INTRODUCTIONNanotechnology is a novel method of producing and manipulating substance at the molecular scale, which can provide for more efficiently functioning mechanical, chemical, and biological components and bring great value to the development of medicine (1). The term "nano," first presented by the famous material scientist Richard P. Feynman (2) in 1959, is a unit used to describe 10 −9 of parameter in the microcosm. Over the past few years, nanotechnology has sparked intense interest among scientists and has been used to overcome biomedical difficulties and treat various diseases such as cancers (3), infectious diseases (4), and cardiovascular diseases (5). Nanoparticles, nano-carriers or nano-materials, defined as substances with a size of 1 to 100 nm, have specific functions at the cellular, atomic and molecular levels and are widely used in the fields of diagnosis and treatment of diseases (6). Nanoparticles or nano-carriers exhibit many advantages, including excellent drug stability and solubility, prolonged half-life of drug systemic circulation, stable and sustained drug-releasing rate, and lower frequency of drug administration, thus minimizing side effects of drug (6). As a result, they have become a promising alternative strategy to improve drug efficiency and minimize side effects in the treatment of diseases.Infective endocarditis (IE) is an infectious disease defined by an infection of the heart valve and the endocardial surface, such as a prosthetic heart valve or an indwelling cardiac device (7). IE remains an infectious and life-threatening disease with an incidence of approximately 3-10 per 100,000 person-years (8, 9). With more prosthetic valve replacements or cardiac electronic device implantations performed for patients who suffer from heart valve diseases or arrhythmia, the incidence of IE is rising (8). IE is still a challenging disease bringing stupendous health and economic burden to the world.With IE recognized as an infectious disease characterized by biofilm formation, the core of antimicrobial therapy for IE has focused on eradicating biofilm and drug-resistant bacteria. Nanoparticles, working as effectively functioning drugs
Atrial fibrillation (AF) is one of the most common sustained tachyarrhythmias worldwide, and its prevalence is positively correlated with aging. AF not only significantly reduces the quality of life of patients but also causes a series of complications, such as thromboembolism, stroke, and heart failure, increases the average number of hospitalizations of patients, and places a huge economic burden on patients and society. Traditional drug therapy and ablation have unsatisfactory success rates, high recurrence rates, and the risk of serious complications. Surgical treatment is highly traumatic. The nano drug delivery system has unique physical and chemical properties, and in the application of AF treatment, whether it is used to assist in enhancing the ablation effect or for targeted therapy, it provides a safer, more effective and more economical treatment strategy.
Purpose The aim of this study was to investigate the effect and mechanism of epigallocatechin-3-gallate (EGCG) on atrial fibrillation (AF) in rats. Methods A rat AF model was established by angiotensin-II (Ang-II) induction, to verify the relationship between atrial fibrosis and the AF. The expression levels of TGF-β/Smad3 pathway molecules and lysyl oxidase (LOX) in AF were detected. Subsequently, EGCG was used to intervene Ang-Ⅱ-induced atrial fibrosis, to explore the role of EGCG in the treatment of AF and its inhibitory mechanism on fibrosis. It was further verified that EGCG inhibited the production of collagen and the expression of LOX through the TGF-β/Smad3 pathway at the cellular level. Results The results showed that the induction rate and maintenance time of AF in rats increased with the increase of the degree of atrial fibrosis. Meanwhile, the expressions of Col I, Col III, molecules related to TGF-β/Smad3 pathway, and LOX increasedsignificantly in the atrial tissues of rats in the Ang-II induced group. EGCG could reduce the occurrence and maintenance time of AF by inhibiting the degree of Ang-induced rat atrial fibrosis. Cell experiments confirmed that EGCG could reduce the synthesis of collagen and the expression of LOX in cardiac fibroblast induced by Ang-II. The possible mechanism is to down-regulate the expression of genes and proteins related to TGF-βSmad3 pathway. Conclusion EGCG could downregulate the expression levels of collagen and LOX by inhibiting the TGF-β/Smad3 signaling pathway, alleviating Ang-II-induced atrial fibrosis, which in turn inhibited the occurrence and curtailed the duration of AF.
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