Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome.

By Yiqing Yan, Wei Jiang, Lei Liu, Xiaqiong Wang, Chen Ding, Zhigang Tian, Rongbin Zhou. Cell, 2015

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Inflammasomes in neuroinflammatory and neurodegenerative diseases (2019, background): “In agreement, NLRP3 knockout mice were resistant to the loss of nigral dopaminergic neurons induced by treatment with the neurotoxin 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP), which was associated with a reduction in caspase-1 activation and IL-1b and IL-18 secretion (Yan et al, 2015).”
Identification of a selective and direct NLRP3 inhibitor to treat inflammatory disorders (2017, methodology): “BMDMs were collected from mice tibia and femoral bone marrow as described elsewhere (Yan et al., 2015) and cultured in DMEM complemented with 10% FBS, 1 mM sodium pyruvate, and 2 mM l-glutamine in the presence of 15% L929 culture supernatants.”
An update on the regulatory mechanisms of NLRP3 inflammasome activation (2021, background): “In addition, dopamine-mediated inhibition of NLRP3 inflammasome activation is mediated through the E3 ligase MARCH7-mediated ubiquitination and degradation of the NLRP3 protein.(43) Cullin1, the key component of the Skp1-Cullin1-F-box E3 ligase, interacts with NLRP3 and promotes the K63‐linked ubiqu”
Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome. (2016, methodology): “and (R)-(-)-rolipram suppressed caspase-1 cleavage and IL-1b secretion in a dose-dependent manner (Figures 3A-3D), in line with previous studies (Sokolowska et al., 2015; Yan et al., 2015).”