1. Senegenin(Sen) promotes proliferation and differentiation of neural progenitor cells in the hippocampus, it contributes to in vitro proliferation of human neural progenitor cells by upregulating phosphorylation of extracellular signal-regulated kinase.
2. Senegenin plays a neuroprotective role in HIR via increasing NR2B expression in rat hippocampus, suggests that senegenin might be a potential agent for prevention and treatment of postoperative cognitive dysfunction (POCD) or other neurodegenerative diseases.
3. Senegenin treatment significantly attenuates CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and MPO activity; it markedly decreases MDA content , serum levels of TNF-α and IL-1β and increases SOD activity and GSH level; it also inhibit the nuclear translocation of NF-κB in the lungs; indicates that senegenin exerts protective effects on CLP-induced septic rats, it may be a potential therapeutic agent against sepsis.
1. Ruscogenin has been found to exert significant anti-inflammatory and anti-thrombotic activities; the possible mechanism of the anti-inflammatory activity is role of intercellular adhesion molecule-1 and nuclear factor-kappaB.
2. Ruscogenin significantly attenuates LPS-induced acute lung injury (ALI )via inhibiting expressions of TF and iNOS and NF-κB p65 activation, indicates that it as a potential therapeutic agent for ALI or sepsis.
3. Ruscogenin can protect the brain against ischemic damage caused by middle cerebral artery occlusion (MCAO), and this effect may be through downregulation of NF-κB-mediated inflammatory responses.
4. Ruscogenin inhibits activation of neutrophil through cPLA 2 , PAK, Akt, MAPKs, cAMP, and PKA signaling pathways.
5. Ruscogenin may attenuate high-fat diet (HFD)-induced steatohepatitis through downregulation of NF- κB-mediated inflammatory responses, reducing hepatic lipogenic gene expression, and upregulating proteins in β-oxidation pathway.
|CFN90399||Tanshinone IIA-sulfonic sodium
1. Sodium tanshinone IIA sulfonate for injection can protect neuron cell against damage. It may be used to treatment brain ischemia disease in clinical.
2. Sodium tanshinone IIA sulfonate pretreatment reduces infarct size and improves cardiac function in an ischemia-reperfusion-induced rat myocardial injury model via activation of Akt/FOXO3A/Bim-mediated signal pathway.
1. Kukoamine B is a potent dual inhibitor for both Lipopolysaccharides (LPS) and oligodeoxynucleotides containing CpG motifs (CpG DNA), LPS and CpG DNA are important pathogenic molecules for the induction of sepsis,are drug targets for sepsis treatment, thus kukoamine B is worthy of further investigation as a potential candidate to treat sepsis.
2. Kukoamine B inhibits inflammation in septic mice by reducing the concentrations of plasma LPS, decreasing leukocyte sequestration and interfering with NFκB activation, and, therefore, suppressing the proadhesive phenotype of endothelial cells.
3. Kukoamine B has protective effects against hydrogen peroxide (H2O2) induced cell injury and potential mechanisms in SH-SY5Y cells, it may potentially serve as an agent for prevention of several human neurodegenerative and other disorders caused by oxidative stress.