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Effect of hydrogen sulphide on beta-amyloid-induced damage in PC12 cells.
Clin Exp Pharmacol Physiol. 2008 Feb; 35(2):180-6.CE

Abstract

1. Hydrogen sulphide (H(2)S) is a well-known cytotoxic gas. Recently, H(2)S has been shown to protect neurons against oxidative stress caused by glutamate, peroxynitrite and HOCl. Considerably lower H(2)S levels have been reported in the brain of Alzheimer's disease (AD) patients with accumulation of beta-amyloid (A beta). 2. The aim of present study was to explore the cytoprotection by H(2)S against A beta(25-35)-induced apoptosis and the molecular mechanisms underlying this effect in PC12 cells. 3. Our findings indicated that A beta(25-35) significantly reduced cell viability and induced apoptosis of PC12 cells, along with dissipation of the mitochondrial membrane potential (MMP) and overproduction of reactive oxygen species (ROS). 4. Sodium hydrosulphide (NaHS), an H(2)S donor, protected PC12 cells against A beta(25-35)-induced cytotoxicity and apoptosis not only by reducing the loss of MMP, but also by attenuating the increase in intracellular ROS. 5. The results of the present study suggest that the cytoprotection by H(2)S is related to the preservation of MMP and attenuation of A beta(25-35)-induced intracellular ROS generation. These findings could significantly advance therapeutic approaches to the neurodegenerative diseases that are associated with oxidative stress, such as AD.

Authors+Show Affiliations

Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, 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

17892504

Citation

Tang, Xiao-Qing, et al. "Effect of Hydrogen Sulphide On Beta-amyloid-induced Damage in PC12 Cells." Clinical and Experimental Pharmacology & Physiology, vol. 35, no. 2, 2008, pp. 180-6.
Tang XQ, Yang CT, Chen J, et al. Effect of hydrogen sulphide on beta-amyloid-induced damage in PC12 cells. Clin Exp Pharmacol Physiol. 2008;35(2):180-6.
Tang, X. Q., Yang, C. T., Chen, J., Yin, W. L., Tian, S. W., Hu, B., Feng, J. Q., & Li, Y. J. (2008). Effect of hydrogen sulphide on beta-amyloid-induced damage in PC12 cells. Clinical and Experimental Pharmacology & Physiology, 35(2), 180-6.
Tang XQ, et al. Effect of Hydrogen Sulphide On Beta-amyloid-induced Damage in PC12 Cells. Clin Exp Pharmacol Physiol. 2008;35(2):180-6. PubMed PMID: 17892504.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of hydrogen sulphide on beta-amyloid-induced damage in PC12 cells. AU - Tang,Xiao-Qing, AU - Yang,Chun-Tao, AU - Chen,Jing, AU - Yin,Wei-Lan, AU - Tian,Shao-Wen, AU - Hu,Bi, AU - Feng,Jian-qiang, AU - Li,Yuan-Jian, Y1 - 2007/09/24/ PY - 2007/9/26/pubmed PY - 2008/2/1/medline PY - 2007/9/26/entrez SP - 180 EP - 6 JF - Clinical and experimental pharmacology & physiology JO - Clin Exp Pharmacol Physiol VL - 35 IS - 2 N2 - 1. Hydrogen sulphide (H(2)S) is a well-known cytotoxic gas. Recently, H(2)S has been shown to protect neurons against oxidative stress caused by glutamate, peroxynitrite and HOCl. Considerably lower H(2)S levels have been reported in the brain of Alzheimer's disease (AD) patients with accumulation of beta-amyloid (A beta). 2. The aim of present study was to explore the cytoprotection by H(2)S against A beta(25-35)-induced apoptosis and the molecular mechanisms underlying this effect in PC12 cells. 3. Our findings indicated that A beta(25-35) significantly reduced cell viability and induced apoptosis of PC12 cells, along with dissipation of the mitochondrial membrane potential (MMP) and overproduction of reactive oxygen species (ROS). 4. Sodium hydrosulphide (NaHS), an H(2)S donor, protected PC12 cells against A beta(25-35)-induced cytotoxicity and apoptosis not only by reducing the loss of MMP, but also by attenuating the increase in intracellular ROS. 5. The results of the present study suggest that the cytoprotection by H(2)S is related to the preservation of MMP and attenuation of A beta(25-35)-induced intracellular ROS generation. These findings could significantly advance therapeutic approaches to the neurodegenerative diseases that are associated with oxidative stress, such as AD. SN - 1440-1681 UR - https://www.unboundmedicine.com/medline/citation/17892504/Effect_of_hydrogen_sulphide_on_beta_amyloid_induced_damage_in_PC12_cells_ DB - PRIME DP - Unbound Medicine ER -