Dopamine inhibits lipopolysaccharide-induced nitric oxide production through the formation of dopamine quinone in murine microglia BV-2 cells

Abstract

Dopamine (DA) has been suggested to modulate functions of glial cells including microglial cells. To reveal the regulatory role of DA in microglial function, in the present study, we investigated the effect of DA on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in murine microglial cell line BV-2. Pretreatment with DA for 24 h concentration-dependently attenuated LPS-induced NO production in BV-2 cells. The inhibitory effect of DA on LPS-induced NO production was not inhibited by SCH-23390 and sulpiride, D1-like and D2-like DA receptor antagonists, respectively. In addition, pretreatment with (-)-(6aR,12bR)-4,6,6a,7,8,12b-Hexahydro-7-methylindolo[4,3-a]phenanthridin (CY 208-243) and bromocriptine, D1-like and D2-like DA receptor agonists, respectively, did not affect the LPS-induced NO production. N-Acetylcysteine, which inhibits DA oxidation, completely inhibited the effect of DA. Tyrosinase, which catalyzes the oxidation of DA to DA quionone (DAQ), accelerated the inhibitory effect of DA on LPS-induced NO production. These results suggest that DA attenuates LPS-induced NO production through the formation of DAQ in BV-2 cells.

Dopamine-melanin nanoparticles scavenge reactive oxygen and nitrogen species and activate autophagy for osteoarthritis therapy

“…36 This includes reduced NO production and protection against LPS-induced cell damage. 37 Previous studies showed that increased levels of ROS and RNS, can modify the Cys residues at the DNA-binding sites and influence the binding between DNA and transcription factors, 38 leading to proteoglycan loss in chondrocytes [39][40][41] and thus cartilage degradation. 42 Interestingly, we found that DM nanoparticles exert anti-inflammatory and chondroprotective effects by autophagy activation, which was demonstrated by the increased production of LC3-Ⅱ/LC3-Ⅰ, ATG7 and Beclin-1 and induced autophagic vesicles formation in chondrocytes (Figure 5e, f, g).…”

l‐DOPA‐induced dyskinesia and neuroinflammation: do microglia and astrocytes play a role?

“…Microglia express all DA receptor subtypes. Presence of D1, D2, D3, D4, and D5 receptor protein and/or mRNA was first demonstrated in cultured microglia, where DA modulates K + current and attenuates NO release through the D1 and D2 receptor (Färber et al ., ; Mastroeni et al ., ; Huck et al ., ; Yoshioka et al ., ). Interestingly, when microglia were investigated in vivo for D2 receptor expression, no expression was detected in unstimulated cells, while an upregulation of D2 receptor mRNA was found in activated microglia after experimental stroke (Huck et al ., ).…”

Automated Synthesis and Initial Evaluation of (4′-Amino-5′,8′-difluoro-1′H-spiro[piperidine-4,2′-quinazolin]-1-yl)(4-[18F]fluorophenyl)methanone for PET/MR Imaging of Inducible Nitric Oxide Synthase

“…The robotic system included a hand station that gripped the Reacti-vials, a syringe station that dispensed the solutions, a vortex station, a heating block station, cap stations that capped and uncapped the Reacti-vials, a solid phase extraction station for primary column purifications, a movable Reacti-vial rack station that collected the eluted fractions, a filtration station that filtered the raw [ 18 F]FBAT product, a filter check station that checked the integrity of the 0.22 μm membrane filters, a solvent rack station, and a water cooling station. [19] and released nitric oxide (NO) in a concentration-dependent manner [20]. Thus, we investigated the dose-dependent increase in NO production in LPS-challenged BV2 cells.…”