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Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells via the Induction of Autophagy.
Neurochem Res. 2016 Sep; 41(9):2311-23.NR

Abstract

Beta-amyloid (Aβ), the hallmark protein in Alzheimer's disease (AD), induces neurotoxicity that involves oxidative stress and mitochondrial dysfunction, leading to cell death. Carnosic acid (CA), a polyphenolic diterpene isolated from the herb rosemary (Rosemarinus officinalis), was investigated in our study to assess its neuroprotective effect and underlying mechanism against Aβ-induced injury in human neuroblastoma SH-SY5Y cells. We found that CA pretreatment alleviated the Aβ25-35-induced loss of cell viability, inhibited both Aβ1-42 accumulation and tau hyperphosphorylation, reduced reactive oxygen species generation, and maintained the mitochondrial membrane potential. Moreover, CA increased the microtubule-associated protein light chain 3 (LC3)-II/I ratio and decreased SQSTM1(p62), indicating that CA could induce autophagy. Autophagy inhibitor 3-methyladenine (3-MA) attenuated the neuroprotective effect of CA, suggesting that autophagy was involved in the neuroprotection of CA. It was also observed that CA activated AMP-activated protein kinase (AMPK) but inhibited mammalian target of rapamycin (mTOR). Furthermore, blocking AMPK with si-AMPKα successfully inhibited the upregulation of LC3-II/I, prevented the downregulation of phosphorylation of mTOR and SQSTM1(p62), indicating that CA induced autophagy in SH-SY5Y cells via the activation of AMPK. These results suggested that CA might be a potential agent for preventing AD.

Authors+Show Affiliations

Department of Neurology, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Rd, Xi'an, 710061, China.Department of Anesthesia and Perioperative Care, Center for Cerebrovascular Research, University of California, San Francisco, San Francisco, CA, USA.Department of Neurology, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Rd, Xi'an, 710061, China. quqiuminxjsn@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27168327

Citation

Liu, Jie, et al. "Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells Via the Induction of Autophagy." Neurochemical Research, vol. 41, no. 9, 2016, pp. 2311-23.
Liu J, Su H, Qu QM. Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells via the Induction of Autophagy. Neurochem Res. 2016;41(9):2311-23.
Liu, J., Su, H., & Qu, Q. M. (2016). Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells via the Induction of Autophagy. Neurochemical Research, 41(9), 2311-23. https://doi.org/10.1007/s11064-016-1945-6
Liu J, Su H, Qu QM. Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells Via the Induction of Autophagy. Neurochem Res. 2016;41(9):2311-23. PubMed PMID: 27168327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Carnosic Acid Prevents Beta-Amyloid-Induced Injury in Human Neuroblastoma SH-SY5Y Cells via the Induction of Autophagy. AU - Liu,Jie, AU - Su,Hua, AU - Qu,Qiu-Min, Y1 - 2016/05/11/ PY - 2016/01/24/received PY - 2016/05/02/accepted PY - 2016/05/01/revised PY - 2016/5/12/entrez PY - 2016/5/12/pubmed PY - 2017/4/18/medline KW - AMP-activated protein kinase KW - Alzheimer’s disease KW - Autophagy KW - Carnosic acid KW - Neuroprotection SP - 2311 EP - 23 JF - Neurochemical research JO - Neurochem Res VL - 41 IS - 9 N2 - Beta-amyloid (Aβ), the hallmark protein in Alzheimer's disease (AD), induces neurotoxicity that involves oxidative stress and mitochondrial dysfunction, leading to cell death. Carnosic acid (CA), a polyphenolic diterpene isolated from the herb rosemary (Rosemarinus officinalis), was investigated in our study to assess its neuroprotective effect and underlying mechanism against Aβ-induced injury in human neuroblastoma SH-SY5Y cells. We found that CA pretreatment alleviated the Aβ25-35-induced loss of cell viability, inhibited both Aβ1-42 accumulation and tau hyperphosphorylation, reduced reactive oxygen species generation, and maintained the mitochondrial membrane potential. Moreover, CA increased the microtubule-associated protein light chain 3 (LC3)-II/I ratio and decreased SQSTM1(p62), indicating that CA could induce autophagy. Autophagy inhibitor 3-methyladenine (3-MA) attenuated the neuroprotective effect of CA, suggesting that autophagy was involved in the neuroprotection of CA. It was also observed that CA activated AMP-activated protein kinase (AMPK) but inhibited mammalian target of rapamycin (mTOR). Furthermore, blocking AMPK with si-AMPKα successfully inhibited the upregulation of LC3-II/I, prevented the downregulation of phosphorylation of mTOR and SQSTM1(p62), indicating that CA induced autophagy in SH-SY5Y cells via the activation of AMPK. These results suggested that CA might be a potential agent for preventing AD. SN - 1573-6903 UR - https://www.unboundmedicine.com/medline/citation/27168327/Carnosic_Acid_Prevents_Beta_Amyloid_Induced_Injury_in_Human_Neuroblastoma_SH_SY5Y_Cells_via_the_Induction_of_Autophagy_ L2 - https://doi.org/10.1007/s11064-016-1945-6 DB - PRIME DP - Unbound Medicine ER -