A chondroprotective effect of moracin on IL-1β-induced primary rat chondrocytes and an osteoarthritis rat model through Nrf2/HO-1 and NF-κB axes

Zhou, Siqi; Shi, Jiaqi; Wen, Haiyan; Han, Xiaotao

doi:10.1039/d0fo01496f

Cited by 23 publications

(21 citation statements)

References 33 publications

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“…The transcription factor NF-κB plays a critical role in the development of inflammation; it promotes the expression of inflammatory cytokines [ 21 ]. LPS-induced generation of pro-inflammatory mediators involves the NF-κB signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

“…After stimulation, P65 is released from the cytoplasm into the nucleus when IκBα is phosphorylated and then degraded. P65 activates the transcription of inflammatory mediators in the nucleus [ 21 ]. Activated NF-κB, which is made up of p50 and p65, is phosphorylated and translocated to the nucleus, where it transcribes inflammation-related genes [ 19 ].…”

Section: Resultsmentioning

confidence: 99%

“…Nrf2 activation can effectively reduce inflammation aside from reducing oxidative stress. Nrf2 is a key transcription factor found primarily in the cytoplasm that protects cells from oxidative damage [ 21 ]. Nrf2 signaling is considered the most sensitive redox pathway implicated in oxidative injury, and NF-κB is a significant regulator of pro-inflammatory mediators [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

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Nepetoidin B from Salvia plebeia R. Br. Inhibits Inflammation by Modulating the NF-κB and Nrf2/HO-1 Signaling Pathways in Macrophage Cells

Kim

Yang

et al. 2021

Antioxidants

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Salvia plebeia has been used to treat a variety of inflammatory diseases, as well as colds and bronchitis. Macrophages have antioxidant defense mechanisms to cope with the intracellular reactive oxygen species (ROS) produced as part of the immune response. The nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 pathway in inflamed macrophages is an appealing target due to its protective effect against ROS-induced cell damage. In this study, nepetoidin B (NeB) was first isolated from S. plebeia and identified by nuclear magnetic resonance spectroscopy. NeB reduced pro-inflammatory mediators (nitric oxide and prostaglandin E2) and cytokines (tumor necrosis factor-α, interleukin (IL)-6, and IL-1β) in LPS-activated RAW 264.7 cells by inhibiting the NF-κB signaling pathway. In the NeB-treated group, catalase and superoxide dismutase levels were significantly higher, and ROS expression decreased. By activating Nrf2 signaling, NeB enhanced HO-1 expression. Furthermore, when the cells were pretreated with tin protoporphyrin (an HO-1 inhibitor), the anti-inflammatory effects of NeB were reduced. Therefore, NeB may activate the Nrf2/ HO-1 pathway. These results reveal the NeB isolated from S. plebeia exerts anti-inflammatory effects by modulating NF-κB signaling and activating the Nrf2/HO-1 pathway in LPS-stimulated RAW 264.7 cells.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Nepetoidin B from Salvia plebeia R. Br. Inhibits Inflammation by Modulating the NF-κB and Nrf2/HO-1 Signaling Pathways in Macrophage Cells

Kim

Yang

et al. 2021

Antioxidants

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“…# P < 0:05 vs. "sh-C" cells. 12 Oxidative Medicine and Cellular Longevity 13 Oxidative Medicine and Cellular Longevity OARSI scores than the DMM group. Furthermore, to investigate the effect of luteolin on ECM in vivo, immunohistochemical staining of Nrf2 and MMP13 in cartilage samples was carried out.…”

Section: Luteolin Ameliorated Oa Progression In the Dmmmentioning

confidence: 96%

“…After binding to antioxidant response elements (AREs) in gene promoters, Nrf2 promotes the transcription and expression of several antioxidant enzymes, such as hem oxygenase 1 (HO-1), NAD (P) H quinone oxidoreductase-1 (NQO1), and γ-glutamyl cysteine ligase catalytic subunit (GCLC) [10,11]. Furthermore, researches have revealed that Nrf2 boost protects chondrocytes against oxidative injury and inflammation, as well as attenuates OA progression in animal models [12,13].…”

Section: Introductionmentioning

confidence: 99%

Luteolin Protects Chondrocytes from H2O2-Induced Oxidative Injury and Attenuates Osteoarthritis Progression by Activating AMPK-Nrf2 Signaling

Zhou

Zhang

Yang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Osteoarthritis (OA) is a chronic degenerative disease featured by cartilage erosion and inflammation. Luteolin, a member of the flavonoid family, has been shown to exert anti-inflammatory and antioxidative activities. However, the potential biological effects and underlying mechanism of luteolin on chondrocytes and OA progression remain largely elusive. In this study, the potential effect and mechanism of luteolin on OA were investigated in vitro and in vivo. Our data revealed that luteolin inhibited H2O2-induced cell death, apoptosis, oxidative stress, programmed necrosis, and inflammatory mediator production in primary murine chondrocytes. In addition, luteolin could activate the AMPK and Nrf2 pathways, and AMPK serves as a positive upstream regulator of Nrf2. In vivo results demonstrated the therapeutic effects of luteolin on OA in the DMM mouse model. Collectively, our findings showed that luteolin might serve as a novel and effective treatment for OA and provided a new research direction for clinical OA therapies.

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Direct Mapping of Cytomechanical Homeostasis Destruction in Osteoarthritis Based on Silicon Nanopillar Array

Yu,

Nie,

Xue

et al. 2023

Adv Healthcare Materials

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Osteoarthritis (OA) is the most prevalent joint degenerative disease characterized by chronic joint inflammation. The pathogenesis of OA has not been fully elucidated yet. Cartilage erosion is the most significant pathological feature in OA, which is considered as the result of the cytomechanical homeostasis destruction. The cytomechanical homeostasis is maintained by the dynamic interaction between cells and the extracellular matrix, which can be reflected by cell traction force (CTF). It is critical to assess the CTF for providing a deeper understanding of the cytomechanical homeostasis destruction and progression in OA. In this study, a silicon nanopillar array (Si‐NP) with high spatial resolution and aspect ratio is fabricated to investigate the CTF in response to OA. We discover the CTF is degraded in OA, which is attributed to the F‐actin reorganization induced by the activation of RhoA/ROCK signaling pathway. Si‐NP also show promising potential as a mechanopharmacological assessment platform for OA drug screening and evaluation.This article is protected by copyright. All rights reserved

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A chondroprotective effect of moracin on IL-1β-induced primary rat chondrocytes and an osteoarthritis rat model through Nrf2/HO-1 and NF-κB axes

Abstract: Osteoarthritis (OA) is a common joint disease characterized by cartilage degeneration and inflammation. Although moracin is known to play a role in anti-inflammation and anti-oxidation in several inflammatory diseases, its...

Cited by 23 publications

References 33 publications

Nepetoidin B from Salvia plebeia R. Br. Inhibits Inflammation by Modulating the NF-κB and Nrf2/HO-1 Signaling Pathways in Macrophage Cells

Nepetoidin B from Salvia plebeia R. Br. Inhibits Inflammation by Modulating the NF-κB and Nrf2/HO-1 Signaling Pathways in Macrophage Cells

Luteolin Protects Chondrocytes from H2O2-Induced Oxidative Injury and Attenuates Osteoarthritis Progression by Activating AMPK-Nrf2 Signaling

Direct Mapping of Cytomechanical Homeostasis Destruction in Osteoarthritis Based on Silicon Nanopillar Array

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