The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

Giuliani, Cesidio

doi:10.3390/antiox8050112

Cited by 92 publications

(59 citation statements)

References 42 publications

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“…Chitosan (CS) has emerged as a strong candidate scaffold for TE applications. Originating from chitin, chitosan is a unique natural polysaccharide with superb properties: high biodegradability, biocompatibility, non-antigenicity, adsorption capabilities, and antimicrobial activity (Giuliani, 2019). Studies have also found no complications, such as inflammation or allergic reactions, Tayeb et al (2018), Dutta et al (2019) following implantation of CS-based scaffolds (Keller et al, 2017).…”

Section: Chitosanmentioning

confidence: 99%

Applications of Biocompatible Scaffold Materials in Stem Cell-Based Cartilage Tissue Engineering

Zhao

et al. 2021

Front. Bioeng. Biotechnol.

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Cartilage, especially articular cartilage, is a unique connective tissue consisting of chondrocytes and cartilage matrix that covers the surface of joints. It plays a critical role in maintaining joint durability and mobility by providing nearly frictionless articulation for mechanical load transmission between joints. Damage to the articular cartilage frequently results from sport-related injuries, systemic diseases, degeneration, trauma, or tumors. Failure to treat impaired cartilage may lead to osteoarthritis, affecting more than 25% of the adult population globally. Articular cartilage has a very low intrinsic self-repair capacity due to the limited proliferative ability of adult chondrocytes, lack of vascularization and innervation, slow matrix turnover, and low supply of progenitor cells. Furthermore, articular chondrocytes are encapsulated in low-nutrient, low-oxygen environment. While cartilage restoration techniques such as osteochondral transplantation, autologous chondrocyte implantation (ACI), and microfracture have been used to repair certain cartilage defects, the clinical outcomes are often mixed and undesirable. Cartilage tissue engineering (CTE) may hold promise to facilitate cartilage repair. Ideally, the prerequisites for successful CTE should include the use of effective chondrogenic factors, an ample supply of chondrogenic progenitors, and the employment of cell-friendly, biocompatible scaffold materials. Significant progress has been made on the above three fronts in past decade, which has been further facilitated by the advent of 3D bio-printing. In this review, we briefly discuss potential sources of chondrogenic progenitors. We then primarily focus on currently available chondrocyte-friendly scaffold materials, along with 3D bioprinting techniques, for their potential roles in effective CTE. It is hoped that this review will serve as a primer to bring cartilage biologists, synthetic chemists, biomechanical engineers, and 3D-bioprinting technologists together to expedite CTE process for eventual clinical applications.

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Section: Chitosanmentioning

confidence: 99%

Applications of Biocompatible Scaffold Materials in Stem Cell-Based Cartilage Tissue Engineering

Zhao

et al. 2021

Front. Bioeng. Biotechnol.

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“…Since Gal-3 recognizes and binds glycoprotein oligosaccharides through the carbohydrate recognition region, the pharmacological inhibitory effect of Gal-3 is mediated by CRD to inhibit the activity of the protein. Given the multiple effects of Gal-3 and its various localizations in tissues, such as intracellular, membrane-bound or extracellular, different inhibitors with different types of cellular uptake have been synthesized [ 98 , 99 ]. At present, these inhibitors are generally classified into carbohydrate and peptidic noncarbohydrate types.…”

Section: Main Textmentioning

confidence: 99%

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

Tan

Zheng

et al. 2021

Cell Biosci

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Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.

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“…A recent study showed that Rg1 could attenuate chronic, unpredictable, mild stress-induced, depressive-like effects in rats via the regulation of the nuclear factor (NF)-κB/NLRP3 pathway (21). It was also seen that Rg1 could protect primary astrocyte cultures against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury, by decreasing ROS generation (22). A recent study also showed that Rg1 could alleviate age-associated neuronal damage by decreasing NOX2-mediated ROS generation and inhibiting NLRP1 inflammasome activation in neurons (23).…”

Section: Ginsenoside Rg1 Alleviates Lipopolysaccharide-induced Neuronal Damage By Inhibiting Nlrp1 Inflammasomes In Ht22 Cellsmentioning

confidence: 99%

Ginsenoside Rg1 alleviates lipopolysaccharide‑induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells

et al. 2021

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Lipopolysaccharide (LPS) is a toxic component of cell walls of Gram-negative bacteria that are widely present in gastrointestinal tracts. Increasing evidence showed that LPS plays important roles in the pathogeneses of neurodegenerative disorders, such as Alzheimer's disease (AD). NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. The NLRP1 inflammasome can be activated in response to an accumulation of ROS in neurons. However, it is still unknown whether LPS exposure can deteriorate neuronal damage by activating NOX2-NLRP1 inflammasomes. Ginsenoside Rg1 (Rg1) has protective effects on neurons, although whether Rg1 alleviates LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes remains unclear. In the present study, the effect of concentration gradients and different times of LPS exposure on neuronal damage was investigated in HT22 cells, and further observed the effect of Rg1 treatment on NOX2-NLPR1 inflammasome activation, ROS production and neuronal damage in LPS-treated HT22 cells. The results demonstrated that LPS exposure significantly induced NOX2-NLRP1 inflammasome activation, excessive production of ROS, and neuronal damage in HT22 cells. It was also shown that Rg1 treatment significantly decreased NOX2-NLRP1 inflammasome activation and ROS production and alleviated neuronal damage in LPS-induced HT22 cells. The present data suggested that Rg1 has protective effects on LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes in HT22 cells, and Rg1 may be a potential therapeutic approach for delaying neuronal damage in AD.

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The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

Cited by 92 publications

References 42 publications

Applications of Biocompatible Scaffold Materials in Stem Cell-Based Cartilage Tissue Engineering

Applications of Biocompatible Scaffold Materials in Stem Cell-Based Cartilage Tissue Engineering

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

Ginsenoside Rg1 alleviates lipopolysaccharide‑induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells

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