Dietary polyphenols for management of rheumatoid arthritis: Pharmacotherapy and novel delivery systems

Maity, Siddharth; Wairkar, Sarika

doi:10.1002/ptr.7444

Cited by 10 publications

(12 citation statements)

References 111 publications

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“…Rheumatoid arthritis (RA), one of the common types of chronic and pharmacologically complex systemic autoimmune disease observed in the elderly population, 242 , 268 , 269 , 270 is characterized by the presence of AAbs such as rheumatoid factor (RF) and anti‐cyclic citrullinated peptide antibody. 271 , 272 Liu et al.…”

Section: Treg Subsets In Autoimmune Diseasementioning

confidence: 99%

“…Rheumatoid arthritis (RA), one of the common types of chronic and pharmacologically complex systemic autoimmune disease observed in the elderly population, 242,[268][269][270] is characterized by the presence of AAbs such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody. 271,272 Liu et al have found that the frequency of circulating CD4 + CXCR5 + FOXP3 + Tfrs (Figure 3) and the ratio of Tfrs/Tfhs were significantly increased in patients with stable RA than in patients with active RA or healthy people.…”

Section: Treg Subsets In Rheumatoid Arthritismentioning

confidence: 99%

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Different subpopulations of regulatory T cells in human autoimmune disease, transplantation, and tumor immunity

Jiang

Zhu

Wang

et al. 2022

MedComm

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CD4 + CD25 + regulatory T cells (Tregs), a subpopulation of naturally CD4 + T cells that characteristically express transcription factor Forkhead box P3 (FOXP3), play a pivotal role in the maintenance of immune homeostasis and the prevention of autoimmunity. With the development of biological technology, the understanding of plasticity and stability of Tregs has been further developed. Recent studies have suggested that human Tregs are functionally and phenotypically diverse. The functions and mechanisms of different phenotypes of Tregs in different disease settings, such as tumor microenvironment, autoimmune diseases, and transplantation, have gradually become hot spots of immunology research that arouse extensive attention. Among the complex functions, CD4 + CD25 + FOXP3 + Tregs possess a potent immunosuppressive capacity and can produce various cytokines, such as IL‐2, IL‐10, and TGF‐β, to regulate immune homeostasis. They can alleviate the progression of diseases by resisting inflammatory immune responses, whereas promoting the poor prognosis of diseases by helping cells evade immune surveillance or suppressing effector T cells activity. Therefore, methods for targeting Tregs to regulate their functions in the immune microenvironment, such as depleting them to strengthen tumor immunity or expanding them to treat immunological diseases, need to be developed. Here, we discuss that different subpopulations of Tregs are essential for the development of immunotherapeutic strategies involving Tregs in human diseases.

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Section: Treg Subsets In Autoimmune Diseasementioning

confidence: 99%

Section: Treg Subsets In Rheumatoid Arthritismentioning

confidence: 99%

Different subpopulations of regulatory T cells in human autoimmune disease, transplantation, and tumor immunity

Jiang

Zhu

Wang

et al. 2022

MedComm

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“…The BCL2 family of proteins is the hallmark of apoptosis regulation. 48 New members of the BCL2 gene family were discovered and cloned and were found to be differentially expressed in many types of cancer. BCL2 protein family, through its role in the regulation of apoptotic pathways, is possibly related to cancer pathophysiology and resistance to conventional chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Withania somnifera Alter BCL2/Bax signaling and trigger apoptosis of MCF-7 and MDA-MB231 breast cancer cells exposed to γ-radiation

et al. 2023

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Treatment strategies encompass synchronization of more than one therapy with specific dependence on zeroing side effects of natural products that might represent a niche in the continuous struggle against cancer. Thus, this study aimed at assessing the role of Withania somnifera; WS (Ashwagandha) in forcing MCF7 or MDA-MB 231 irradiated breast cancer cells to outweigh the route of programmed cell death. We check to what extent SIRT1-BCL2/Bax signaling pathway was interrelated to form apoptotic cancer cells. MDA or MCF7 cells are categorized into four groups: gp1, Control (C): MDA-MB-231 or MCF7 cells not treated with WS or exposed to γ-rays, gp2 (WS): cells challenged with WS for MDA-MB-231 or MCF7 cells respectively, gp3: irradiated (R) MDA-MB-231 or MCF7 cells exposed to γ-rays (4 Gy; one shot) and gp4 WS and irradiated (WS + R): cells challenged with WS as in gp2 and exposed to gamma rays as in gp3. The results revealed that, WS established IC50 equivalent to 4897.8 μg/ml in MDA-MB-231 cells or equivalent to 3801.9 μg/ml in MCF7 cells. The flowcytometric analysis (Annexin V and cell cycle) showed that WS induces apoptosis at pre-G phase and induces cell arrest at G2/M and preG1 phases for MDA-MB-231 and at the preG1 for MCF7 cells. Furthermore, the WS + R group of cells (MDA-MB-231 and MCF7) showed significant increases in the expression of SIRT1, and BCL2 and a decrease in BAX compared with WS or R group. It could be concluded that WS has an anti-proliferative action on MDA-MB-231 and MCF7 cells because of its capability to enhance apoptosis.

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“…Recent studies suggest that also many naturally occurring compounds may be promising therapeutic options for the improvement of CVD risk. Antioxidant and anti-inflammatory effects of flavonoid and non-flavonoid polyphenols are well-documented [ 535 ]. Mainly in patients with chronic inflammatory conditions, polyphenols could improve HDL function, enhance RCT or protect HDL particles against dysfunction.…”

Section: Currently Available Hdl-targeted Therapiesmentioning

confidence: 99%

Alterations of HDL’s to piHDL’s Proteome in Patients with Chronic Inflammatory Diseases, and HDL-Targeted Therapies

2022

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Chronic inflammatory diseases, such as rheumatoid arthritis, steatohepatitis, periodontitis, chronic kidney disease, and others are associated with an increased risk of atherosclerotic cardiovascular disease, which persists even after accounting for traditional cardiac risk factors. The common factor linking these diseases to accelerated atherosclerosis is chronic systemic low-grade inflammation triggering changes in lipoprotein structure and metabolism. HDL, an independent marker of cardiovascular risk, is a lipoprotein particle with numerous important anti-atherogenic properties. Besides the essential role in reverse cholesterol transport, HDL possesses antioxidative, anti-inflammatory, antiapoptotic, and antithrombotic properties. Inflammation and inflammation-associated pathologies can cause modifications in HDL’s proteome and lipidome, transforming HDL from atheroprotective into a pro-atherosclerotic lipoprotein. Therefore, a simple increase in HDL concentration in patients with inflammatory diseases has not led to the desired anti-atherogenic outcome. In this review, the functions of individual protein components of HDL, rendering them either anti-inflammatory or pro-inflammatory are described in detail. Alterations of HDL proteome (such as replacing atheroprotective proteins by pro-inflammatory proteins, or posttranslational modifications) in patients with chronic inflammatory diseases and their impact on cardiovascular health are discussed. Finally, molecular, and clinical aspects of HDL-targeted therapies, including those used in therapeutical practice, drugs in clinical trials, and experimental drugs are comprehensively summarised.

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Dietary polyphenols for management of rheumatoid arthritis: Pharmacotherapy and novel delivery systems

Cited by 10 publications

References 111 publications

Different subpopulations of regulatory T cells in human autoimmune disease, transplantation, and tumor immunity

Different subpopulations of regulatory T cells in human autoimmune disease, transplantation, and tumor immunity

Withania somnifera Alter BCL2/Bax signaling and trigger apoptosis of MCF-7 and MDA-MB231 breast cancer cells exposed to γ-radiation

Alterations of HDL’s to piHDL’s Proteome in Patients with Chronic Inflammatory Diseases, and HDL-Targeted Therapies

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