Coronary atherosclerotic heart disease, cerebrovascular disease, and peripheral artery disease are common diseases with high morbidity and mortality rates and must be addressed. Their most frequent complications, including myocardial infarction and stroke, are caused by spontaneous thrombotic occlusion and are the most frequent cause of death worldwide. Atherosclerosis (AS) is the most widespread underlying pathological change for the above diseases. Therefore, drugs that interfere with this pathophysiological process must be incorporated in the treatment. Chinese traditional and herbal drugs can effectively treat AS. With the development of traditional Chinese medicine, the active ingredients in common Chinese medicinal materials must be thoroughly purified prior to their application in western medicine. Various proprietary Chinese medicine preparations with remarkable effects have been used in AS treatment. Catalpol, the active component of Rehmannia glutinosa, belongs to iridoid terpene and has anti-inflammatory, antioxidant, insulin resistance improvement, and other related effects. Several reviews have been conducted on this compound and its actions against osteoporosis, neurodegenerative diseases, Alzheimer's disease (AD), Parkinson's disease (PD) and diabetes and its complications. The current review focused on catalpol’s effect on atherosclerotic plaque formation in different animal models. The potential mechanisms of catalpol to ameliorate AS were also summarized in terms of oxidative stress, inflammation, cell aging, apoptosis, and activation of the silent information regulator factor 2-related enzyme 1 (SIRT1) pathway.
Myocardial remodeling refers to structural and functional disorders of the heart caused by molecular biological changes in the cardiac myocytes in response to neurological and humoral factors. A variety of heart diseases, such as hypertension, coronary artery disease, arrhythmia, and valvular heart disease, can cause myocardial remodeling and eventually lead to heart failure. Therefore, counteracting myocardial remodeling is essential for the prevention and treatment of heart failure. Sirt1 is a nicotinamide adenine dinucleotide+-dependent deacetylase that plays a wide range of roles in transcriptional regulation, energy metabolism regulation, cell survival, DNA repair, inflammation, and circadian regulation. It positively or negatively regulates myocardial remodeling by participating in oxidative stress, apoptosis, autophagy, inflammation, and other processes. Taking into account the close relationship between myocardial remodeling and heart failure and the involvement of SIRT1 in the development of the former, the role of SIRT1 in the prevention of heart failure via inhibition of myocardial remodeling has received considerable attention. Recently, multiple studies have been conducted to provide a better understanding of how SIRT1 regulates these phenomena. This review presents the progress of research involving SIRT1 pathway involvement in the pathophysiological mechanisms of myocardial remodeling and heart failure.
It has been found that a Mannich-type reaction catalyzed by an intramolecular phenolic hydroxy group involves simply heating a hydroxybenzaldehyde with a secondary amine and a dialkyl phosphite in alcohol, produced highly substituted a-aminomethylphosphonates. The corresponding reaction can hardly be detected if the hydoxy group of the benzaldehyde is absent or blocked, or the hydroxybenzaldehyde is replaced by 2¢-hydroxyacetophenone.
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