Dr. Roubille, et al reply

Roubille, Camille; Richer, Vincent; Starnino, Tara; McCourt, Collette; McFarlane, Alexandra; Fleming, Patrick; Siu, Stephanie; Kraft, John; Lynde, Charles; Pope, Janet; Gulliver, Wayne; Keeling, Stephanie; Dutz, Jan P.; Bessette, Louis; Bissonnette, Robert

doi:10.3899/jrheum.151347

Cited by 5 publications

(6 citation statements)

References 21 publications

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“…1,2 Although corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin, and disease-modifying antirheumatic drugs (DMARDs) such as methotrexate suppress the symptoms of RA, their clinical use is limited due to the continuous progression of the disease despite ongoing therapy or the emergence of side effects, which discourages long-term compliance or use by patients. 3,4 A better understanding of the important role of pro-inflammatory cytokines in the pathophysiology of RA in recent times has vastly improved treatment options, as evidenced by the development of proinflammatory cytokine blockers. 5,6 However, these drugs achieve disease remission in only a minority of patients due to infectious adverse events, rebound of symptoms, short halflives, or high treatment costs.…”

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confidence: 99%

Effects of Koumine on Adjuvant- and Collagen-Induced Arthritis in Rats

et al. 2016

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To examine the effect of koumine, a Gelsemium alkaloid, on two experimental models of rheumatoid arthritis (RA), rats with adjuvant-induced arthritis (AIA) and collagen-induced arthritis (CIA) were administered koumine (0.6, 3, or 15 mg/kg/day) or vehicle through gastric gavage (i.g.). Clinical evaluation was performed via measurements of hind paw volume, arthritis index (AI) score, mechanical withdrawal threshold, organ weight, and by radiographic and histological examinations. Levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and antitype II collagen (CII) antibody were also examined. In rats with AIA, koumine reduced the AI score and mechanical allodynia of the injected hind paw in a dose-dependent manner and significantly inhibited increase in thymus and liver weights. In rats with CIA, koumine inhibited increase in hind paw volume, AI score, and mechanical allodynia in a dose-dependent manner and reduced joint space narrowing. Furthermore, koumine also attenuated the increase in the expression of IL-1β and TNF-α, as well as the robust increase of serum anti-CII antibodies in response to immunization. These results suggested that koumine effectively attenuated arthritis progression in two rat models of RA and that this therapeutic effect may be associated with its immunoregulatory action.

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confidence: 99%

Effects of Koumine on Adjuvant- and Collagen-Induced Arthritis in Rats

et al. 2016

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“…In the 210−360 nm region of the ECD spectra, both the experimental and calculated ECD curves of 9 showed sequential negative and positive Cotton effects around 245 and 270 nm, suggesting (M)-configurations for both of the HHDP moieties (Figure 2). Brevipetin F (10) was assigned as an isomer of 9, as it has the same molecular formula (C 49 H 42 O 26 ) according to its HRESIMS data. Analysis of the NMR spectroscopic and hydrolysis data of 10 revealed that its structure is similar to 9, and the only difference was that the allyl moiety (C-7″−C-8′C-9′) in 9 was replaced by an (E)-1-propenyl unit (C-7′C-8″−C-9′) in 10 (Tables 1 and 2).…”

Section: ■ Results and Discussionmentioning

confidence: 99%

“…7−9 At present, RA is treated with five different drug classes, namely, nonsteroidal anti-inflammatory drugs, antibiotics, corticosteroids, slow acting antirheumatic drugs (SAARDs), and disease-modifying antirheumatic drugs (DMARDs). 10,11 However, due to the toxicities and drug resistance, only a small number of patients with the disease benefit from the drugs in clinical use, and there is still a lack of sufficient effective drugs for the treatment of RA. 12−14 Medicinal plants have been regarded as promising sources of novel antiarthritic lead compounds for the treatment of RA.…”

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confidence: 99%

Anti-inflammatory Ellagitannins from Cleidion brevipetiolatum for the Treatment of Rheumatoid Arthritis

et al. 2019

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Six new ellagitannins, brevipetins B–G (5 and 7–11), and a new phenolic glucoside, brevipetin A (4), along with six known compounds were isolated from the traditional Chinese medicinal plant Cleidion brevipetiolatum. Their structures and absolute configurations were determined by spectroscopic analyses, chemical methods, and TD-DFT-ECD calculations. Compounds 5–11 exhibited NO inhibitory effects with IC50 values of 1.9–8.2 μM, and 9 showed the most potent inhibitory effect (IC50: 1.9 μM). An in vivo anti-inflammatory assessment of 9 showed that it exerts therapeutic effects in both the carrageenan-induced rat paw edema and collagen-induced arthritis (CIA) models at 50 mg/kg oral administration. The enhanced protein and mRNA expression levels of iNOS (inducible nitric oxide synthase) and COX-2 (cyclooxygenase-2) in LPS-stimulated RAW 264.7 cells were dose-dependently suppressed by 9. An anti-inflammatory mechanistic study revealed that 9 suppressed NF-κB activity by inhibiting IκBα phosphorylation and blocking translocation of p65 from the cytosol to the nucleus. Therefore, 9 might have the potential to be developed as a lead compound for relieving rheumatoid arthritis.

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“…[7] Among them, NSAIDs and glucocorticoids are often used as adjunctive therapies and are less frequently used because of their serious side effects. [8] The commonly-used disease-modifying antirheumatic drugs include traditional disease-modifying antirheumatic drugs (csDMARDs) [9][10][11] , for example, hydroxychloroquine, methotrexate (MTX), and salazosulfapyridine; biological disease-modifying antirheumatic drugs [12][13][14] , including B-cell depleting and inhibiting antibodies, tumor necrosis factor-α inhibitors and tocilizumab, and kinase inhibitors [15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

A multifunctional nanoaggregate‐based system for detection of rheumatoid arthritis via Optoacoustic/NIR‐II fluorescent imaging and therapy via inhibiting JAK‐STAT/NF‐κB/NLRP3 pathways

Chen,

She

et al. 2023

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Rheumatoid arthritis (RA) is a debilitating autoimmune disease that causes chronic pain and serious complications, presenting a significant challenge to treat. Promising approaches for treating RA involve signaling pathways modulation and targeted therapy. To this end, a multifunctional nanosystem, TPC‐U@HAT, has been designed for RA therapy, featuring multitargeting, dual‐stimuli response, and on‐demand drug release capabilities. TPC‐U@HAT is composed of a probe/prodrug TPC, a JAK1 kinase inhibitor upadacitinib, and the drug carrier HAT. TPC is composed of an aggregation‐induced emission (AIE)‐active NIR‐II chromophore TPY and an NF‐κB/NLRP3 inhibitor caffeic acid phenethyl ester (CAPE), connected via boronic ester bond which serves as the reactive‐oxygen‐species‐responsive linker. The carrier, HAT, is created by grafting bone‐targeting alendronate and hydrophobic tocopheryl succinate onto hyaluronic acid chains, which can encapsulate TPC and upadacitinib to form TPC‐U@HAT. Upon intravenous injection into mice, TPC‐U@HAT accumulates at inflamed lesions of RA through both active and passive targeting, and the overexpressed hyaluronidase and H2O2 therein cleave the hyaluronic acid polymer chains and boronate bonds, respectively. This generates an AIE‐active chromophore for detection and therapeutic evaluation of RA via both optoacoustic imaging and NIR‐II fluorescent imaging and concomitantly releases CAPE and upadacitinib to exert efficacious therapy by inhibiting NF‐κB/NLRP3 and JAK‐STAT pathways.

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Dr. Roubille, et al reply

Cited by 5 publications

References 21 publications

Effects of Koumine on Adjuvant- and Collagen-Induced Arthritis in Rats

Effects of Koumine on Adjuvant- and Collagen-Induced Arthritis in Rats

Anti-inflammatory Ellagitannins from Cleidion brevipetiolatum for the Treatment of Rheumatoid Arthritis

A multifunctional nanoaggregate‐based system for detection of rheumatoid arthritis via Optoacoustic/NIR‐II fluorescent imaging and therapy via inhibiting JAK‐STAT/NF‐κB/NLRP3 pathways

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