查找使用阿拉丁产品的科研文献

Sanweidoukou decoction, a Chinese herbal formula, ameliorates β-amyloid protein-induced neuronal insult via modulating MAPK/NF-κB signaling pathways: Studies in vivo and in vitro

Feng-mao An,Zheng Liu,Xin-ran Xuan,Qing-shan Liu,Cheng-xi Wei

Ethnopharmacological relevance The traditional Chinese medicine Sanweidoukou decoction (DK-3) was a classical formula for the treatment of nervous system diseases , recorded in the Chinese medical classic Sibu Yidian . Aim of the study The present study is aim to investigate the neuroprotective effects of DK-3 on β-amyloid (Aβ) protein -induced AD-like pathologies and underlying molecular mechanisms both in vitro and in vivo studies. Materials and methods Hydrolysates of DK-3 were analyzed by LC-ESI-MS/MS. In vitro , MTT was utilized to examine effects of DK-3 on Aβ 25-35 -induced cytotoxicity in PC12 cells. In vivo , male Sprague-Dawley rats were administered with Aβ 25-35 to induce AD-like pathologies and behavioral evaluations were conducted via Morris water maze (MWM) test. Histopathological changes were observed by Hematoxylin-eosin (HE) straining. Immunohistochemistry (IHC) was used to detect the tau hyperphosphorylation at Thr181 site. The expression levels of tau hyperphosphorylation, inflammation-related cytokines such as COX-2, iNOS , TNF-α, IL-1β, IL-6, the phosphorylated state of various mitogen-activated protein kinase (MAPK) signaling molecules (p38 MAPK, ERK, and JNK) and activation of nuclear factor κB (NF-κB) in vitro and in vivo were assessed via Western blot . Results In vitro , DK-3 dose-dependently increased cell viability of PC12 cells induced by Aβ 25-35 . In vivo , DK-3 improved learning and memory abilities of Aβ 25-35 -induced AD-like rats. Moreover, DK-3 reversed hyperphosphorylation of tau and reduced the production of inflammation-related cytokines through significantly inhibited MAPK and NF-κB signaling pathways both in vitro and in vivo studies. Conclusion The present study suggested that the traditional Chinese medicine DK-3 may play a role in preventing and treating AD by reducing the hyperphosphorylation of tau protein and the expressions of inflammation-related cytokines via modulating the MAPK/NF-κB signaling pathways.