Effects of genistein on neuronal apoptosis, and expression of Bcl-2 and Bax proteins in the hippocampus of ovariectomized rats

Yun Peng; Bo Jiang; Huiling Wu; Ruchun Dai; Liming Tan

doi:10.3969/j.issn.1673-5374.2012.36.004

Effects of genistein on neuronal apoptosis, and expression of Bcl-2 and Bax proteins in the hippocampus of ovariectomized rats

Neural Regen Res. 2012 Dec 25;7(36):2874-81. doi: 10.3969/j.issn.1673-5374.2012.36.004.

Authors

Yun Peng¹, Bo Jiang¹, Huiling Wu¹, Ruchun Dai², Liming Tan¹

Affiliations

¹ Department of Neurology, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.
² Institute of Endocrinology and Metabolism, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.

PMID: 25317139
PMCID: PMC4190945
DOI: 10.3969/j.issn.1673-5374.2012.36.004

Abstract

Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-2 in the hippocampus of rats decreased and Bax expression increased, with an obvious upregulation of apoptosis. However, intraperitoneal injection of genistein or 17β-estradiol for 15 consecutive weeks from the second day after operation upregulated Bcl-2 protein expression, downregulated Bax protein expression, and attenuated hippocampal neuron apoptosis. Our experimental findings indicate that long-term intervention with genistein can lead to a decrease in apoptosis in hippocampal neurons following ovariectomy, upregulate the expression of Bcl-2, and downregulate the expression of Bax. In addition, genistein and 17β-estradiol play equal anti-apoptotic and neuroprotective roles.

Keywords: 17β-estradiol; Bax; Bcl-2; apoptosis; brain injury; genistein; hippocampus; neural regeneration; ovariectomized model; rats.