ABSTRACT
Objective::To observe the effect of icariin on damaged neurons from the perspective of endoplasmic reticulum stress, in order to explore some mechanisms for repairing damaged neurons. Method::PC12 cells were induced by nerve growth factor (NGF) to differentiate into neurons, and the positive rate of microtubule associated protein-2 (MAP2) and neuron-specific enolase (NSE) expressions was determined by flow cytometry. The experiment was divided into 4 groups, blank control group: PC12 induced differentiation into neuronal cells, solvent control group: PC12 induced differentiation into neurons+ 0.1% dimethyl sulfoxide (DMSO), thapsigargin group: PC12 induced differentiation into nerves Yuan+ 2 μmol·L-1 thapsigargin, and icariin group: PC12 induced differentiation into neurons+ 2 μmol·L-1 thapsigargin+ 0.1 μmol·L-1 icariin. The proliferation of the cells was detected by using cell counting kit-8(CCK-8) method, the apoptosis of the cells was detected by flow cytometry, the protein expressions of CCAAT/enhace-binding protein homologous protein(CHOP) and glucoseregulated protein 78(Grp78) were detected by Western blot, and the mRNA expressions of CHOP and Grp78 were detected by real-time quantitative PCR (Real-time PCR). Result::Compared with the solvent control group, the thapsigargin group inhibited the proliferation of neuron-like PC12 cells induced by NGF, promoted apoptosis, and up-regulated the expressions of CHOP and Grp78 (P<0.05, P<0.01). Compared with the thapsigargin group, the icariin group can alleviate the inhibition of neurotrophic activity by thapsigargin, reduce neuronal apoptosis, and down-regulate the expressions of CHOP and Grp78 (P<0.05, P<0.01). Conclusion::Icariin can inhibit endoplasmic reticulum stress by down-regulating the expressions of CHOP and Grp78 and promote the repair of damaged neurons.