scholarly journals Restoration of the Phenotype of Dedifferentiated Rabbit Chondrocytes by Sesquiterpene Farnesol

Pharmaceutics ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 186
Author(s):  
Guan-Xuan Wu ◽  
Chun-Yu Chen ◽  
Chun-Shien Wu ◽  
Lain-Chyr Hwang ◽  
Shan-Wei Yang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Prostaglandin E2 ◽  
Proinflammatory Cytokine ◽  
Collagen Synthesis ◽  
Therapeutic Agent ◽  
Interleukin 1Β ◽  
Morphology Change ◽  
Progressive Degeneration ◽  
Joint Disorder ◽  
Inflammatory Effect

Osteoarthritis (OA) is a joint disorder characterized by the progressive degeneration of articular cartilage. The phenotype and metabolism behavior of chondrocytes plays crucial roles in maintaining articular cartilage function. Chondrocytes dedifferentiate and lose their cartilage phenotype after successive subcultures or inflammation and synthesize collagen I and X (COL I and COL X). Farnesol, a sesquiterpene compound, has an anti-inflammatory effect and promotes collagen synthesis. However, its potent restoration effects on differentiated chondrocytes have seldom been evaluated. The presented study investigated farnesol’s effect on phenotype restoration by examining collagen and glycosaminoglycan (GAG) synthesis from dedifferentiated chondrocytes. The results indicated that chondrocytes gradually dedifferentiated through cellular morphology change, reduced expressions of COL II and SOX9, increased the expression of COL X and diminished GAG synthesis during four passages of subcultures. Pure farnesol and hyaluronan-encapsulated farnesol nanoparticles promote COL II synthesis. GAG synthesis significantly increased 2.5-fold after a farnesol treatment of dedifferentiated chondrocytes, indicating the restoration of chondrocyte functions. In addition, farnesol drastically increased the synthesis of COL II (2.5-fold) and GAG (15-fold) on interleukin-1β-induced dedifferentiated chondrocytes. A significant reduction of COL I, COL X and proinflammatory cytokine prostaglandin E2 was observed. In summary, farnesol may serve as a therapeutic agent in OA treatment.

Anticatabolic Effects of Morin through the Counteraction of Interleukin-1β-Induced Inflammation in Rat Primary Chondrocytes

2019 ◽  
Vol 207 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Gyeong-Je Lee ◽  
In-A Cho ◽  
Ji-Su Oh ◽  
Yo-Seob  Seo ◽  
Jae-Seek You ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Articular Cartilage ◽  
Cellular Mechanism ◽  
Interleukin 1Β ◽  
Potential Candidate ◽  
Primary Chondrocytes ◽  
Progressive Degeneration ◽  
Herbal Plants ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Morin, a flavonoid isolated from various medicinal herbal plants, has an anti-inflammatory effect. This study aimed to elucidate the anticatabolic effects and cellular mechanism of morin against interleukin-1β (IL-1β) in rat primary chondrocytes. Morin at 10–100 μM did not affect the viability of rat primary chondrocytes. Treatment with morin for 21 days ameliorated the IL-1β-induced decrease in extracellular matrix. Furthermore, treatment with morin attenuated IL-1β-induced proteoglycan loss in the articular cartilage through suppression of catabolic factors, such as matrix metalloproteinases, inflammatory mediators, and pro-inflammatory cytokines. These data indicated that morin exerted anticatabolic effects that can prevent and reduce progressive degeneration of the articular cartilage, and thus may be a potential candidate treatment for osteoarthritis.

The Interleukin 1β Pathway in the Pathogenesis of Osteoarthritis

2008 ◽  
Vol 35 (12) ◽  
pp. 2306-2312 ◽  
Author(s):  
MASSOUD DAHESHIA ◽  
JIAN Q. YAO
Keyword(s):  
Chronic Pain ◽  
Articular Cartilage ◽  
Functional Impairment ◽  
Proinflammatory Cytokine ◽  
Joint Space ◽  
Persistent Pain ◽  
Current Understanding ◽  
Interleukin 1Β ◽  
Structural Remodeling ◽  
Joint Friction

Osteoarthritis (OA) is a major disabling disease and is ranked as a major cause of chronic pain in adults. The pathology of the illness is characterized by a loss of articular cartilage leading to narrowing of joint space, increased joint friction, potential structural remodeling, persistent pain, and functional impairment. The proinflammatory cytokine interleukin 1β (IL-1β) has several chemical and bioactive characteristics allowing this catabolic protein to be involved in initiation and progression of OA. We review the current understanding of the pathogenesis of OA, and how upregulation of IL-1β initiates a cascade of intracellular events that can culminate in activation…

Endogenous nitric oxide and prostaglandin E2 do not regulate the synthesis of each other in interleukin-1β-stimulated rat articular cartilage

Inflammation ◽  
1996 ◽  
Vol 20 (6) ◽  
pp. 683-692 ◽  
Author(s):  
Tero A. H. Järvinen ◽  
Teemu Moilanen ◽  
Teppo L. N. Järvinen ◽  
Eeva Moilanen
Keyword(s):  
Nitric Oxide ◽  
Articular Cartilage ◽  
Prostaglandin E2 ◽  
Interleukin 1Β ◽  
Endogenous Nitric Oxide

scholarly journals α-Ketoheterocycles Able to Inhibit the Generation of Prostaglandin E2 (PGE2) in Rat Mesangial Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 275
Author(s):  
Anastasia Psarra ◽  
Maria A. Theodoropoulou ◽  
Martin Erhardt ◽  
Marina Mertiri ◽  
Christiana Mantzourani ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Mesangial Cells ◽  
Cellular Level ◽  
Interleukin 1Β ◽  
Novel Agents

Prostaglandin E2 (PGE2) is a key mediator of inflammation, and consequently huge efforts have been devoted to the development of novel agents able to regulate its formation. In this work, we present the synthesis of various α-ketoheterocycles and a study of their ability to inhibit the formation of PGE2 at a cellular level. A series of α-ketobenzothiazoles, α-ketobenzoxazoles, α-ketobenzimidazoles, and α-keto-1,2,4-oxadiazoles were synthesized and chemically characterized. Evaluation of their ability to suppress the generation of PGE2 in interleukin-1β plus forskolin-stimulated mesangial cells led to the identification of one α-ketobenzothiazole (GK181) and one α-ketobenzoxazole (GK491), which are able to suppress the PGE2 generation at a nanomolar level.

scholarly journals Prostaglandin E2 receptor type 2-selective agonist prevents the degeneration of articular cartilage in rabbit knees with traumatic instability

2011 ◽  
Vol 13 (5) ◽  
pp. R146 ◽  
Author(s):  
Hiroto Mitsui ◽  
Tomoki Aoyama ◽  
Moritoshi Furu ◽  
Kinya Ito ◽  
Yonghui Jin ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Prostaglandin E2 ◽  
Receptor Type ◽  
Selective Agonist ◽  
Prostaglandin E2 Receptor

scholarly journals Up-regulation of P21-activated kinase 1 in osteoarthritis chondrocytes is responsible for osteoarthritic cartilage destruction

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Wanli Ma ◽  
Xiaohe Wang ◽  
Chunhui Wang ◽  
Mingzhi Gong ◽  
Peng Ren
Keyword(s):  
Articular Cartilage ◽  
Cartilage Destruction ◽  
Related Factors ◽  
Osteoarthritic Cartilage ◽  
Resident Cell ◽  
Joint Disorder ◽  
Osteoarthritis Chondrocytes ◽  
P21 Activated Kinase ◽  
Pak1 Expression

Abstract Osteoarthritis is mainly caused by a degenerative joint disorder, which is characterized by the gradual degradation of articular cartilage and synovial inflammation. The chondrocyte, the unique resident cell type of articular cartilage, is crucial for the development of osteoarthritis. Previous studies revealed that P21-activated kinase-1 (PAK1) was responsible for the initiation of inflammation. The purpose of the present study was to determine the potential role of PAK1 in osteoarthritis. The level of PAK1 expression was measured by Western blot and quantitative real-time PCR in articular cartilage from osteoarthritis model rats and patients with osteoarthritis. In addition, the functional role of aberrant PAK1 expression was detected in the chondrocytes. We found that the expression of PAK1 was significantly increased in chondrocytes treated with osteoarthritis-related factors. Increased expression of PAK1 was also observed in knee articular cartilage samples from patients with osteoarthritis and osteoarthritis model rats. PAK1 was found to inhibit chondrocytes proliferation and to promote the production of inflammatory cytokines in cartilages chondrocytes. Furthermore, we found that PAK1 modulated the production of extracellular matrix and cartilage degrading enzymes in chondrocytes. Results of the present studies demonstrated that PAK1 might play an important role in the pathogenesis of osteoarthritis.

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