IndraLab

Statements

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"Proteomic analysis revealed that amitriptyline promoted anabolic changes and blocked basal TLR4 and NLRP3 signalling."
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"Interestingly, amitriptyline also depleted TLR4‐enriched pathways like ‘IL‐1 signalling’ and ‘The NLRP3 inflammasome’ (Figure 2d), which are key pathways involved in diverse articular inflammatory processes, such as microcrystals‐induced IL‐1β secretion (Aouba et al., 2015; Mangan et al., 2018; Szekanecz et al., 2019; Zamyatina & Heine, 2020) (Figure 2d)."
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"Underpinning the clinical relevance of amitriptyline blockade of TLR4/NLRP3 axis, amitriptyline intake significantly reduced colchicine consumption in a dose‐dependent manner."
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"Antidepressant Amitriptyline Does Not Inhibit NLRP3 Dependent Caspase-1 Activation but Suppresses LPS Triggered IL-1beta mRNA Production."
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"Amitriptyline blocks TLR4-, IL-1 receptor and NLRP3-dependent innate immune responses."
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"Meanwhile, it was remarkable that cartilages from wild-type mice could not produce active IL-1β, which is consistent with the limited efficacy of IL-1β inhibitors in OA treatment.The antidepressant am[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In fact, an algorithm that associates proteome signatures to known diseases (Pathan et al., 2017) suggested that amitriptyline might prevent or block processes linked to osteoarthritis, gout and/or osteoporosis (Figure 4i).3.8 Amitriptyline blocks NLRP3 inflammasome signalling."
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"Amitriptyline depleted basal and induced NLRP3 signalling, which is involved in osteoarthritis (McAllister et al., 2018) and gout (So & Martinon, 2017) pathogenesis."
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"Furthermore, in the same human synoviocyte cell line and without cytotoxic effects, treatment with amitriptyline also blocked basal and induced NLRP3 and IL‐1β mRNA expression elicited by synovial liquids from osteoarthritis and gout patients (Figure 5l–n).3.9 Clinical data mining identifies evidence about amitriptyline anti-innate immune response in gout patients."
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