JSH-23

JSH-23 is a nuclear factor-kappa B (NF-κB) nuclear translocation inhibitor. JSH-23 inhibits LPS and cytokine-induced nuclear translocation of the p65 subunit of NF-kB as analyzed by EMSA and western blot. JSH-23 treatment significantly reversed the nerve conduction and nerve blood flow deficits seen in diabetic animals. Reduction in mechanical pain threshold was also partially corrected by the treatment. Protein expression studies showed that nuclear translocation of p65/p50 subunit was inhibited by JSH-23 treatment in the sciatic nerve. The treatment also lowered the elevated IL-6, TNF-α, cyclo-oxygenase (COX-2) and inducible nitric oxide synthase (iNOS) levels/expression, indicating reduction in the inflammatory damage of the sciatic nerve. Apart from these effects, JSH-23 also increased Nrf2 and hemeoxygenase-1 (HO-1) levels which could imply its potential in increasing the strength of antioxidant defence.

NF-κB Inhibitors Related Products:

Bortezomib; Bortezomib pinanediol ester; TPCA-1; Bardoxolone methyl; Curcumin; QNZ (EVP4593); Triptolide; Benfotiamine; Omaveloxolone; Erdosteine

[1]. Shin, H.M., et al. Inhibitory action of novel aromatic diamine compound on lipopolysaccharide-induced nuclear translocation of NF-kappaB without affecting IkappaB degradation. FEBS Lett, 2004. 571(1-3): p. 50-4.

[2]. Arias-Salvatierra, D., et al. Role of nitric oxide produced by iNOS through NF-kappaB pathway in migration of cerebellar granule neurons induced by Lipopolysaccharide. Cell Signal, 2011. 23(2): p. 425-35.