Aloe-emodin attenuates myocardial infarction and apoptosis via up-regulating miR-133 expression

Yu, Yang; Liu, Huibin; Yang, Di; He, Fang; Yuan, Ye; Guo, Jing; Hu, Juan; Yu, Jie; Yan, Xiuwei; Wang, Shuo; Du, Zhenhong

doi:10.1016/j.phrs.2019.104315

Cited by 51 publications

(40 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bai's findings suggested a novel pharmacological role of AE in high-fat diet-induced cardiac electrical remodelling (Bai et al, 2017). Yu et al (2019) findings indicated that AE can protect against myocardial infarction via the upregulation of miR-133, inhibition of ROS production and suppression of caspase-3 apoptotic signaling pathway. Zhang et al (2020) results revealed that inhibiting the activation of NLRP3 inflammasome and reducing the release of HMGB1 by promoting NLRP3 ubiquitination, thereby restoring the endothelial tight junction proteins and permeability, which indicated that AE exhibited immense potential therapeutic value in hypertensionrelated cardiovascular disease and the development of innovative drugs ( Table 3).…”

Section: Emodin Derivativesmentioning

confidence: 99%

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Emodin is a natural occurring anthraquinone derivative isolated from roots and barks of numerous plants, molds, and lichens. It is found to be an active ingredient in different Chinese herbs including Rheum palmatum and Polygonam multiflorum, and it is a pleiotropic molecule with diuretic, vasorelaxant, anti-bacterial, anti-viral, antiulcerogenic, anti-inflammatory, and anti-cancer effects. Moreover, emodin has also been shown to have a wide activity of anti-cardiovascular diseases. It is mainly involved in multiple molecular targets such as inflammatory, anti-apoptosis, anti-hypertrophy, antifibrosis, anti-oxidative damage, abnormal, and excessive proliferation of smooth muscle cells in cardiovascular diseases. As a new type of cardiovascular disease treatment drug, emodin has broad application prospects. However, a large amount of evidences detailing the effect of emodin on many signaling pathways and cellular functions in cardiovascular disease, the overall understanding of its mechanisms of action remains elusive. In addition, by describing the evidence of the effects of emodin in detail, the toxicity and poor oral bioavailability of mice have been continuously discovered. This review aims to describe a timely overview of emodin related to the treatment of cardiovascular disease. The emphasis is to summarize the pharmacological effects of emodin as an anticardiovascular drug, as well as the targets and its potential mechanisms. Furthermore, the treatment of emodin compared with conventional cardiovascular drugs or target inhibitors, the toxicity, pharmacokinetics and derivatives of emodin were discussed.

show abstract

Section: Emodin Derivativesmentioning

confidence: 99%

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Consistent with our finding, Yuan et al also demonstrated that chrysophanol ameliorated the abnormal changes in cardiac structure and function in rats [ 16 ]. In addition to chrysophanol, other anthraquinone compounds with anti-inflammatory properties, such as kanglexin, aloe-emodin, and diacerein, also improve cardiac function by reducing the inflammatory response after myocardial injury [ 26 – 28 ]. The protective role of chrysophanol is further supported by the above evidence.…”

Section: Discussionmentioning

confidence: 99%

“…Generally, pathological changes are visible and have a unique diagnostic significance in heart failure. Therefore, it is important to measure the myocardial damage related to the AHF episode [ 28 ]. Histological analysis revealed that chrysophanol relieved the pathological injury of myocardial tissue, which is further supported by the chrysophanol-induced reduction of CK-MB and LDH activity.…”

Section: Discussionmentioning

confidence: 99%

Chrysophanol Protects Against Acute Heart Failure by Inhibiting JNK1/2 Pathway in Rats

Xie

2020

Med Sci Monit

View full text Add to dashboard Cite

Background Acute heart failure (AHF) usually requires urgent therapy. Myocardial damage, oxidative stress, and inflammation are major components in the pathology of AHF. This study was designed to investigate the effects of chrysophanol on AHF. Material/Methods Sprague-Dawley rats were injected with isoprenaline hydrochloride to construct AHF rat models. AHF rats were treated with normal saline (negative control), chrysophanol, the combination of chrysophanol and SP600125, or benazepril (positive control) using sham rats as blank controls. Echocardiography, histological staining, and enzyme activity analysis were performed to assess the heart functions and myocardial damage. Effects on apoptosis, oxidative stress (OS), and inflammation were evaluated by biochemical analysis, TUNEL staining, and ELISA. Results Chrysophanol improved the parameters of cardiac functions and alleviated the myocardial damage accompanied by the reduction of creatine kinase and lactate dehydrogenase activity. Meanwhile, chrysophanol inhibited the myocardial apoptosis along with the upregulation of Bcl-2 and downregulation of Bax and cleaved caspase-3. AHF-induced abnormal changes of OS parameters (MDA, GPx, CAT, SOD) and inflammatory markers (IL-6, IL-1β, TNF-α, IFN-γ) were alleviated by chrysophanol. Benazepril treatment showed similar results with chrysophanol, while the addition of SP600125 enhanced the chrysophanol-mediated protection effects in AHF rats. Western blot analysis demonstrated that chrysophanol inhibited the phosphorylation of JNK1/2 and its upstream/downstream factors. Conclusions Chrysophanol improved cardiac functions and protected against myocardial damage, apoptosis, OS, and inflammation by inhibiting activation of the JNK1/2 pathway in AHF rat models. These finding indicate that chrysophanol may be a promising approach for treatment of AHF.

show abstract

“…MiR-133b is expressed in the brain and is known to regulate the development of midbrain dopaminergic neurons [177]. Interestingly, miR-133b is also regulated after myocardial infarction and dampens reactive oxygen species production [178,179]. Therefore, miR-133b has roles both in the brain and the heart.…”

Section: Non-coding Rnas In the Brain-heart Axis In Pdmentioning

confidence: 99%

Non-Coding RNAs in the Brain-Heart Axis: The Case of Parkinson’s Disease

Acharya

Salgado-Somoza

Stefanizzi

et al. 2020

IJMS

View full text Add to dashboard Cite

Parkinson’s disease (PD) is a complex and heterogeneous disorder involving multiple genetic and environmental influences. Although a wide range of PD risk factors and clinical markers for the symptomatic motor stage of the disease have been identified, there are still no reliable biomarkers available for the early pre-motor phase of PD and for predicting disease progression. High-throughput RNA-based biomarker profiling and modeling may provide a means to exploit the joint information content from a multitude of markers to derive diagnostic and prognostic signatures. In the field of PD biomarker research, currently, no clinically validated RNA-based biomarker models are available, but previous studies reported several significantly disease-associated changes in RNA abundances and activities in multiple human tissues and body fluids. Here, we review the current knowledge of the regulation and function of non-coding RNAs in PD, focusing on microRNAs, long non-coding RNAs, and circular RNAs. Since there is growing evidence for functional interactions between the heart and the brain, we discuss the benefits of studying the role of non-coding RNAs in organ interactions when deciphering the complex regulatory networks involved in PD progression. We finally review important concepts of harmonization and curation of high throughput datasets, and we discuss the potential of systems biomedicine to derive and evaluate RNA biomarker signatures from high-throughput expression data.

show abstract

Aloe-emodin attenuates myocardial infarction and apoptosis via up-regulating miR-133 expression

Cited by 51 publications

References 31 publications

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Chrysophanol Protects Against Acute Heart Failure by Inhibiting JNK1/2 Pathway in Rats

Non-Coding RNAs in the Brain-Heart Axis: The Case of Parkinson’s Disease

Contact Info

Product

Resources

About