Changqin NO. 1 inhibits neuronal apoptosis via suppressing GAS5 expression in traumatic brain injury mice model.

Changqin NO. 1 inhibits neuronal apoptosis via suppressing GAS5 expression in traumatic brain injury mice model. Biol Chem. 2018 Dec 01;: Authors: Dai X, Yi M, Wang D, Chen Y, Xu X Abstract The present study was designed to investigate the mechanism of traditional Chinese medicine Changqin NO. 1 on amelioration of traumatic brain injury (TBI). Adult male C57BL/6J mice and newborn mice were used to generate a mouse TBI model and harvest primary neurons, respectively. The localizations of specific neural markers neuropilin-1 (Nrp-1), growthassociated protein-43 (GAP-43) and microtubule-associated protein Tau (Tau) were examined in brain tissues by immunohistochemistry. TUNEL apoptotic cell detection in tissue sections and CCK-8 cell viability assay were performed to examine neuronal apoptosis. Quantitative real-time PCR (qRT-PCR) and western blot were also carried out in this study. The association between long non-coding RNA (lncRNA) growth-arrest specific 5 (GAS5), miR- 335 and RAS p21 GTPase activating protein 1 (Rasa1) was disclosed by dual-luciferase reporter assay. Changqin NO. 1 inhibited TBI-induced neuronal apoptosis in vivo and in vitro. GAS5 functioned as a competing endogenous RNA (ceRNA) by sponging miR-335 to upregulate Rasa1 expression in mouse neuronal cells. Further investigations demonstrated that GAS5 promoted neuronal apoptosis following TBI via miR-335/Rasa1 axis. In vivo experiments indicated that Changqin NO. 1 e...
Source: Biological Chemistry - Category: Chemistry Tags: Biol Chem Source Type: research