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IC50: 3.2 μM: blocks NF-κB signaling via inhibition of IκBα phosphorylation

Narasin, isolated from certain Streptomyces sp. is an ionophore antibiotic. As a coccidiostat, it can be used in veterinary practice for gastrointestinal parasites. Narasin has been shown to induce tumor necrosis factor-related apoptosis-induced ligand (TRAIL)-mediated apoptosis by ER stress in glioma cells and to dampen NF-κB signaling by suppressing the phosphorylation of IκBα. NF-κB, as a transcription factor, plays a vital role across many cellular processes which are involved in neuronal and embryonic development, cell proliferation, apoptosis, and immune responses to infection and inflammation.

In vitro: Narasin caused suicidal erythrocyte death or eryptosis. When human erythrocytes were exposed to narasin, it was shown that narasin resulted in the increase of annexin-V-binding indicating cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface and the decrease of forward scatter reflecting cell shrinkage, which indicated the death of erythrocyte [1]. Narasin blocked NF-κB signaling via inhibition of IκBα phosphorylation at a lower concentration [2].

In vivo: New Zealand White rabbits were given narasin 4-48 p. p. m, in pelleted feed. After 4 weeks, the experiments indicated that narasin protected rabbits from severe coccidiosis induced by E. flavescens, E. perforans E. magna, E. intestinalis, and E. stiedai. In addition, narasin reduced oocyst output in a highly effective fashion [3].

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