HC-030031 is a selective TRPA1 channel blocker, antagonizing formalin-evoked calcium influx and formalin-induced pain. IC50 is 5 μM. TRPA1 antagonism is a promising therapeutic target for chronic inflammatory or neurogenic pain.
HC-030031 is a selective TRPA1 channel blocker.
HC-030031 is a selective TRPA1 channel blocker. HC-030031 antagonizes formalin-evoked calcium influx. IC50 is 5 μM.
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Eyeshields, Faceshields, Gloves, type P2 (EN 143) respirator cartridges
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 66(4), 311-322 (2016-12-03)
Although TRPA1, SP, histamine and 5-hydroxytryptamine (5-HT) have recognized contribution to nociceptive mechanisms, little is known about how they interact with each other to mediate inflammatory pain in vivo. In this study we evaluated whether TRPA1, SP, histamine and 5-HT
The transient receptor potential (TRP) channels family are cationic channels involved in various physiological processes as pain, inflammation, metabolism, swallowing function, gut motility, thermoregulation or adipogenesis. In the oral cavity, TRP channels are involved in chemesthesis, the sensory chemical transduction
Frontiers in pharmacology, 11, 594479-594479 (2021-02-02)
The tachykinin hemokinin-1 (HK-1) is involved in immune cell development and inflammation, but little is known about its function in pain. It acts through the NK1 tachykinin receptor, but several effects are mediated by a yet unidentified target. Therefore, we
The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 29(6), 692-700 (2018-11-02)
Transient receptor potential ankyrin 1 (TRPA1) and substance P (SP), both expression in sensory neurons, have important roles in stress-induced duodenal lesions. The possible contribution of TRPA1 and SP to stress-induced duodenal lesions was explored by using the water immersion
Excessive synaptic loss is thought to be one of the earliest events in Alzheimer's disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes
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