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Protective effects of aloin on oxygen and glucose deprivation-induced injury in PC12 cells.
Brain Res Bull. 2016 Mar; 121:75-83.BR

Abstract

The present study aims to determine whether aloin could protect cells from ischemic and reperfusion injury in vitro and to elucidate the related mechanisms. Oxygen and glucose deprivation model in PC12 cells was used in the present study. 2-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH) assay and Hoechst 33342 nuclear staining were used to evaluate the protective effects of aloin, at concentrations of 10, 20, or 40 μg/mL in PC12 cells. PCR was applied to detect fluorescence caspase-3, Bax and Bcl-2 mRNA expression in PC12 cells. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) activity were evaluated by biochemical method. The concentration of intracellular-free calcium [Ca(2+)]i, mitochondrial membrane potential (MMP) were determined to estimate the degree of neuronal damage. It was shown that aloin (10, 20, and 40 μg/mL) significantly attenuated PC12 cells damage with characteristics of an increased injured cells absorbance of MTT and releases of LDH, decreasing cell apoptosis, and antagonizing decreases in SOD activity and increase in MDA level induced by OGD-reoxygenation. Meanwhile pretreatment with aloin significantly reduced injury-induced intracellular ROS, increased MMP (P<0.01), but it inhibited [Ca(2+)]i (P<0.01) elevation in a dose-dependent manner. Furthermore, pre-treatment with aloin significantly up-regulated Bcl-2 mRNA expression, down-regulated Bax mRNA expression and consequently activated caspase-3 mRNA expression in a dose-dependent manner. The results indicated that the protection of aloin on OGD-induced apoptosis in PC12 cells is associated with its suppression on OGD-induced oxidative stress and protection on mitochondrial function and inhibition of caspase activity. Alion could be a promising candidate in the development of a novel class of anti-ischemic agent.

Authors+Show Affiliations

Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China.Ningxia Key Lab of Craniocerebral Diseases of Ningxia Hui Autonomous Region, Yinchuan, China.College of Nursing, Ningxia Medical University, Yinchuan, China. Electronic address: li_yuxiang@163.com.Department of Pharmacology, College of Pharmacy, Ningxia Medical University, Yinchuan, China; Ningxia Hui Medicine Modern Engineering Research Center, Ningxia Medical University, Yinchuan, China. Electronic address: yujq910315@163.com.

Pub Type(s)

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

Language

eng

PubMed ID

26772628

Citation

Chang, Renyuan, et al. "Protective Effects of Aloin On Oxygen and Glucose Deprivation-induced Injury in PC12 Cells." Brain Research Bulletin, vol. 121, 2016, pp. 75-83.
Chang R, Zhou R, Qi X, et al. Protective effects of aloin on oxygen and glucose deprivation-induced injury in PC12 cells. Brain Res Bull. 2016;121:75-83.
Chang, R., Zhou, R., Qi, X., Wang, J., Wu, F., Yang, W., Zhang, W., Sun, T., Li, Y., & Yu, J. (2016). Protective effects of aloin on oxygen and glucose deprivation-induced injury in PC12 cells. Brain Research Bulletin, 121, 75-83. https://doi.org/10.1016/j.brainresbull.2016.01.001
Chang R, et al. Protective Effects of Aloin On Oxygen and Glucose Deprivation-induced Injury in PC12 Cells. Brain Res Bull. 2016;121:75-83. PubMed PMID: 26772628.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effects of aloin on oxygen and glucose deprivation-induced injury in PC12 cells. AU - Chang,Renyuan, AU - Zhou,Ru, AU - Qi,Xue, AU - Wang,Jing, AU - Wu,Fan, AU - Yang,Wenli, AU - Zhang,Wannian, AU - Sun,Tao, AU - Li,Yuxiang, AU - Yu,Jianqiang, Y1 - 2016/01/06/ PY - 2015/11/13/received PY - 2015/12/28/revised PY - 2016/01/04/accepted PY - 2016/1/17/entrez PY - 2016/1/17/pubmed PY - 2016/12/15/medline KW - Aloin KW - Apoptosis KW - Ischemic injury KW - Oxidative stress KW - Oxygen and glucose deprivation KW - PC12 cells SP - 75 EP - 83 JF - Brain research bulletin JO - Brain Res. Bull. VL - 121 N2 - The present study aims to determine whether aloin could protect cells from ischemic and reperfusion injury in vitro and to elucidate the related mechanisms. Oxygen and glucose deprivation model in PC12 cells was used in the present study. 2-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH) assay and Hoechst 33342 nuclear staining were used to evaluate the protective effects of aloin, at concentrations of 10, 20, or 40 μg/mL in PC12 cells. PCR was applied to detect fluorescence caspase-3, Bax and Bcl-2 mRNA expression in PC12 cells. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) activity were evaluated by biochemical method. The concentration of intracellular-free calcium [Ca(2+)]i, mitochondrial membrane potential (MMP) were determined to estimate the degree of neuronal damage. It was shown that aloin (10, 20, and 40 μg/mL) significantly attenuated PC12 cells damage with characteristics of an increased injured cells absorbance of MTT and releases of LDH, decreasing cell apoptosis, and antagonizing decreases in SOD activity and increase in MDA level induced by OGD-reoxygenation. Meanwhile pretreatment with aloin significantly reduced injury-induced intracellular ROS, increased MMP (P<0.01), but it inhibited [Ca(2+)]i (P<0.01) elevation in a dose-dependent manner. Furthermore, pre-treatment with aloin significantly up-regulated Bcl-2 mRNA expression, down-regulated Bax mRNA expression and consequently activated caspase-3 mRNA expression in a dose-dependent manner. The results indicated that the protection of aloin on OGD-induced apoptosis in PC12 cells is associated with its suppression on OGD-induced oxidative stress and protection on mitochondrial function and inhibition of caspase activity. Alion could be a promising candidate in the development of a novel class of anti-ischemic agent. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/26772628/Protective_effects_of_aloin_on_oxygen_and_glucose_deprivation_induced_injury_in_PC12_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(16)30001-6 DB - PRIME DP - Unbound Medicine ER -