Tags

Type your tag names separated by a space and hit enter

1,5-dicaffeoylquinic acid protects primary neurons from amyloid β 1-42-induced apoptosis via PI3K/Akt signaling pathway.
Chin Med J (Engl). 2011 Sep; 124(17):2628-35.CM

Abstract

BACKGROUND

Recently, 1,5-dicaffeoylquinic acid (1,5-DQA), a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have not yet been clearly identified. The purpose of this study was to explore the protective mechanisms of 1,5-DQA on neuronal culture.

METHODS

We investigated the neuroprotective effects of 1,5-DQA against amyloid β(1-42) (Aβ(42))-induced neurotoxicity in primary neuronal culture. To evaluate the neuroprotective effects of 1,5-DQA, primary cultured cortical neurons from neonate rats were pretreated with 1,5-DQA for 2 hours and then treated with 40 µmol/L Aβ(42) for 6 hours. Cell counting kit-8, Hoechst staining and Western blotting were used for detecting the protective mechanism. Comparisons between two groups were evaluated by independent t test, and multiple comparisons were analyzed by one-way analysis of variance (ANOVA).

RESULTS

1,5-DQA treated neurons showed increased neuronal cell viability against Aβ(42) toxicity in a concentration-dependent manner, both phosphoinositide 3-kinase (PI3K)/Akt and extracellular regulated protein kinase 1/2 (Erk1/2) were activated by 1,5-DQA with stimulating their upstream tyrosine kinase A (Trk A). However, the neuroprotective effects of 1,5-DQA were blocked by LY294002, a PI3K inhibitor, but not by PD98059, an inhibitor of mitogen-activated protein kinase kinase. Furthermore, 1,5-DQA's anti-apoptotic potential was related to the enhanced inactivating phosphorylation of glycogen synthase kinase 3β (GSK3β) and the modulation of expression of apoptosis-related protein Bcl-2/Bax.

CONCLUSION

These results suggest that 1,5-DQA prevents Aβ(42)-induced neurotoxicity through the activation of PI3K/Akt followed by the stimulation of Trk A, then the inhibition of GSK3β as well as the modulation of Bcl-2/Bax.

Authors+Show Affiliations

Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22040415

Citation

Xiao, Hai-bing, et al. "1,5-dicaffeoylquinic Acid Protects Primary Neurons From Amyloid Β 1-42-induced Apoptosis Via PI3K/Akt Signaling Pathway." Chinese Medical Journal, vol. 124, no. 17, 2011, pp. 2628-35.
Xiao HB, Cao X, Wang L, et al. 1,5-dicaffeoylquinic acid protects primary neurons from amyloid β 1-42-induced apoptosis via PI3K/Akt signaling pathway. Chin Med J (Engl). 2011;124(17):2628-35.
Xiao, H. B., Cao, X., Wang, L., Run, X. Q., Su, Y., Tian, C., Sun, S. G., & Liang, Z. H. (2011). 1,5-dicaffeoylquinic acid protects primary neurons from amyloid β 1-42-induced apoptosis via PI3K/Akt signaling pathway. Chinese Medical Journal, 124(17), 2628-35.
Xiao HB, et al. 1,5-dicaffeoylquinic Acid Protects Primary Neurons From Amyloid Β 1-42-induced Apoptosis Via PI3K/Akt Signaling Pathway. Chin Med J (Engl). 2011;124(17):2628-35. PubMed PMID: 22040415.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 1,5-dicaffeoylquinic acid protects primary neurons from amyloid β 1-42-induced apoptosis via PI3K/Akt signaling pathway. AU - Xiao,Hai-bing, AU - Cao,Xu, AU - Wang,Lei, AU - Run,Xiao-qin, AU - Su,Ying, AU - Tian,Cheng, AU - Sun,Sheng-gang, AU - Liang,Zhi-hou, PY - 2011/11/2/entrez PY - 2011/11/2/pubmed PY - 2012/5/2/medline SP - 2628 EP - 35 JF - Chinese medical journal JO - Chin Med J (Engl) VL - 124 IS - 17 N2 - BACKGROUND: Recently, 1,5-dicaffeoylquinic acid (1,5-DQA), a caffeoylquinic acid derivative isolated from Aster scaber, was found to have neuroprotective effects. However, the protective mechanisms of 1,5-DQA have not yet been clearly identified. The purpose of this study was to explore the protective mechanisms of 1,5-DQA on neuronal culture. METHODS: We investigated the neuroprotective effects of 1,5-DQA against amyloid β(1-42) (Aβ(42))-induced neurotoxicity in primary neuronal culture. To evaluate the neuroprotective effects of 1,5-DQA, primary cultured cortical neurons from neonate rats were pretreated with 1,5-DQA for 2 hours and then treated with 40 µmol/L Aβ(42) for 6 hours. Cell counting kit-8, Hoechst staining and Western blotting were used for detecting the protective mechanism. Comparisons between two groups were evaluated by independent t test, and multiple comparisons were analyzed by one-way analysis of variance (ANOVA). RESULTS: 1,5-DQA treated neurons showed increased neuronal cell viability against Aβ(42) toxicity in a concentration-dependent manner, both phosphoinositide 3-kinase (PI3K)/Akt and extracellular regulated protein kinase 1/2 (Erk1/2) were activated by 1,5-DQA with stimulating their upstream tyrosine kinase A (Trk A). However, the neuroprotective effects of 1,5-DQA were blocked by LY294002, a PI3K inhibitor, but not by PD98059, an inhibitor of mitogen-activated protein kinase kinase. Furthermore, 1,5-DQA's anti-apoptotic potential was related to the enhanced inactivating phosphorylation of glycogen synthase kinase 3β (GSK3β) and the modulation of expression of apoptosis-related protein Bcl-2/Bax. CONCLUSION: These results suggest that 1,5-DQA prevents Aβ(42)-induced neurotoxicity through the activation of PI3K/Akt followed by the stimulation of Trk A, then the inhibition of GSK3β as well as the modulation of Bcl-2/Bax. SN - 2542-5641 UR - https://www.unboundmedicine.com/medline/citation/22040415/15_dicaffeoylquinic_acid_protects_primary_neurons_from_amyloid_β_1_42_induced_apoptosis_via_PI3K/Akt_signaling_pathway_ L2 - https://Insights.ovid.com/pubmed?pmid=22040415 DB - PRIME DP - Unbound Medicine ER -