Effects of FM0807, a novel curcumin derivative, on lipopolysaccharide-induced inflammatory factor release via the ROS/JNK/p53 pathway in RAW264.7 cells

Wu, Yilong; Liu, Zhiwei; Wu, Weifang; Su, Lin; Zhang, Nanwen; Wang, Honglin; Tan, Shuangyu; Lin, Peimin; Chen, Xiaole; Wu, Lixian; Xu, Jianhua

doi:10.1042/bsr20180849

Cited by 9 publications

(6 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Curcumin can improve the condition in sepsis due to its anti-inflammatory, antioxidant and immunomodulatory properties. Curcumin inhibits the secretion of plasma TNF-α and IL-6, the activation of MAPKs, and the production of reactive oxygen species (ROS) which relate to inflammatory response [ 9 , 10 ]. Curcumin acts on MAPK p38 pathway modulating COX-2 and iNOS expression in chronic experimental colitis [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Protective role of curcumin against lipopolysaccharide-induced inflammation and apoptosis in human neutrophil

et al. 2020

View full text Add to dashboard Cite

Background Sepsis, an uncontrolled host response to infection, may be life-threatening organ injury. Neutrophils play a critical role in regulation of host immune response to infection. Curcumin, known as a spice and food coloring agent, possesses anti-inflammatory properties. In this study, we investigated the effects of curcumin on lipopolysaccharide (LPS)-induced neutrophil activation with its signaling pathways. Methods Isolated human neutrophils were incubated without or with LPS and curcumin, and the expression of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-8 were assessed by enzyme-linked immunosorbent assays. The expression of mitogen-activated protein kinases such as p38, extracellularsignal-regulated kinase (ERK)1/2, and c-Jun N-terminal kinase (JNK) were evaluated by Western blot analysis. Neutrophil apoptosis was also measured by fluorescence-activated cell sorting (annexin V/propidium iodide) in LPS-stimulated neutrophils under treatment with curcumin. Results Curcumin attenuated expression of TNF-α, IL-6, and IL-8 and the phosphorylation levels of p38 and JNK, but not ERK1/2, in LPS-stimulated neutrophils. Additionally, curcumin restored the delayed neutrophil apoptosis by LPS-stimulated neutrophils(19.7 ± 3.2 to 38.2 ± 0.5%, P < 0.05). Conclusions Our results reveal the underlying mechanism of how curcumin attenuate neutrophil activation and suggest potential clinic applications of curcumin supplementation for patients with severe sepsis and septic shock. Additional clinical studies are required to confirm these in vitro findings.

show abstract

Section: Introductionmentioning

confidence: 99%

Protective role of curcumin against lipopolysaccharide-induced inflammation and apoptosis in human neutrophil

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The half-life of FM0807 in various solutions of pH 2–9 was longer than 2 days. FM0807 is more stable than its precursor: curcumin [16]. It was shown that FM0807 had a substantial inhibitory effect on acute and chronic inflammation [17,18].…”

Section: Introductionmentioning

confidence: 99%

FM0807 decelerates experimental arthritis progression by inhibiting inflammatory responses and joint destruction via modulating NF-κB and MAPK pathways

et al. 2019

Self Cite

View full text Add to dashboard Cite

Background: Rheumatoid arthritis (RA) is a chronic articular synovial inflammatory disease. The precise etiology underlying the pathogenesis of RA remains unknown. We aimed to investigate the inhibitory effect of curcumin analog FM0807 (curcumin salicylate monoester, 2-hydroxy-, 4-[(1E,6E)-7-(4-hydroxy-3-methoxyphenyl)-3,5-dioxo-1,6-heptadien-1-yl]-2-methoxyphenyl ester) on experimental RA and investigate its possible mechanisms of action. Method: Rats with Freund’s complete adjuvant (FCA)-induced arthritis (AIA) were administered aspirin (0.1 mmol.kg−1), curcumin (0.1 mmol.kg−1), FM0807 (0.1, 0.2 mmol.kg−1) and vehicle via gastric gavage, from days 7 to 21, once daily. The hind paw volume and arthritis index (AI) were measured, and radiographic and histological examinations were performed. Twenty-one days later, the animals were killed and left ankle joints were removed to measure protein expression of the elements of the nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathway by Western blot analysis. The enzyme-linked immunosorbent assay (ELISA) was employed to measure synovial fluid levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β and IL-10. Results: Compared with AIA group, FM0807 reduced the AI and swelling of the injected hind paw in a dose-dependent manner, and inhibited increases in inflammatory cell infiltration, pannus formation and cartilage destruction. FM0807 also potently attenuated the increase in the expression of inflammatory factors TNF-α, IL-6 and IL-1β in synovial fluid, while IL-10 levels were also elevated. FM0807 significantly suppressed phosphorylation of extracellular-signal-regulated kinase (ERK) 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK) 1/2 (JNK1/2), p38MAPK, inhibitor of NF-κB kinase (IKK), IκB and NF-κB p65 protein, (all P<0.05), which displayed more potential effects compared with those of the aspirin and curcumin groups. Conclusion: FM0807 exerts its therapeutic effects on RA by inhibiting cartilage degeneration. FM0807 treatment might be an effective therapeutic approach for RA.

show abstract

“…Oxidative stress and inflammation are intertwined and affect each other. Studies have shown that ROS is the major inducement of inflammation [ 37 ], while TNF-α is the main cytokine that induces inflammation; the increase of TNF-α promotes the production of ROS and up-regulates the oxidative stress response [ 38 ]. IL-1β is the main active form of interleukin-1 (IL-1), an important pro-inflammatory cytokine in the body that participates in the regulation of the immune response and inflammatory reaction process [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Procyanidin B2 Alleviates Heat-Induced Oxidative Stress through the Nrf2 Pathway in Bovine Mammary Epithelial Cells

Wang

Hao²,

Li³

et al. 2022

IJMS

View full text Add to dashboard Cite

The objective of this study was to investigate the protective effects and potential molecular mechanisms of procyanidin B2 (PB2) in MAC-T (mammary alveolar cells-large T antigen) cells during heat stress (HS). The MAC-T cells were divided into three treatment groups: control (37 °C), HS (42 °C), and PB2 + HS (42 °C). Compared with MAC-T cells that were consistently cultured at 37 °C, acute HS treatment remarkably decreased cell viability, reduced activities of catalase (CAT), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC), and elevated intracellular levels of malondialdehyde (MDA) and reactive oxygen species (ROS). Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) was activated and translocated to the nucleus, in accompaniment with upregulation of Nrf2, heme oxygenase 1 (HO-1), thioredoxin reductase 1 (Txnrd1), and heat shock protein 70 (HSP70). In parallel, both mRNA transcript and actual protein secretion of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were increased by heat stress. Pretreatment of MAC-T cells with 0~25 μM PB2 alleviated the decline of cell viability by HS in a dose-dependent fashion and protected cells against HS-induced oxidative stress, as evidenced by significantly improved CAT, SOD, and T-AOC activity, as well as with decreased MDA and ROS generation. Furthermore, PB2 further activated the Nrf2 signaling pathway and reversed the inflammatory response induced by HS. Silencing of Nrf2 by si-Nrf2 transfection not only exacerbated HS-induced cell death and provoked oxidative stress and the inflammatory response, but also greatly abolished the cytoprotective effects under HS of PB2. In summary, PB2 protected MAC-T cells against HS-induced cell death, oxidative stress, and inflammatory response, partially by operating at the Nrf2 signal pathway.

show abstract

Effects of FM0807, a novel curcumin derivative, on lipopolysaccharide-induced inflammatory factor release via the ROS/JNK/p53 pathway in RAW264.7 cells

Cited by 9 publications

References 37 publications

Protective role of curcumin against lipopolysaccharide-induced inflammation and apoptosis in human neutrophil

Protective role of curcumin against lipopolysaccharide-induced inflammation and apoptosis in human neutrophil

FM0807 decelerates experimental arthritis progression by inhibiting inflammatory responses and joint destruction via modulating NF-κB and MAPK pathways

Procyanidin B2 Alleviates Heat-Induced Oxidative Stress through the Nrf2 Pathway in Bovine Mammary Epithelial Cells

Contact Info

Product

Resources

About