Rui Cao

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (8)17.45 Total impact

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    ABSTRACT: Accumulating evidence suggested that hyperglycemia played a critical role in hippocampus dysfunction in patients with diabetes mellitus. However, the multifactorial pathogenesis of hyperglycemia induced the impairments of hippocampal neurons has not been fully elucidated. Docosahexaenoic acid (DHA) has been shown to enhance learning and memory and affect neural function in various experimental conditions. The present study investigated the effects of DHA on the lipid peroxidation, the level of inflammatory cytokines and neuron apoptosis in the hippocampal neurons in high glucose condition. High glucose administration increased the level of TNF-α and IL-6, induced oxidative stress and apoptosis of hippocampal neurons in vitro. DHA treatment reduced oxidative stress and TNF-α expression, protected the hippocampal neurons by increasing AKT phosphorylation and decreasing caspase-3 and caspase-9 expression. These results suggested that high glucose exposure induced injury of hippocampal neurons in vitro, and the principle mechanisms involved in the neuroprotective effect of DHA were its antioxidant and anti-apoptotic potential. DHA may thus be of use in preventing or treating neuron-degeneration resulting from hyperglycemia.
    Neuroscience 05/2014; · 3.12 Impact Factor
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    ABSTRACT: Accumulating evidence suggested that hyperglycemia played a critical role in hippocampus dysfunction in patients with diabetes mellitus. However, the multifactorial pathogenesis of hyperglycemia-induced impairments of hippocampal neurons has not been fully elucidated. Docosahexaenoic acid (DHA) has been shown to enhance learning and memory and affect neural function in various experimental conditions. The present study investigated the effects of DHA on the lipid peroxidation, the level of inflammatory cytokines and neuron apoptosis in the hippocampal neurons in high-glucose condition. High-glucose administration increased the level of tumor necrosis factor α (TNF-α) and IL-6, induced oxidative stress and apoptosis of hippocampal neurons in vitro. DHA treatment reduced oxidative stress and TNF-α expression, protected the hippocampal neurons by increasing AKT phosphorylation and decreasing caspase-3 and caspase-9 expression. These results suggested that high-glucose exposure induced injury of hippocampal neurons in vitro, and the principle mechanisms involved in the neuroprotective effect of DHA were its antioxidant and anti-apoptotic potential. DHA may thus be of use in preventing or treating neuron-degeneration resulting from hyperglycemia.
    Neuroscience 01/2014; 274:218–228. · 3.12 Impact Factor
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    ABSTRACT: Dietary ratios of n-3/n-6 polyunsaturated fatty acids (PUFAs) have been implicated in controlling markers of metabolic disorders, including obesity, insulin resistance (IR), inflammation, and lipid profiles, which are also presumed to be partly related to type 2 diabetes mellitus (T2DM). However, molecular mechanisms of the different PUFAs related to metabolic disorders have not been systematically addressed. The present study aimed to investigate the impact of dietary n-3/n-6 PUFA ratios on obesity and IR and, further, to determine the underlying mechanisms. For 16 weeks, 32 SD male rats, randomly divided into four groups (n = 8 per group), received one of the following diets: normal chow, high saturated fatty acid (SFA), high n-3/n-6 PUFA ratio (1∶1, PUFA(1:1)), or low n-3/n-6 PUFA ratio (1∶4, PUFA(1:4)). Following the experimental diet period, metabolic parameters related to obesity and IR were measured. Compared to SFA diet-fed rats, PUFA(1:1) diet-fed rats exhibited decreased body and visceral fat weight, lowered blood lipids, and improved glucose tolerance and insulin sensitivity. Interestingly, these changes were accompanied with decreased expression levels of circulating pro-inflammatory cytokines, including tumor necrosis factor α, interleukin-6, and C-reactive protein. Moreover, the TLR4 protein and mRNA levels were markedly down-regulated by PUFA(1:1) compared with SFA; however, PUFA(1:4) diet-fed rats failed to exhibit these changes. Cumulatively, our data highlight a role for a PUFA(1:1) diet in the prevention of obesity and related metabolic disorders by suppressing the activation of TLR4, a critical modulator of pro-inflammatory cytokines.
    Nutrition research (New York, N.Y.) 10/2013; 33(10):849-58. · 1.20 Impact Factor
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    ABSTRACT: The etiological role of dysregulated autophagy in neurodegenerative diseases has been a subject of intense investigation. While manganese (Mn) is known to cause dopaminergic (DAergic) neurodegeneration, it has yet to be determined whether the dysregulation of autophagy plays a role in Mn-induced neuronal injury. In this study, we investigated the effect of Mn on autophagy in a rat model of manganism, a neurodegenerative disease associated with excessive exposure to Mn. After a single intrastriatal injection of Mn, the short- (4-12 h) and long-term (1-28 days) effect of Mn on DAergic neurons and autophagy were examined. Marked reduction in the number of TH-immunoreactive neurons in the substantia nigra pars compacta (SNpc) as well as TH protein expression, and a significant increase of apomorphine-induced rotations were observed in rats after Mn injection. Manganese also induced the down-regulation of dopamine levels and D1 dopamine receptor expression. In addition, autophagy was dysregulated and inhibited, as evidenced by increased number of abnormal lysosomes, decreased protein expression of Beclin1, and decreased ratio of microtubule-associated protein 1 light chain 3 (LC3) II over LC3 I, concomitant with activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70s6k) signaling. In contrast, in the early phase of Mn exposure, the level of autophagy was not be suppressed but compensatorily activated. Although the morphology of the DAergic neuron was intact in the early phase, Mn caused a significant decrease in TH-immunoreactivity and a significant increase in apomorphine-induced rotations in the presence of wortmannin, an inhibitor of autophagy. Taken together, these results demonstrate, for the first time, that autophagy may play a protective role against Mn-induced neuronal damage, whilst dysregulation of autophagy at later phases may mediate DAergic neurodegeneration.
    Neurotoxicity Research 04/2013; · 2.87 Impact Factor
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    ABSTRACT: Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. Diabetes impaired spatial learning and memory of rats. Diabetes increased the expression of Bax and caspase-3, which led the apoptosis of the CA1 pyramidal neurons, and further contributed to the deficits in learning and memory processing. Fish oil dietary supplementation in diabetic rats conducts neuron-protective function through an anti-apoptotic pathway and significantly improves the ability of learning and memory. These results partially explain the mechanism of the effect of diabetes and fish oil treatment on learning and memory, supporting a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications.
    Brain research 04/2012; 1457:33-43. · 2.46 Impact Factor
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    ABSTRACT: Increasing evidence indicates that neuroinflammation plays an important role in neurotoxins-induced neurodegenerations. Microglia are a type of glial cells in the brain and play as the first and main form of active immune defense in the central nervous system. Accumulated data suggest that the activation of microglia plays a critical role in neurotoxicities induced by environmental toxicants. So the inhibition of microglia has been proven to be an effective strategy against neurotoxic effects. In the present study, we found that n-3 polyunsaturated fatty acids can inhibit both microglial activation and dopaminergic injury in the substantia nigra of Sprague-Dawley rats induced by lipopolysaccharide, one of the major constituents of the outer membrane of Gram-negative bacteria. Moreover, n-3 polyunsaturated fatty acids inhibited lipopolysaccharide-induced activation of nuclear factor-κB, an important transcription factor involved in microglial activation. Taken together, our results provided the first in vivo evidence that n-3 polyunsaturated fatty acids can inhibit the damage of dopaminergic neurons induced by lipopolysaccharide through their inhibitory effects on nuclear factor-κB-dependent microglial activation.
    NeuroToxicology 03/2012; 33(4):780-8. · 2.65 Impact Factor
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    ABSTRACT: To study the inhibition effect of equol on MDA-MB-231 cells, a human breast cancer cell line with estrogen-independent receptor. Cultured MDA-MB-231 cells were treated with different contents of equol. The cell viability was assessed with MTT method. The apoptosis was detected by flow cytometry and immunofluorescence. Western Blot was used to assess the expression of NF-kappaB. The growth of MDA-MB-231 cells was inhibited by equol in a does-and time-dependent manner. The apoptosis of MDA-MB-231 cells induced by equol was the result of inhibiting the expression of NF-kappaB. The apoptosis of MDA-MB-231 cells might be the reduced expression of NF-kappaB induced by equol.
    Wei sheng yan jiu = Journal of hygiene research 01/2011; 40(1):95-8.
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    ABSTRACT: Dietary conjugated linoleic acid (CLA) has been investigated for its beneficial effects on disease prevention and treatment, and now obesity is one of the most perspective researching highlights. In a variety of experimental models, the results of studies on the effects of CLA on food intakes are somewhat inconsistent. Our experiment was conducted to extend these observations to hypothalamus and other regions within the central nervous system so that the mechanism of the actions of CLA might be more easily elucidated. In the experiment, a permanent cannula was inserted into the lateral ventricle of each rat. For the experiment, animals received intracerebroventricular injections of either 150nmol (n=16) CLA, or LA as non-conjugated control, or normal saline as vehicle. Hypothalamus and blood samples were collected at the 2nd, 4th, 8th, and 14th day. The results show that CLA in cerebral ventricle can inhibit food intake of experimented rats and this inhibition is related with the decreased expression of neuropeptides Y (NPY) and agouti-related protein (AgRP). The circulating leptin level was also increased by this tentative treatment (2.94+/-0.71 versus 1.18+/-0.18ng/ml). However, the glucose metabolism was not affected by ICV CLA. It is concluded that CLA in brain can inhibit the appetite of rats through the mechanism of decreasing the expression of NPY and AgRP.
    Neuroscience Letters 06/2007; 418(3):217-21. · 2.03 Impact Factor