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Estrogen receptor beta treats Alzheimer's disease

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neural Regeneration Research 2013年第5期8卷 420-426页

作者： Zhu Tian Jia Fan Yang Zhao Sheng Bi Lihui Si Qun Liu Department of Neurology the First Hospital of Jilin University Department of Neurology the Second Hospital of Jilin University Department of Obstetrics and Gynecology the Second Hospital of Jilin University

In vitro studies have shown that estrogen receptor β can attenuate the cytotoxic effect of amyloid protein on PC12 cells through the Akt pathway without estrogen stimulation. In this study, we aimed to observe the effect of estrogen receptor β in Alzheimer＇s disease rat models established by intraventricular injection of amyloid β protein. Estrogen receptor β lentiviral particles delivered via intraventricular injection increased Akt content in the hippocampus, decreased interleukin-1β mRNA tumor necrosis factor a mRNA and amyloid β protein levels in the hippocampus, and improved the learning and memory capacities in AIzheimer＇s disease rats. Estrogen receptor β short hairpin RNA lentiviral particles delivered via intraventricular injection had none of the above impacts on AIzheimer＇s disease rats. These experimental findings indicate that estrogen receptor β, independent from estrogen, can reduce inflammatory reactions and amyloid β deposition in the hJppocampus of AIzheimer＇s disease rats, and improve learning and memory capacities. This effect may be mediated through activation of the Akt pathway.

关键词： neural regeneration neurodegenerative diseases estrogen estrogen receptor β Alzheimer＇s disease amyloid β protein inflammatory cytokines Akt signaling pathway cognition neural protection photographs-containing paper neuroregeneration

Hypothermic intervention for 3 hours inhibits apoptosis in neonatal rats with hypoxic-ischemic brain damage

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neural Regeneration Research 2011年第22期6卷 1709-1714页

作者： Yale Guo Zhankui Li Ruilin Li Baoshan Su Shaoping Huang Jianping Zhou Department of Pediatrics Second Affiliated Hospital of Medical College of Xi＇an Jiaotong University Xi＇an 710004 Shaanxi Province China Department of Neonatology Maternal and Child Health Hospital of Shaanxi Province Xi＇an 710004 Shaanxi Province China Department of Pathology Second Affifiated Hospital of Medical College of Xi＇an Jiaotong University Xi＇an 710004 Shaanxi Province China

A neonatal rat model of hypoxic-ischemic brain damage was designed and implemented in this study. Rats were subjected to hypothermia at 31℃ immediately following hypoxia-ischemia for either 3, 6 or 15 hours. TdT-mediated dUTP nick end labeling demonstrated that the number of apoptotic cells was reduced in the rat cerebral cortex, hippocampus and periventricular white matter following hypothermia. Immunohistochemistry revealed that Bcl-2 and p16 expression were decreased. Inhibition of apoptosis was greatest with the 3 hour hypothermic treatment, followed by hypothermia for 6 hours. In contrast, hypothermia for 15 hours led to a decrease in neuronal number in the cerebral cortex. The results demonstrate that hypothermic intervention at 31℃ protects brain tissue against hypoxic-ischemic brain damage by inhibiting apoptosis, and that the optimal length of treatment is 3 hours.

关键词： hypothermia hypoxia ischemia neural protection neural regeneration

Triptolide protects astrocytes from hypoxia/reoxygenation injury

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neural Regeneration Research 2011年第21期6卷 1623-1627页

作者： Minfang Guo Hongcui Fan Jiezhong Yu Ning Ji Yongsheng Sun Liyun Liang Baoguo Xiao Cungen Ma Institute of Brain Science Department of Neurology Medical School Shanxi Datong University Datong 037008 Shanxi Province China Institute of Neurology Huashan Hospital Fudan University Shanghai 200025 China

Astrocytes in an in vitro murine astrocyte model of oxygen and glucose deprivation/hypoxia and reoxygenation were treated with different concentrations of triptolide （250, 500, 1 000 ng/mL） in a broader attempt to elucidate the protection and mechanism underlying triptolide treatment on astrocytes exposed to hypoxia/reoxygenation injury. The results showed that the matrix metalloproteinase-9, interleukin-1β, tumor necrosis factor α and interleukin-6 expressions were significantly decreased after triptolide treatment in the astrocytes exposed to hypoxia/ reoxygenation injury, while interleukin-10 expression was upregulated. In addition, the vitality of the injured astrocytes was enhanced, the triptolide＇s effect was apparent at 500 ng/mL. These experimental findings indicate that triptolide treatment could protect astrocytes against hypoxia/ reoxygenation injury through the inhibition of inflammatory response and the reduction of matrix metalloproteinase-9 expression.

关键词： triptolide hypoxia/reoxygenation astrocyte matrix metalloproteinase-9 inflammatory factor neural protection neural regeneration