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Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus.
Neurosci Lett. 2008 Jun 13; 438(1):116-20.NL

Abstract

Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of genistein against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Sprague-Dawley rats by four-vessel-occlusion for 10min. At various times of reperfusion, the histopathological changes and the levels of mitochondria-generated reactive oxygen species (ROS), malondialdehyde (MDA), cytosolic cytochrome c and caspase-3 activity in hippocampus were measured. We found extensive neuronal death in the CA1 region at day 5 after I/R. The ischemic changes were preceded by increases in ROS generation and MDA concentration and followed by increased cytosolic cytochrome c, and subsequently caspase-3 activation and apoptosis. Treatment with genistein (15mg/kg, i.p.) significantly attenuated ischemia-induced neuronal death. Genistein administration also decreased ROS generation, MDA concentration and the apoptotic indices. These results suggest that genistein protects neurons from transient global cerebral I/R injury in rat hippocampus by attenuating oxidative stress, lipid peroxidation and the signaling cascade leading to apoptotic cell death.

Authors+Show Affiliations

Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310058, China.No 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

18467029

Citation

Liang, Hua-Wei, et al. "Genistein Attenuates Oxidative Stress and Neuronal Damage Following Transient Global Cerebral Ischemia in Rat Hippocampus." Neuroscience Letters, vol. 438, no. 1, 2008, pp. 116-20.
Liang HW, Qiu SF, Shen J, et al. Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. Neurosci Lett. 2008;438(1):116-20.
Liang, H. W., Qiu, S. F., Shen, J., Sun, L. N., Wang, J. Y., Bruce, I. C., & Xia, Q. (2008). Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. Neuroscience Letters, 438(1), 116-20. https://doi.org/10.1016/j.neulet.2008.04.058
Liang HW, et al. Genistein Attenuates Oxidative Stress and Neuronal Damage Following Transient Global Cerebral Ischemia in Rat Hippocampus. Neurosci Lett. 2008 Jun 13;438(1):116-20. PubMed PMID: 18467029.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. AU - Liang,Hua-Wei, AU - Qiu,Shui-Feng, AU - Shen,Jia, AU - Sun,Li-Na, AU - Wang,Jing-Ye, AU - Bruce,Iain C, AU - Xia,Qiang, Y1 - 2008/04/20/ PY - 2008/02/26/received PY - 2008/04/03/revised PY - 2008/04/07/accepted PY - 2008/5/10/pubmed PY - 2008/9/9/medline PY - 2008/5/10/entrez SP - 116 EP - 20 JF - Neuroscience letters JO - Neurosci Lett VL - 438 IS - 1 N2 - Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of genistein against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Sprague-Dawley rats by four-vessel-occlusion for 10min. At various times of reperfusion, the histopathological changes and the levels of mitochondria-generated reactive oxygen species (ROS), malondialdehyde (MDA), cytosolic cytochrome c and caspase-3 activity in hippocampus were measured. We found extensive neuronal death in the CA1 region at day 5 after I/R. The ischemic changes were preceded by increases in ROS generation and MDA concentration and followed by increased cytosolic cytochrome c, and subsequently caspase-3 activation and apoptosis. Treatment with genistein (15mg/kg, i.p.) significantly attenuated ischemia-induced neuronal death. Genistein administration also decreased ROS generation, MDA concentration and the apoptotic indices. These results suggest that genistein protects neurons from transient global cerebral I/R injury in rat hippocampus by attenuating oxidative stress, lipid peroxidation and the signaling cascade leading to apoptotic cell death. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/18467029/Genistein_attenuates_oxidative_stress_and_neuronal_damage_following_transient_global_cerebral_ischemia_in_rat_hippocampus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(08)00483-7 DB - PRIME DP - Unbound Medicine ER -