JSH-23 - CAS 749886-87-1
Catalog number: 749886-87-1
Category: Inhibitor
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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.
white solid powder
JSH-23; JSH 23; JSH23.
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1.Anti-Inflammatory Effect of ETAS®50 by Inhibiting Nuclear Factor-
Shirato K;Koda T;Takanari J;Sakurai T;Ogasawara J;Imaizumi K;Ohno H;Kizaki T Evid Based Complement Alternat Med. 2018 Jun 3;2018:5072986. doi: 10.1155/2018/5072986. eCollection 2018.
Ultraviolet (UV) irradiation induces proinflammatory responses in skin cells, including dermal fibroblasts, accelerating premature skin aging (photoaging). ETAS 50, a standardized extract from the ;Asparagus officinalis; stem, is a novel and unique functional food that suppresses proinflammatory responses of hydrogen peroxide-stimulated skin fibroblasts and interleukin- (IL-) 1;β;-stimulated hepatocytes. To elucidate its antiphotoaging potencies, we examined whether ETAS 50 treatment after UV-B irradiation attenuates proinflammatory responses of normal human dermal fibroblasts (NHDFs). UV-B-irradiated NHDFs showed reduced levels of the cytosolic inhibitor of nuclear factor-;κ;B ;α; (I;κ;B;α;) protein and increased levels of nuclear p65 protein. The nuclear factor-;κ;B nuclear translocation inhibitor JSH-23 abolished UV-B irradiation-induced IL-1;β; mRNA expression, indicating that p65 regulates transcriptional induction. ETAS 50 also markedly suppressed UV-B irradiation-induced increases in IL-1;β; mRNA levels. Immunofluorescence analysis revealed that ETAS 50 retained p65 in the cytosol after UV-B irradiation. Western blotting also showed that ETAS 50 suppressed the UV-B irradiation-induced increases in nuclear p65 protein.
2.Long noncoding RNA NKILA enhances the anti-cancer effects of baicalein in hepatocellular carcinoma via the regulation of NF-κB signaling.
Yu X;Tang W;Yang Y;Tang L;Dai R;Pu B;Feng C;Xia J Chem Biol Interact. 2018 Apr 1;285:48-58. doi: 10.1016/j.cbi.2018.02.027. Epub 2018 Feb 23.
Hepatocellular carcinoma (HCC) is one of the most common cancer and leading cause of cancer-related death worldwide. Baicalein, a principle flavonoid, has shown attractive anti-cancer effects on HCC. However, the underlying molecular mechanisms and influencing factors contributing to the anti-cancer effects of baicalein on HCC are still largely unknown. Long noncoding RNAs (lncRNAs) have been revealed to be fascinating therapeutic targets for cancers. The roles of NF-κB Interacting LncRNA (NKILA) are recently explored in several cancers. However, the expressions, clinical significances, roles and action mechanisms of NKILA in the anti-cancer effects of baicalein on HCC are unknown. In this study, we found that NKILA is down-regulated in HCC and reduced expression of NKILA indicts poor survival of HCC patients. Functional assays showed that overexpression of NKILA enhances the roles of baicalein on HCC cell proliferation inhibition, apoptosis induction, and migration inhibition in vitro and tumor growth suppression in vivo. Conversely, knockdown of NKILA suppresses the effects of baicalein. Mechanistically, we found that NKILA inhibits IκBα phosphorylation, NF-κB nuclear translocation, and NF-κB activity.
3.A synthetic diosgenin primary amine derivative attenuates LPS-stimulated inflammation via inhibition of NF-κB and JNK MAPK signaling in microglial BV2 cells.
Cai B;Seong KJ;Bae SW;Chun C;Kim WJ;Jung JY Int Immunopharmacol. 2018 Aug;61:204-214. doi: 10.1016/j.intimp.2018.05.021. Epub 2018 Jun 8.
Diosgenin, a precursor of steroid hormones in plants, is known to exhibit diverse pharmacological activities including anti-inflammatory properties. In this study, (3β, 25R)‑spirost‑5‑en‑3‑oxyl (2‑((2((2‑aminoethyl)amino)ethyl)amino)ethyl) carbamate (DGP), a new synthetic diosgenin derivative incorporating primary amine was used to investigate its anti-inflammatory effects and underlying mechanisms of action in lipopolysaccharide (LPS)-stimulated microglial BV2 cells. Pretreatment with DGP resulted in significant inhibition of nitric oxide (NO) synthesis, and down-regulation of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated microglial BV2 cells. In addition, DGP decreased the production of reactive oxygen species (ROS) and pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor alpha (TNF-α). The inhibitory effects of DGP on these inflammatory mediators in LPS-stimulated microglial BV2 cells were regulated by NF-κB signaling through blocking p65 nuclear translocation and NF-κB p65/DNA binding activity. DGP also blocked the phosphorylation of c-Jun amino-terminal kinase (JNK), but not p38 kinase or extracellular signal-regulated kinases (ERK).
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CAS 749886-87-1 JSH-23

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