The analgesic and anti-inflammatory effects of Litsea japonica fruit are mediated via suppression of NF-κB and JNK/p38 MAPK activation

Koo, Hyun Jung; Yoon, Weon‐Jong; Sohn, Eun‐Hwa; Ham, Young-Min; Jang, Seon‐A; Kwon, Jae Wan; Jeong, Yong Seok; Kwak, Jong Hwan; Sohn, Eunsoo; Park, Soo‐Young; Jang, Ki‐Hyo; Namkoong, Seung; Han, Hyo-Sang; Jung, Yong‐Hwan; Kang, Se Chan

doi:10.1016/j.intimp.2014.06.007

Cited by 40 publications

(34 citation statements)

References 47 publications

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“…Activated NF-κB is involved in immune regulation, inflammatory response, cell growth, and antiapoptosis via phosphorylating IκB and shifting into the nucleus [40][41][42]. Notably, previous studies have shown that the suppression of NF-κB pathway is associated with anti-inflammatory responses [43][44][45][46]. Therefore, we explored whether GEA could regulate NF-κB signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages

Lei¹,

Zhao²,

Zhang³

et al. 2016

ABBS

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Inflammation is a response of body tissues to injury and infection. Compounds that can inhibit inflammation have been shown to have potential therapeutic clinical application. Gambogenic acid (GEA) has potent antitumor and anti-inflammatory activities. Herein, the molecular mechanisms of GEA's anti-inflammatory effect were investigated in lipopolysaccharide (LPS)-stimulated macrophage cells. The results showed that pretreatment with GEA could markedly inhibit interleukin (IL)-1α, IL-1β, tumor necrosis factor-α, IFN-β, IL-12b, and IL-23a production in a dose-dependent manner in LPS-induced model. Furthermore, this drug significantly reduced the release of nitric oxide (NO), and impaired the protein level of inducible NO synthase and the cyclooxygenase 2. The finding also showed that the effect of GEA may be related to the suppression of the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathway. These results indicate that GEA could suppress LPS-simulated inflammatory response partially by attenuating NO synthesis and NF-κB and MAPK activation, suggesting that it may become a potent therapeutic agent for the treatment of inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages

Lei¹,

Zhao²,

Zhang³

et al. 2016

ABBS

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“…In this microenvironment, tumor cells and their associated stromal cells, as well as osteocytes, release large quantities of factors including TNF-α, IL-6, bradykinin, endothelins, cannabinoids, granulocyte-macrophage colony-stimulating factor, nerve growth factor, and parathyroid hormone-related protein (10,28–30). Although pain signals are processed in the nervous system, it is considered that inflammatory mediators and cytokines released from cancer cells, immunocytes, osteoclasts or injured tissues in the local microenvironment are able to stimulate the nociceptor terminals of peripheral afferent sensory neurons (8,30,31). The electrochemical signals converted by local nociceptors are subsequently transmitted to the spinal cord and the central nervous system, and pain sensitivity is enhanced (31).…”

Section: Discussionmentioning

confidence: 99%

“…However, traditional non-selective NSAIDs are associated with gastrointestinal ulceration, renal dysfunction and impaired platelet aggregation (8,39). Using COX-2 selective inhibitors may reduce the risk of gastrointestinal bleeding, but this advantage appears to reduce after 6 months of treatment, and there is also an increased risk of cardiovascular events with prolonged use of COX-2 inhibitors (39).…”

Section: Discussionmentioning

confidence: 99%

“…Denosumab is superior to zoledronic acid in reducing skeletal-related events in patients with bone metastasis, but hypocalcemia occurs more frequently in patients receiving denosumab (7). NSAIDs are frequently considered to be more efficacious in reducing bone cancer pain compared with other pain states, but they are associated with gastrointestinal injury and myocardial infarction (5,8). In this regard, alternative drugs that are able to assist the treatment for bone metastasis are required.…”

Section: Introductionmentioning

confidence: 99%

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Anti-rheumatic drug iguratimod protects against cancer-induced bone pain and bone destruction in a rat model

Sun

Zhang

et al. 2017

Oncology Letters

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The bone is one of the most common sites of metastasis in patients with cancer. Current treatments for bone metastases include bisphosphonates, denosumab, non-steroidal anti-inflammatory drugs and analgesics, but each of them has certain limitations. Cytokines and mediators released from various cells in the bone microenvironment may drive a vicious cycle of osteolytic bone metastases. Iguratimod (T-614), a novel disease-modifying anti-rheumatic drug, has demonstrated therapeutic effects by suppressing the production of inflammatory cytokines in rats and patients with rheumatoid arthritis. Therefore, the current study evaluated the hypothesis that iguratimod may protect against cancer-induced bone pain and bone metastasis in a rat model. For this purpose, rats inoculated with Walker 256 cells were treated with iguratimod from days 11–17 post-surgery. Mechanical paw withdrawal thresholds and expression levels of phosphorylated extracellular signal-related kinase (pERK) and c-Fos in the spinal cord were investigated to detect changes in bone pain. Bone destruction levels were detected using X-rays, hematoxylin and eosin and tartrate-resistant acid phosphatase staining. The results revealed that mechanical paw withdrawal thresholds and the expression levels of pERK and c-Fos declined in a dose-dependent manner in rats treated with iguratimod, and bone destruction severity was also reduced. These findings may provide important new insights into the treatment of bone metastasis symptoms.

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“…The qualities of Litsea (genus of the Laurel family, Lauraceae), mostly in the form of the ethanolic (EtOH) or hexane fragmentations of the plant, as an antioxidant agent with anti-inflammatory characteristics, have been evaluated, inter alia, within the setting of OA [52][53][54][55][56][57][58]. Data reported from in vitro research, investigating the anti-inflammatory assets of a variety of fractions (EtOH or other) of this plant within the context of lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, suggest a considerable inhibitory activity of the intervention on modulators of inflammation (NO and PGE 2 , iNOS, and COX-2), expression levels, along with pro-inflammatory cytokines, IL-1β, IL-6, TNF-α, and NF-κB (p65 and p50) activation, and mitogen-activated protein kinase (MAPK) phosphorylation [52][53][54].…”

Section: Litsea Japonicamentioning

confidence: 99%

Unraveling Natural Products’ Role in Osteoarthritis Management—An Overview

et al. 2020

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The natural process of aging gradually causes changes in living organisms, leading to the deterioration of organs, tissues, and cells. In the case of osteoarthritis (OA), the degradation of cartilage is a result of both mechanical stress and biochemical factors. Natural products have already been evaluated for their potential role in the prevention and treatment of OA, providing a safe and effective adjunctive therapeutic approach. This review aimed to assess the therapeutic potential of natural products and their derivatives in osteoarthritis via a systematic search of literature after 2008, including in vitro, in vivo, ex vivo, and animal models, along with clinical trials and meta-analysis. Overall, 170 papers were obtained and screened. Here, we presented findings referring to the preventative and therapeutic potential of 17 natural products and 14 naturally occurring compounds, underlining, when available, the mechanisms implicated. The nature of OA calls to initially focus on the management of symptoms, and, in that context, several naturally occurring compounds have been utilized. Underlying a global need for more sustainable natural sources for treatment, the evidence supporting their chondroprotective potential is still building up. However, arriving at that kind of solution requires more clinical research, targeting the implications of long-term treatment, adverse effects, and epigenetic implications.

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The analgesic and anti-inflammatory effects of Litsea japonica fruit are mediated via suppression of NF-κB and JNK/p38 MAPK activation

Cited by 40 publications

References 47 publications

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages

Anti-rheumatic drug iguratimod protects against cancer-induced bone pain and bone destruction in a rat model

Unraveling Natural Products’ Role in Osteoarthritis Management—An Overview

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The analgesic and anti-inflammatory effects of Litsea japonica fruit are mediated via suppression of NF-κB and JNK/p38 MAPK activation

Cited by 40 publications

References 47 publications

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-&kappa;B and MAPK in macrophages

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-&kappa;B and MAPK in macrophages

Anti-rheumatic drug iguratimod protects against cancer-induced bone pain and bone destruction in a rat model

Unraveling Natural Products’ Role in Osteoarthritis Management—An Overview

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Product

Resources

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Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages

Gambogenic acid inhibits LPS-simulated inflammatory response by suppressing NF-κB and MAPK in macrophages