Dihydromyricetin Inhibits High Glucose Induced PC12 Cells Apoptosis by Down-regulating JNK Pathway

作者：Lu Hui-Jie; Zhu Ze-Mei; Chen Wei-Zhao; He Jian-Qin; Yang Si-Si; Zhang Kai-Fang; Feng Shui-Dong; Ling Hong-Yan^*

来源：Progress in Biochemistry and Biophysics, 2018, 45(6): 663-671.

DOI：10.16476/j.pibb.2017.0477

• dihydromyricetin
• high glucose
• PC12 cell apoptosis
• INK signal

To investigate whether dihydromyricetin(DHM)inhibits high glucose induced PC12 cell apoptosis by downregulating INK signaling. The cell viabilities of PC12 cells were assessed by MTT assay. The apoptotic rates of PC12 cells were measured after Annexin-V/PI (propidium iodide) staining by flow cytometry (FCM). Hoechst 33258 staining was used to detect the morphology of apoptotic PC12 cells. The expression of apoptosis-related proteins (Bax, Bcl-2, cleaved-Caspase-3) and the level of p-JNK in PC12 cells were detected by Western blotting assay. After PC12 cells were treated with different concentrations of glucose (4.5, 9, 13.5, 18 g/L) at 24, 48, 72 and 96 h respectively, the results showed that 13.5 g/L high glucose treatment for 72 h could significantly change the cell morphology, reduce cell viability, increase the apoptosis rate, at the same time, the expression of pro-apoptotic protein (Bax, Caspase-3) was increased and anti-apoptotic protein Bcl-2 was decreased, indicating that long-term high glucose treatment induced PC12 cell apoptosis. However, pretreatment with DHM (15 mu mol/l) could significantly improve high glucose induced PC12 cell apoptosis and decrease the expression of INK and p-INK high glucose induced PC12 cell. Further treatment with JNK agonists (Anisomycin), which could eliminate the protective effect of DHM on apoptosis induced by high glucose in PC12 cells. In conclusion, DHM antagonizes high glucose-induced PC12 cell apoptosis by down-regulating JNK signaling.

• 出版日期2018-6
• 单位南华大学