cordycepin suppresses oxidative stress both in vitro and in vivo, we hypothesized that cordycepin would inhibit cardiac hypertrophy by blocking oxidative stress‐dependent related signalling. In our study, a mouse model of cardiac hypertrophy was induced by aortic banding (AB) surgery. Mice were intraperitoneally injected with cordycepin (20 mg/kg/d) or the same volume of vehicle 3 days after‐surgery for 4 weeks. Our data demonstrated that cordycepin prevented cardiac hypertrophy induced by AB, as assessed by haemodynamic parameters analysis and echocardiographic, histological and molecular analyses. Oxidative stress was estimated by detecting superoxide generation, superoxide dismutase (SOD) activity and malondialdehyde levels, and by detecting the protein levels of gp91 phox and SOD. Mechanistically, we found that cordycepin activated activated protein kinase α (AMPKα) signalling and attenuated oxidative stress both in vivo in cordycepin‐treated mice and in vitro in cordycepin treated cardiomyocytes. Taken together, the results suggest that cordycepin protects against post‐AB cardiac hypertrophy through activation of the AMPKα pathway, which subsequently attenuates oxidative stress.

show abstract

Arctiin protects against cardiac hypertrophy through inhibiting MAPKs and AKT signaling pathways

Abstract: In conclusion, arctiin can improve cardiac function and prevent the development of cardiac hypertrophy by blocking the MAPKs and AKT signaling pathways.

Cited by 29 publications

References 39 publications

Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways

Galangin ameliorates cardiac remodeling via the MEK1/2–ERK1/2 and PI3K–AKT pathways

Arctiin Antagonizes Triptolide‐Induced Hepatotoxicity via Activation of Nrf2 Pathway

Cordycepin ameliorates cardiac hypertrophy via activating the AMPKα pathway

Contact Info

Product

Resources

About