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    25 October 2012, Volume 7 Issue 30 Previous Issue    Next Issue
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    Osthole improves synaptic plasticity in the hippocampus and cognitive function of Alzheimer’s disease rats via regulating glutamate
    Xiaohua Dong, Danshen Zhang, Li Zhang, Wei Li, Xianyong Meng
    2012, 7 (30):  2325-2332. 
    Abstract ( 222 )   PDF (279KB) ( 934 )   Save

    Osthole, an effective monomer in Chinese medicinal herbs, can cross the blood-brain barrier and protect against brain injury, with few toxic effects. In this study, a rat model of Alzheimer’s disease was established after intracerebroventricular injection of β-amyloid peptide (25–35). Subsequently, the rats were intraperitoneally treated with osthole (12.5 or 25.0 mg/kg) for 14 successive days. Results showed that osthole treatment significantly improved cognitive impairment and protected hippocampal neurons of Alzheimer’s disease rats. Also, osthole treatment alleviated suppressed long-term potentiation in the hippocampus of Alzheimer’s disease rats. In these osthole-treated Alzheimer’s disease rats, the level of glutamate decreased, but there was no significant change in γ-amino-butyric acid. These experimental findings suggest that osthole can improve learning and memory impairment, and increase synaptic plasticity in Alzheimer’s disease rats. These effects of osthole may be because of its regulation of central glutamate and γ-amino-butyric acid levels.

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    Oxymatrine reduces neuroinflammation in rat brain A signaling pathway
    Jiahui Mao, Yae Hu, Ailing Zhou, Bing Zheng, Yi Liu, Yueming Du, Jia Li, Jinyang Lu, Pengcheng Zhou
    2012, 7 (30):  2333-2339. 
    Abstract ( 282 )   PDF (217KB) ( 853 )   Save

    Cerebral neuroinflammation models were established by injecting 10 μg lipopolysaccharide into the hippocampus of male Sprague-Dawley rats. The rats were treated with an intraperitoneal injection of 120, 90, or 60 mg/kg oxymatrine daily for three days prior to the lipopolysaccharide injection. Twenty-four hours after model induction, the hippocampus was analyzed by real-time quantitative PCR, and the cerebral cortex was analyzed by enzyme-linked immunosorbent assay and western blot assay. The results of the enzyme-linked immunosorbent assay and the real-time quantitative PCR showed that the secretion and mRNA expression of the pro-inflammatory cytokines interleu-kin-1β and tumor necrosis factor-α were significantly decreased in the hippocampus and cerebral cortex of model rats treated with oxymatrine. Western blot assay and real-time quantitative PCR analysis indicated that toll-like receptor 4 mRNA and protein expression were significantly de-creased in the groups receiving different doses of oxymatrine. Additionally, 120 and 90 mg/kg oxymatrine were shown to reduce protein levels of nuclear factor-κB p65 in the nucleus and of phosphorylated IκBα in the cytoplasm of brain cells, as detected by western blot assay. Experi-mental findings indicate that oxymatrine may inhibit neuroinflammation in rat brain via downregu-lating the expression of molecules in the toll-like receptor 4/nuclear factor-κB signaling pathway.

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    Ginsenoside Rb1 relieves glucose fluctuation- induced oxidative stress and apoptosis in Schwann cells
    Bing Xue, Lianqing Sun, Xiaojin Li, Xuan Wang, Ying Zhang, Yiming Mu, Linlang Liang
    2012, 7 (30):  2340-2346. 
    Abstract ( 215 )   PDF (206KB) ( 998 )   Save

    Cultured Schwann cells were treated with 5.6 mM and 50 mM glucose alternating every 8 hours to simulate intermittent high glucose. The present study analyzed the neuroprotective effects of 1, 10 and 100 μM ginsenoside Rb1 on oxidative damage and apoptosis in Schwann cells induced by in-termittent high glucose. Flow cytometry demonstrated that ginsenoside Rb1 reduced intermittent high glucose-mediated reactive oxygen species production. Enzyme linked immunosorbent assay showed that 8-hydroxy-2-deoxy guanosine levels in Schwann cells decreased following ginseno-side Rb1 treatment. Quantitative real-time reverse transcription-PCR and western blot assay results revealed that ginsenoside Rb1 inhibited intermittent high glucose-upregulated Bax expression, but antagonized intermittent high glucose-downregulated Bcl-2 expression in Schwann cells. These effects were most pronounced with 100 μM ginsenoside Rb1. These results indicate that ginseno-side Rb1 inhibits intermittent high glucose-induced oxidative stress and apoptosis in Schwann cells.

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    Expressions of apoptosis-related proteins in rats with focal cerebral ischemia after Angong Niuhuang sticker point application
    Dongshu Zhang, Maodong Fu, Chenglong Song, Caiyun Wang, Xiaochun Lin, Yuanliang Liu
    2012, 7 (30):  2347-2353. 
    Abstract ( 286 )   PDF (157KB) ( 997 )   Save

    In this study, we extracted and purified components in the Angong Niuhuang pill. Then we applied transdermal enhancers to Angong Niuhuang stickers by modern technology. The Angong Niuhuang sticker includes extracts from curcuma, berberine hydrochloride, baicalin, geniposide, borneol, and musk. Angong Niuhuang stickers at different point application doses (1.35, 2.7, and 5.4 g/kg) were administered to Dazhui (DU14), Qihai (RN6) and Mingmen (DU4). Rats in the different dose point application and acupuncture groups were continuously administered for 7 days. Then a middle ce-rebral artery occlusion model was prepared for simulating human cerebral ischemia. Twelve hours later, expressions of Bcl-2, Bax and p53 protein in hippocampal CA1 were detected with immuno-histochemistry. The expression level of Bcl-2, an anti-apoptotic protein, significantly increased in the high-, medium- and low-dose point application groups and the acupuncture group, while the ex-pression of the pro-apoptotic proteins, Bax and p53, significantly decreased compared with the middle cerebral artery occlusion rats; and the Bcl-2/Bax ratio was significantly increased. The dif-ference was noticeable for the high-dose point application group, which showed statistical differ-ence compared with the low-dose point application group and the acupuncture group. Our experi-mental findings indicate that point application with Angong Niuhuang stickers promotes the expres-sion of Bcl-2, and inhibits the expressions of Bax and p53 in the hippocampal CA1 area of rats after focal cerebral ischemia. Thus, point application of Angong Niuhang stickers protects brain tissues from cerebral ischemia.

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    Tea polyphenols increase X-ray repair cross-complementing protein 1 and apurinic/apyrimidinic endonuclease/redox factor-1 expression in the hippocampus of rats during cerebral ischemia/reperfusion injury
    Zhi Wang, Rongliang Xue, Xi Lei, Jianrui Lv, Gang Wu, Wei Li, Li Xue, Xiaoming Lei, Hongxia Zhao, Hui Gao, Xin Wei
    2012, 7 (30):  2355-2361. 
    Abstract ( 232 )   PDF (250KB) ( 841 )   Save

    Recent studies have shown that tea polyphenols can cross the blood-brain barrier, inhibit apoptosis and play a neuroprotective role against cerebral ischemia. Furthermore, tea polyphenols can decrease DNA damage caused by free radicals. We hypothesized that tea polyphenols repair DNA damage and inhibit neuronal apoptosis during global cerebral ischemia/reperfusion. To test this hypothesis, we employed a rat model of global cerebral ischemia/reperfusion. We demonstrated that intraperitoneal injection of tea polyphenols immediately after reperfusion significantly reduced apoptosis in the hippocampal CA1 region; this effect started 6 hours following reperfusion. Immunohistochemical staining showed that tea polyphenols could reverse the ischemia/reperfusion-induced reduction in the expression of DNA repair proteins, X-ray repair cross-complementing protein 1 and apurinic/apyrimidinic endonuclease/redox factor-1 starting at 2 hours. Both effects lasted at least 72 hours. These experimental findings suggest that tea polyphenols promote DNA damage repair and protect against apoptosis in the brain.

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    Activated and deactivated functional brain areas in the Deqi state A functional MRI study
    Yong Huang, Tongjun Zeng, Guifeng Zhang, Ganlong Li, Na Lu, Xinsheng Lai, Yangjia Lu, Jiarong Chen
    2012, 7 (30):  2362-2369. 
    Abstract ( 232 )   PDF (278KB) ( 846 )   Save

    We compared the activities of functional regions of the brain in the Deqi versus non-Deqi state, as reported by physicians and subjects during acupuncture. Twelve healthy volunteers received sham and true needling at the Waiguan (TE5) acupoint. Real-time cerebral functional MRI showed that compared with non-sensation after sham needling, true needling activated Brodmann areas 3, 6, 8, 9, 10, 11, 13, 20, 21, 37, 39, 40, 43, and 47, the head of the caudate nucleus, the parahippocampal gyrus, thalamus and red nucleus. True needling also deactivated Brodmann areas 1, 2, 3, 4, 5, 6, 7, 9, 10, 18, 24, 31, 40 and 46.

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    Effects of pre-moxibustion at Zusanli (ST36) on heat shock protein 70 expression in rats with gastric mucosal lesions after neurotomy
    Liang Peng, Mi Liu, Xiaorong Chang, Zhou Yang, Shouxiang Yi, Jie Yan, Yan Peng
    2012, 7 (30):  2370-2376. 
    Abstract ( 186 )   PDF (193KB) ( 901 )   Save

    Studies have shown that pre-moxibustion protects the gastric mucosa by up-regulating the expression of heat shock protein 70. However, the signaling pathway underlying this effect remains unclear. Rats were intragastrically administered absolute alcohol, causing obvious lesion of the gastric mucosa. Following pre-moxibustion at Zusanli (ST36) for 8 days, the ulcer index decreased to different degrees. The results of an enzyme linked immunosorbent assay and western blotting showed significant upregulation of heat shock protein 70 expression in the gastric mucosa and serum. None out of transection of the spinal cord, damage to the nucleus of the solitary tract, neurotomy of the vagal nerve and neurotomy of the common peroneal nerve affected the decrease in ulcer index or the increase in heat shock protein 70 expression in serum after pre-moxibustion at Zusanli, and heat shock protein 70 expression was obviously decreased in the gastric mucosa. These findings suggest that pre-moxibustion at Zusanli can protect the gastric mucosa against lesioning, and that the mechanism underlying this effect involves its induction of heat shock protein 70 expression. Neural pathways participate in the regulatory effects of moxibustion on heat shock protein 70 expression in the gastric mucosa.

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    Genetic association of urokinase-type plasminogen activator gene rs2227564 site polymorphism with sporadic Alzheimer’s disease in the Han Chinese population
    Xuelian Ji, Longfei Jia, Jianping Jia, Li Qi
    2012, 7 (30):  2377-2383. 
    Abstract ( 312 )   PDF (267KB) ( 891 )   Save

    A missense C/T polymorphism in exon 6 (the NCBI rsID is rs2227564) of the urokinase-type plas-minogen activator gene has been identified as a possible hot spot for Alzheimer’s disease risk. The present study analyzed urokinase-type plasminogen gene polymorphisms of rs2227564 with spo-radic Alzheimer’s disease by PCR-restriction fragment length polymorphism. Results showed that CC, CT and TT genotype distribution frequencies had significant differences between sporadic Alzheimer’s disease patients and healthy controls. In-depth analysis of the association between urokinase-type plasminogen gene rs2227564 polymorphisms and sporadic Alzheimer’s disease in-dicated that people with the C-positive genotype CC + CT were at a higher risk for developing sporadic Alzheimer’s disease. These results support the contribution of the polymorphisms of rs2227564 in the urokinase-type plasminogen gene to the pathogenesis of sporadic Alzheimer’s disease in the Han Chinese population.

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    Is the C677T polymorphism in methylenetetrahydrofolate reductase gene or plasma homocysteine a risk factor for diabetic peripheral neuropathy in Chinese individuals
    Hongli Wang, Dongsheng Fan, Tianpei Hong
    2012, 7 (30):  2384-2391. 
    Abstract ( 166 )   PDF (167KB) ( 996 )   Save

    The present study enrolled 251 diabetic patients, including 101 with neuropathy and 150 without neuropathy. Of the 150 patients, 100 had no complications, such as retinopathy, nephropathy, or neuropathy. Polymerase chain reaction restriction fragment length polymorphism analysis was used to identify methylenetetrahydrofolate reductase gene variants. Plasma homocysteine levels were also measured. Homocysteine levels and the frequency of hyperhomocysteinemia were significantly higher in patients with diabetic peripheral neuropathy compared with diabetic patients without neuropathy (P < 0.05). In logistic regression analysis with neuropathy as the dependent variable,the frequency of C677T in methylenetetrahydrofolate reductase was significantly higher in patients with diabetic peripheral neuropathy compared with patients without diabetic complications. Homocysteine levels were significantly higher in patients with diabetic peripheral neuropathy carrying the 677T allele and low folic acid levels. In conclusion, hyperhomocysteinemia is an independent risk factor for diabetic neuropathy in Chinese patients with diabetes. The C677T polymorphism in methylenetetrahydrofolate reductase and low folic acid levels may be risk factors for diabetic peripheral neuropathy in Chinese patients with diabetes.

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    Neuroimaging diagnosis for cerebral infarction An 8-year bibliometric analysis
    Yan Du, Xiaoxia Yang, Hong Song, Bo Chen, Lin Li, Yue Pan, Qiong Wu, Jia Li
    2012, 7 (30):  2392-2399. 
    Abstract ( 186 )   PDF (169KB) ( 1180 )   Save

    OBJECTIVE: To identify global research trends in neuroimaging diagnosis for cerebral infarction using a bibliometric analysis of the Web of Science.
    DATA RETRIEVAL: We performed a bibliometric analysis of data retrieval for neuroimaging diag-nosis for cerebral infarction containing the key words “CT, magnetic resonance imaging, MRI, transcranial Doppler, transvaginal color Doppler, digital subtraction angiography, and cerebral in-farction” using the Web of Science.
    SELECTION CRITERIA: Inclusion criteria were: (a) peer-reviewed articles on neuroimaging diag-nosis for cerebral infarction which were published and indexed in the Web of Science; (b) original research articles and reviews; and (c) publication between 2004–2011. Exclusion criteria were: (a) articles that required manual searching or telephone access; and (b) corrected papers or book chapters.
    MAIN OUTCOME MEASURES: (1) Annual publication output; (2) distribution according to country; (3) distribution according to institution; (4) top cited publications; (5) distribution according to jour-nals; and (6) comparison of study results on neuroimaging diagnosis for cerebral infarction.
    RESULTS: Imaging has become the predominant method used in diagnosing cerebral infarction. The most frequently used clinical imaging methods were digital subtraction angiography, CT, MRI, and transcranial color Doppler examination. Digital subtraction angiography is used as the gold standard. However, it is a costly and time-consuming invasive diagnosis that requires some radia-tion exposure, and is poorly accepted by patients. As such, it is mostly adopted in interventional therapy in the clinic. CT is now accepted as a rapid, simple, and reliable non-invasive method for use in diagnosis of cerebrovascular disease and preoperative appraisal. Ultrasonic Doppler can be used to reflect the hardness of the vascular wall and the nature of the plaque more clearly than CT and MRI.
    CONCLUSION: At present, there is no unified standard of classification of cerebral infarction im-aging. Detection of clinical super-acute cerebral infarction remains controversial due to its changes on imaging, lack of specificity, and its similarity to a space-occupying lesion. Neuroimaging diagno-sis for cerebral infarction remains a highly active area of research and development.

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