TRP ion channel related to the pathogenic mechanism of small intestinal ulceration induced by NSAIDs use

By the permeability experiment with small intestinal epithelial cells, NSAIDs accelerated the permeability via the accumulation of 8, 9 EET, which is the metabolites of membrane arachidonic acids and activated TRPV4. The activated TRPV4 is attributed to the increase of permeability. By this assay system, one candidate drug was selected, which showed the inhibition of TRPV4 activation and inhibited the increased permeability of intestinal epithelial cells induced by NSAIDs. Clinical trials are planning to confirm the preventing effect of the candidate.

本研究から小腸上皮細胞膜透過性亢進にはイオンチャネルであるTRPV4活性化が引き金であり、ある既存薬（米国で発売、他疾患治療に使用されている）がNSAIDｓによるTRPV4活性化、細胞膜透過性亢進を阻害することが明らかとなり、新規のNSAIDｓ起因性小腸潰瘍予防薬として有望であり、臨床試験が計画中である。