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Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Neurochem+Res 2015 ; 40 (9): 1954-65 Nephropedia Template TP
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Magnesium Lithospermate B Protects Neurons Against Amyloid beta (1-42)-Induced Neurotoxicity Through the NF-kappaB Pathway #MMPMID26285901
Jiang F; Mao Y; Liu H; Xu P; Zhang L; Qian X; Sun X
Neurochem Res 2015[Sep]; 40 (9): 1954-65 PMID26285901show ga
Magnesium lithospermate B (MLB) is one of the major bioactive components of Radix Salviae miltiorrhizae, a Chinese traditional herbal medicine colloquially known as Dan Shen. In this study, we investigated the neuroprotective effect of MLB against oligomeric amyloid beta (Abeta) (1-42)-induced neurotoxicity in cultured FVB mouse hippocampal neurons. We found that pretreatment with MLB not only prevents a loss in neuronal cell viability following exposure to Abeta (1-42), but also attenuates Abeta (1-42)-induced release of pro-inflammatory cytokines and neuronal apoptosis in a dose-dependent manner. Mechanistic studies show that MLB counteracts Abeta (1-42)-induced activation of the nuclear factor kappa B (NF-kappaB) pathway, evidenced by the suppression of NF-kappaB luciferase reporters, decreased expression of phosphorylated Inhibitor kappaB alpha and IkappaB kinase alpha, and reduced nuclear translocation of p65 in response to pre-treatment with 50 mug/ml MLB prior to Abeta (1-42) exposure. MLB was able to reverse the increase in phosphorylated c-Jun N-terminal kinase (JNK) levels as well as the decrease in phosphorylated Akt levels that are induced by Abeta (1-42), although this finding did not extend to extracellular signal-regulated kinase or p38 kinases. Furthermore, combining MLB with the JNK inhibitor SP600125 synergistically counteracts the Abeta (1-42)-induced reduction in cell viability and neurite growth, and the neuroprotective effects of MLB could be attenuated by the Akt inhibitor triciribine. In conclusion, these results suggest that MLB can protect against Abeta (1-42)-induced neuronal damage, which is most likely to be mediated by the NK-kappaB pathway.