Stability of glycosylated complexes loaded with Epigallocatechin 3-gallate (EGCG)

Zhang, Jianyong; Cui, Hongchun; Qiu, Jiahuan; Wang, Xiaoqing; Zhong, Yixin; Yao, Caiping; Yao, Lanying; Zheng, Qingdong; Xiong, Chunhua

doi:10.1016/j.foodchem.2022.135364

Cited by 11 publications

(3 citation statements)

References 34 publications

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“…Second, further experiments are needed to determine the effect of EGCG on arterial calcification by using JunBknockout mice to better understand the molecular mechanisms by which EGCG inhibits MAC. Finally, EGCG has several disadvantages, such as low stability in aqueous solution and low oral bioavailability in vivo, which limit its application in the treatment of several diseases [34]. Therefore, researchers have combined EGCG with liposomes or nanoparticles to prepare a variety of novel EGCG-based complex materials, such as EGCG nanoliposomes and Fe-EGCG nanocomplexes, which have greatly improved the bioavailability of EGCG [35,36].…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB

Li,

Fang,

Yin

et al. 2024

ABBS

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Medial arterial calcification (MAC) accompanying chronic kidney disease (CKD) leads to increased vessel wall stiffness, myocardial ischemia, heart failure, and increased cardiovascular morbidity and mortality. Unfortunately, there are currently no drugs available to treat MAC. The natural polyphenol epigallocatechin-3-gallate (EGCG) has been demonstrated to protect against cardiovascular disease; however, whether EGCG supplementation inhibits MAC in CKD remains unclear. In this study, we utilize a CKD-associated MAC model to investigate the effects of EGCG on vascular calcification and elucidate the underlying mechanisms involved. Our findings demonstrate that EGCG treatment significantly reduces calcium phosphate deposition and osteogenic differentiation of VSMCs in vivo and in vitro in a dose-dependent manner. In addition, through RNA sequencing (RNA-seq) analysis, we show a significant activation of the transcription factor JunB both in CKD mouse arteries and in osteoblast-like VSMCs. Notably, EGCG effectively suppresses CKD-associated MAC by inhibiting the activity of JunB. In addition, overexpression of JunB can abolish while knockdown of JunB can enhance the inhibitory effect of EGCG on the osteogenic differentiation of VSMCs. Furthermore, EGCG supplementation inhibits MAC in CKD via modulation of the JunB-dependent Ras/Raf/MEK/ERK signaling pathway. In conclusion, our study highlights the potential therapeutic value of EGCG for managing CKD-associated MAC, as it mitigates this pathological process through targeted inactivation of JunB.

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Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB

Li,

Fang,

Yin

et al. 2024

ABBS

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“…In addition, the inhibitory effect of EGCG on EndMT has been confirmed, providing more possibilities for the prevention and treatment of cardiovascular diseases in the future [ 129 ]. The multi-type nanoparticle carriers developed for EGCG have been tested in simulated gastric and intestinal fluid environments to enhance their stability in acid–base and enzymatic hydrolysis environments, which is conducive to improving bioavailability in the human body [ 130 , 131 ].…”

Section: Protective Effects Of Flavonoids On Endothelial Cellsmentioning

confidence: 99%

Research Progress of Flavonoids Regulating Endothelial Function

Li,

Zhang

2023

Pharmaceuticals

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The endothelium, as the guardian of vascular homeostasis, is closely related to the occurrence and development of cardiovascular diseases (CVDs). As an early marker of the development of a series of vascular diseases, endothelial dysfunction is often accompanied by oxidative stress and inflammatory response. Natural flavonoids in fruits, vegetables, and Chinese herbal medicines have been shown to induce and regulate endothelial cells and exert anti-inflammatory, anti-oxidative stress, and anti-aging effects in a large number of in vitro models and in vivo experiments so as to achieve the prevention and improvement of cardiovascular disease. Focusing on endothelial mediation, this paper introduces the signaling pathways involved in the improvement of endothelial dysfunction by common dietary and flavonoids in traditional Chinese medicine and describes them based on their metabolism in the human body and their relationship with the intestinal flora. The aim of this paper is to demonstrate the broad pharmacological activity and target development potential of flavonoids as food supplements and drug components in regulating endothelial function and thus in the prevention and treatment of cardiovascular diseases. This paper also introduces the application of some new nanoparticle carriers in order to improve their bioavailability in the human body and play a broader role in vascular protection.

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“…Not only can OMVs derived from EcN be used as the tumor-targeting drug delivery vehicle, but also they can effectively reprogramme M2-like TAMs to M1-like TAMs [ 23 ]. EGCG, as a tea polyphenol substance, has been widely used in clinical treatment and is a potential anticancer drug for development [ 24 ]. EGCG has been testified to inhibit tumor growth by suppressing the NF-κB pathway [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Tea polyphenol-engineered hybrid cellular nanovesicles for cancer immunotherapy and androgen deprivation therapy

Guo,

Wu,

Chen

et al. 2024

J Nanobiotechnol

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Androgen deprivation therapy (ADT) is a crucial and effective strategy for prostate cancer, while systemic administration may cause profound side effects on normal tissues. More importantly, the ADT can easily lead to resistance by involving the activation of NF-κB signaling pathway and high infiltration of M2 macrophages in tumor microenvironment (TME). Herein, we developed a biomimetic nanotherapeutic platform by deriving cell membrane nanovesicles from cancer cells and probiotics to yield the hybrid cellular nanovesicles (hNVs), loading flutamide (Flu) into the resulting hNVs, and finally modifying the hNVs@Flu with Epigallocatechin-3-gallate (EGCG). In this nanotherapeutic platform, the hNVs significantly improved the accumulation of hNVs@Flu-EGCG in tumor sites and reprogramed immunosuppressive M2 macrophages into antitumorigenic M1 macrophages, the Flu acted on androgen receptors and inhibited tumor proliferation, and the EGCG promoted apoptosis of prostate cancer cells by inhibiting the NF-κB pathway, thus synergistically stimulating the antitumor immunity and reducing the side effects and resistance of ADT. In a prostate cancer mouse model, the hNVs@Flu-EGCG significantly extended the lifespan of mice with tumors and led to an 81.78% reduction in tumor growth compared with the untreated group. Overall, the hNVs@Flu-EGCG are safe, modifiable, and effective, thus offering a promising platform for effective therapeutics of prostate cancer. Graphical Abstract

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Stability of glycosylated complexes loaded with Epigallocatechin 3-gallate (EGCG)

Cited by 11 publications

References 34 publications

Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB

Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB

Research Progress of Flavonoids Regulating Endothelial Function

Tea polyphenol-engineered hybrid cellular nanovesicles for cancer immunotherapy and androgen deprivation therapy

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