JSH-23 (Synonyms: NFκB Activation Inhibitor II)

JSH-23, exhibited inhibitory effect on nuclear translocation and NF-κB transcriptional activity with an IC50 value of 7.1 µM in lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7 ^[1].

JSH-23 (1 µM) monotherapy significantly reduced the chemotactic sensitivity of the cells to SDF1. The co-treatment with cordycepin (10 µM) and JSH-23 (1 µM) significantly inhibited the expression of CXCR4 ^[2].

JSH-23 (1 and 3 mg/kg) treatment significantly reversed the nerve conduction and nerve blood flow deficits seen in diabetic animals ^[1]. 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 ^[1]. Mice were treated with JSH-23 (20 or 40 mg/kg) which directly affects NF-κB transcriptional activity. Kidney function, tubular injury (ATN, serum neutrophil gelatinase-associated lipocalin [NGAL], but not apoptosis) and myeloperoxidase (MPO) activity were significantly improved by JSH-23 (40 mg/kg) ^[3].

References:
[1]. Kumar A, Negi G, Sharma S S. JSH©\23 targets nuclear factor©\kappa B and reverses various deficits in experimental diabetic neuropathy: effect on neuroinflammation and antioxidant defence[J]. Diabetes, Obesity and Metabolism, 2011, 13(8): 750-758.
[2]. Guo Z, Chen W, Dai G, et al. Cordycepin suppresses the migration and invasion of human liver cancer cells by downregulating the expression of CXCR4[J]. International journal of molecular medicine, 2020, 45(1): 141-150.
[3]. Ozkok A, Ravichandran K, Wang Q, et al. NF-κB transcriptional inhibition ameliorates cisplatin-induced acute kidney injury (AKI)[J]. Toxicology letters, 2016, 240(1): 105-113.