Rhodiola rosea: A Therapeutic Candidate on Cardiovascular Diseases.

Cardiovascular diseases, also known as circulatory diseases, are diseases of the heart and blood vessels, and its etiology is hyperlipidemia, thick blood, atherosclerosis, and hypertension. Due to its high prevalence, disability, and mortality, it seriously threatens human health. According to reports, the incidence of cardiovascular disease is still on the rise. Rhodiola rosea is a kind of traditional Chinese medicine, which has the effects of antimyocardial ischemia-reperfusion injury, lowering blood fat, antithrombosis, and antiarrhythmia. Rhodiola rosea has various chemical components, and different chemical elements have the same pharmacological effects and medicinal values for various cardiovascular diseases. This article reviews the research on the pharmacological effects of Rhodiola rosea on cardiovascular diseases and provides references for the clinical treatment of cardiovascular diseases.

GSK-3ß inhibition by curcumin mitigates amyloidogenesis via TFEB activation and anti-oxidative activity in human neuroblastoma cells.

The translocation of transcription factor EB (TFEB) to the nucleus plays a pivotal role in the regulation of basic cellular processes, such as lysosome biogenesis and autophagy. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome, which is important in maintaining cellular homeostasis during environmental stress. Furthermore, oxidative stress is a critical cause for the progression of neurodegenerative diseases. Curcumin has anti-oxidative and anti-inflammatory activities, and is expected to have potential therapeutic effects in various diseases. In this study, we demonstrated that curcumin regulated TFEB export signalling via inhibition of glycogen synthase kinase-3ß (GSK-3ß); GSK-3ß was inactivated by curcumin, leading to reduced phosphorylation of TFEB. We further showed that H2O2-induced oxidative stress was reduced by curcumin via the Nrf2/HO-1 pathway in human neuroblastoma cells. In addition, we showed that curcumin induced the degradation of amyloidogenic proteins, including amyloid-ß precursor protein and α-synuclein, through the TFEB-autophagy/lysosomal pathway. In conclusion, curcumin regulates autophagy by controlling TFEB through the inhibition of GSK-3ß, and increases antioxidant gene expression in human neuroblastoma cells. These results contribute to the development of novel cellular therapies for neurodegenerative diseases.