The protective effect and underlying mechanism of Hainan papaya water extract against neuronal apoptosis induced by A β 40

被引:1
作者
Zhao, Jiu-Hong [1 ]
Zhang, Hai-Ying [1 ]
Zhang, Xian-Fang [1 ]
Dong, Xu [2 ]
Liu, Qi-Bing [3 ]
Liu, Yue-Li
Huang, Yi-Di [1 ]
Zhang, Quan-Peng [1 ]
Luo, Gang [1 ]
Ma, Zhi-Jian [1 ,2 ]
Yi, Xi-Nan [1 ,2 ]
机构
[1] Hainan Med Coll, Dept Anat, Xueyuan Rd, Haikou 571199, Peoples R China
[2] Hainan Med Coll, Neurosci Res Inst, Haikou 571199, Peoples R China
[3] Hainan Med Coll, Sch Pharm, Haikou 571101, Peoples R China
基金
中国国家自然科学基金;
关键词
A beta peptide; Neuron protection; ERK signaling pathway; ANTIOXIDANT; ERK; DYSFUNCTION; STRESS; BRAIN; MODEL;
D O I
10.1016/j.apjtm.2016.05.001
中图分类号
R1 [预防医学、卫生学];
学科分类号
100235 [预防医学];
摘要
Objective: To investigate whether Hainan papayas has protective effects in an A beta 40-induced primary neuron injury model and elucidate the underlying molecular mechanism. Methods: Cultured primary neurons from the dorsal root ganglia (DRG) of Sprague-Dawley (SD) rats were treated with 20 mu M A beta 40 peptide, 100 mu g/L Hainan papaya water extract, peptide plus extract, or culture medium for 24 h. Cell viability was measured by MTT assay, and neuronal apoptosis was evaluated by DAPI staining. ERK signaling pathway-associated molecule activation and changes in Bax expression were analyzed by Western blotting and immunofluorescence. Results: A cell viability rate of (44.11 +/- 6.59)% in the A beta 40 group was rescued to (79.13 +/- 6.64)% by adding different concentrations of the extract. DAPI showed pyknotic nuclei in 39.5% of A beta 40-treated cells; the fraction dropped to 17.4% in the 100 mu g/L extract group. ERK phosphorylation was observed in the A beta 40 group but was ameliorated by pretreatment with 100 mu g/L extract. Hainan papaya water extract also prevented A beta 40-induced phosphorylation of MEK, RSKI and CREB associated with ERK signaling and downregulated Bax expression in the neurons. Conclusion: The resultss suggest that Hainan papaya water extract has protective effects on neurons; the mechanism may be related to suppression of ERK signaling activation.
引用
收藏
页码:653 / 658
页数:6
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