Objectives : The aim of this study was to investigate the effects of Guibi-Tang(GBT) on focal brain ischemic injury induced by intraluminal filament insertion in rats. Methods : The ischemia was induced by intraluminal filament insertion into middle cerebral artery. Sprague-Dawley rats were divided into five groups, normal group(n=8); control group was ischemia induced and no treatment(n=8); GBT 1X group was ischemia induced and administrated 42.2 mg/ml/kg of Guibi-Tang orally(n=8); GBT 3X group was ischemia induced and administrated 126.6 mg/ml/kg of Guibi-Tang orally(n=8); GBT 6X group was ischemia induced and administrated 253.2 mg/ml/kg of Guibi-Tang orally(n=8) for 21 days. mGluR5, Bax, Bcl-2 and cytochrome C were investigated to observe the effects of Guibi-Tang on apoptosis. The effects of Guibi-Tang on neuroprotective/apoptotic agents in cresyl violet, choline acetyltranferase(ChAT) with ischemic injury were investigated. Results : The intensity of mGluR5 mRNA in the hippocampal CA1 was increased in normal and GBT(Guibi-Tang) 1X groups compared with the control group. The intensity of Bax mRNA in the hippocampal CA1 was decreased in normal and GBT 1X groups compared with the control group. However it was increased unexpectedly in GBT 3X group. The intensity of Bcl-2 mRNA in the hippocampal CA1 was increased in normal and GBT 1X groups compared with the control group. The intensity of Bax/Bcl-2 ratio in the hippocampal CA1 was decreased in normal and GBT 1X groups compared with the control group. The intensity of cytochrome C protein in the hippocampal CA1 was decreased in normal, GBT 1X and GBT 6X groups compared with the control group. The density of neurons stained by cresyl violet and ChAT was increased in normal and GBT 1X groups compared with the control group. Conclusions : These results suggest that Guibi-Tang may have protective effect on vascular dementia.
Journal of Physiology & Pathology in Korean Medicine
/
v.25
no.2
/
pp.300-305
/
2011
The present study was investigated the neuroprotective effects of acupuncture at ST36 on learning and memory deficits after transient cerebral ischemia in a gerbil model. The animals were randomly divided into three groups (n=7 in each group): the sham operation group (SHAM), ischemia-induced and ST36 acupuncture group (ISC + ST36), and the ischemia-induced and Tail-acupuncture group (ISC + TAIL). For the acupuncture stimulation, stainless steel needles, 0.3 mm in diameter, were inserted bilaterally into the ST36 locus or the tail and stimulated for 1 min/day for 14 days. Using the Morris water maze test, the animals were tested on spatial learning and memory. In addition, the effects of acupuncture on memory storage and the choline acetyltransferase (ChAT) activity, in the hippocampal CA1 area, were investigated by ChAT immunohistochemistry. Transient cerebral ischemia produced impaired performance on the MWM test (DAY 5: p<0.01 and retention test: p<0.05) and severely decreased ChAT immunoreactivity in the CA1 hippocampal area compared to the SHAM group (p<0.05). However, improved learning and memory were observed (DAY 5: p<0.05 and retention test: p<0.01) as well as a significantly reduced loss of ChAT immunoactivity in the hippocampal CA1 region (p<0.001) after acupuncture stimulation at ST36 were observed. These results show that acupuncture at ST36 ameliorated the learning and memory deficits at least in part through the cholinergic system. The findings of this study provide potential data that acupuncture is useful for the treatment of some of the behavioral impairs of transient cerebral ischemia.
This study investigated whether ferulic acid modulates the heme oxygenase (HO)-1 and HO-2 expression in middle cerebral artery occlusion (MCAO)-induced brain injury. Rats (Sprague-Dawley, male) were treated with vehicle or ferulic acid (100 mg/kg, i.v.) before MCAO, and cerebral cortex tissues were collected 24 h after MCAO. This study clearly confirmed the protective effects of ferulic acid during MCAO-induced damage using hematoxylin and eosin staining. MCAO induces nuclear chromatin condensations and necrotic changes with scalloped shrunken form. However, ferulic acid prevented MCAO-induced histopathological changes. HO-1 and HO-2 expression levels were measured using reverse-transcription PCR and Western blot analyses. HO-1 levels were decreased in vehicle-treated animals after MCAO, whereas this decrease in HO-1 levels was attenuated by ferulic acid treatment. However, the level of HO-2 was consistently maintained in the cerebral cortex of vehicle- and ferulic acid-treated animals after MCAO. These results demonstrated that ferulic acid regulates HO-1 expression in ischemic brain injury, while ferulic acid do not modulate HO-2 expression in MACO. In conclusion, these findings suggest that ferulic acid exerts a neuroprotective effect by preventing the MCAO-induced decrease of HO-1 expression.
Background: Gintonin is a ginseng-derived exogenous ligand of the G protein-coupled lysophosphatidic acid (LPA) receptor. We previously reported that gintonin stimulates gliotransmitter release in primary cortical astrocytes. Astrocytes play key roles in the functions of neurovascular systems. Although vascular endothelial growth factor (VEGF) is known to influence the normal growth and maintenance of cranial blood vessels and the nervous system, there is little information about the effect of gintonin on VEGF regulation in primary astrocytes, under normal and hypoxic conditions. Methods: Using primary cortical astrocytes of mice, the effects of gintonin on the release, expression, and distribution of VEGF were examined. We further investigated whether the gintonin-mediated VEGF release protects astrocytes from hypoxia. Results: Gintonin administration stimulated the release and expression of VEGF from astrocytes in a concentration- and time-dependent manner. The gintonin-mediated increase in the release of VEGF was inhibited by the LPA1/3 receptor antagonist, Ki16425; phospholipase C inhibitor, U73122; inositol 1,4,5- triphosphate receptor antagonist, 2-APB; and intracellular $Ca^{2+}$ chelator, BAPTA. Hypoxia further stimulated astrocytic VEGF release. Gintonin treatment stimulated additional VEGF release and restored cell viability that had decreased due to hypoxia, via the VEGF receptor pathway. Altogether, the regulation of VEGF release and expression and astrocytic protection mediated by gintonin under hypoxia are achieved via the LPA receptor-VEGF signaling pathways. Conclusion: The present study shows that the gintonin-mediated regulation of VEGF in cortical astrocytes might be neuroprotective against hypoxic insults and could explain the molecular basis of the beneficial effects of ginseng on the central nervous system.
Xianan Dong ;Liangliang Kong ;Lei Huang ;Yong Su ;Xuewang Li;Liu Yang;Pengmin Ji ;Weiping Li ;Weizu Li
Journal of Ginseng Research
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v.47
no.3
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pp.458-468
/
2023
Background: As a complication of Type II Diabetes Mellitus (T2DM), the etiology, pathogenesis, and treatment of cognitive dysfunction are still undefined. Recent studies demonstrated that Ginsenoside Rg1 (Rg1) has promising neuroprotective properties, but the effect and mechanism in diabetes-associated cognitive dysfunction (DACD) deserve further investigation. Methods: After establishing the T2DM model with a high-fat diet and STZ intraperitoneal injection, Rg1 was given for 8 weeks. The behavior alterations and neuronal lesions were judged using the open field test (OFT) and Morris water maze (MWM), as well as HE and Nissl staining. The protein or mRNA changes of NOX2, p-PLC, TRPC6, CN, NFAT1, APP, BACE1, NCSTN, and Ab1-42 were investigated by immunoblot, immunofluorescence or qPCR. Commercial kits were used to evaluate the levels of IP3, DAG, and calcium ion (Ca2+) in brain tissues. Results: Rg1 therapy improved memory impairment and neuronal injury, decreased ROS, IP3, and DAG levels to revert Ca2+ overload, downregulated the expressions of p-PLC, TRPC6, CN, and NFAT1 nuclear translocation, and alleviated Aβ deposition in T2DM mice. In addition, Rg1 therapy elevated the expression of PSD95 and SYN in T2DM mice, which in turn improved synaptic dysfunction. Conclusions: Rg1 therapy may improve neuronal injury and DACD via mediating PLC-CN-NFAT1 signal pathway to reduce Aβ generation in T2DM mice.
Influenza virus is the major cause of seasonal and pandemic flu. Currently, oseltamivir, a potent and selective inhibitor of neuraminidase of influenza A and B viruses, is the drug of choice for treating patients with influenza virus infection. However, recent emergence of oseltamivir-resistant influenza viruses has limited its efficacy. Morin hydrate (3,5,7,2',4'-pentahydroxyflavone) is a flavonoid isolated from Morus alba L. It has antioxidant, anti-inflammatory, neuroprotective, and anticancer effects partly by the inhibition of the NF-κB signaling pathway. However, its effects on influenza virus have not been studied. We evaluated the antiviral activity of morin hydrate against influenza A/Puerto Rico/8/1934 (A/PR/8; H1N1) and oseltamivir-resistant A/PR/8 influenza viruses in vitro. To determine its mode of action, we carried out time course experiments, and time of addition, hemolysis inhibition, and hemagglutination assays. The effects of the co-administration of morin hydrate and oseltamivir were assessed using the murine model of A/PR/8 infection. We found that morin hydrate reduced hemagglutination by A/PR/8 in vitro. It alleviated the symptoms of A/PR/8-infection, and reduced the levels of pro-inflammatory cytokines and chemokines, such as TNF-α and CCL2, in infected mice. Co-administration of morin hydrate and oseltamivir phosphate reduced the virus titers and attenuated pulmonary inflammation. Our results suggest that morin hydrate exhibits antiviral activity by inhibiting the entry of the virus.
Won, Beom Young;Shin, Ki Young;Ha, Hyun Jee;Wee, Ji-Hyang;Yun, Yeo Sang;Kim, Ye Ri;Park, Yong Jin;Jung, Kyoung Ok;Sung, Hea Mi;Lee, Hyung Gun
Journal of the Korean Society of Food Science and Nutrition
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v.45
no.1
/
pp.1-11
/
2016
This study was conducted to investigate effect of the acetylcholinesterase inhibitor activity, the protective effect of the extract on SH-SY5Y cell death by $H_2O_2$, the memory improvement from scopolamine-induced rat. Moreover, the antioxidant activity of isorhamnetin from the dropwort (Oenanthe javanica) was investigated. Acetylcholinesterase inhibitor activity was highest (28.59%) in Hwasun O. javanica extract (H-OJE). H-OJE and Naju O. javanica extract (N-OJE) were not significantly different. SH-SY5Y cell death deceased to 37.23% and 36.68% for H-OJE and N-OJE, respectively, following treatment with the extracts. O. javanica extracts showed a protective effect against $H_2O_2$-induced neurotoxicity. Treatment with O. javanica extracts slightly improved scopolamine-induced (1 mg/kg, i.p.) memory impairment in rats. H-OJE contained the highest total phenolic and flavonoid contents of 117 mg/g and 30 mg gallic acid equivalents/g, respectively, and had a DPPH radical scavenging activity ($SC_{50}$) of $113.8{\mu}g/mL$ and ABTS radical scavenging activity of $48.2{\mu}g/mL$, which was higher than the other extracts. The thiobarbituric acid reactive substances value was highest (50.2%) in H-OJE. Antioxidant activity differed significantly among dropwort extracts. Isorhamnetin was known as one of the flavonoid and for having neuroprotective effect. So we analyzed acid-hydrolyzed O. javanica extract HPLC. The results were that peak at 14 min and spectrum of the extracts was consistent with standard solution. The results of LC/MS/MS analysis were that the extract and standard solution were confirmed total ion chromatogram at identical time, precursor ion was 317 $[M-H]^+$ m/z, product ion was 302 $[M-H]^+$ m/z. Overall, the results showed that the dropwort extract led to memory improvement and had antioxidant activity. Based on these finding, further research to investigate the production of ethanol extract of dropwort as a processed food is warranted.
Purpose : Transcranial electromagnetic stimulation(TMS) is a noninvasive method which stimulates the central nervous system through pulsed magnetic fields without direct effect on the neurons. Although the neurobiologic mechanisms of magnetic stimulation are unknown, the effects on the brain are variable according to the diverse stimulation protocols. This study aims to observe the effect of the magnetic stimulation with two different stimulation methods on the cultured hippocampal slices. Methods : We obtained brains from 8-days-old Spague-Dawley rats and dissected the hippocampal tissue under the microscope. Then we chopped the tissue into 450 µm thickness slices and cultured the hippocampal tissue by Stoppini's method. We divided the inserts, which contained five healthy cultured hippocampal slices respectively, into magnetic stimulation groups and a control group. To compare the different effects according to the frequency of magnetic stimulation, stimulation was done every three days from five days in vitro at 0.67 Hz in the low stimulation group and at 50 Hz in the high stimulation group. After N-methyl-D-aspartate exposure to the hippocampal slices at 14 days in vitro, magnetic stimulation was done every three days in one and was not done in another group. To evaluate the neuronal activity after magnetic stimulation, the $NeuN/{\beta}$-actin ratio was calculated after western blotting in each group. Results : The expression of NeuN in the magnetic stimulation group was stronger than that of the control group, especially in the high frequency stimulation group. After N-methyl-D-aspartate exposure to hippocampal slices, the expression of NeuN in the magnetic stimulation group was similar to that of the control group, whereas the expression in the magnetic non-stimulation group was lower than that of the control group. Conclusion : We suggest that magnetic stimulation increases the neuronal activity in cultured hippocamal slices, in proportion to the stimulating frequency, and has a neuroprotective effect on neuronal damage.
The nutritional components, antioxidant, and neuroprotective effects of water and a 50% methanol extract from litchi fruit pericarp were investigated. The most abundant mineral, amino acid, and fatty acid were K, proline, and palmitic acid, respectively. In addition, the total water phenolics and 50% methanol extracts were 8.02 and 12.28 mg/g, respectively. The DPPH, ABTS radical scavenging activities and ferric reducing antioxidant power of the water and 50% methanol extracts showed dose-dependent antioxidant activity. In a cell viability assay using MTT, almost all extracts showed a protective effect against $H_2O_2$-induced neurotoxicity, and lactate dehydrogenase leakage was also inhibited by the pericarp extracts. In particular, the 50% methanol extract showed a higher cell membrane protective effect than the water extract at the highest concentration. Consequently, these data suggest that litchi fruit pericarp can be utilized as an effective and safe functional food substances for natural antioxidants and may reduce the risk of neurodegenerative disorders.
Objectives : Neuronal changes that result from treadmill exercise for patients with Parkinson's disease(PD) have not been well documented, although some clinical and laboratory reports suggest that regular exercise may produce a neuroprotective effect and restore dopaminergic and motor functions. However, it is not clear if the improvements are due to neuronal alterations within the affected nigrostriatal region or result from a more general effect of exercise on affect areas and motivation. In this study, we demonstrate that motorized treadmill exercise improves the neuronal outcomes in rodent models of PD. Methods : We used a chronic mouse model of parkinsonism, which was induced by injecting male C57BL/6 mice with 10 doses(Every 12 hour) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (30 mg/kg) and probenecid (20 mg/kg) over 5 days. These mice were able to sustain an exercise training program on a motorized rodent treadmill at a speed of 18 m/min, $0^{\circ}$ of inclination, 40 min/day, 5 days/week for 4 weeks. At the end of exercise training, we extracted the brain and compared their neuronal and neurochemical changes with the control(saline and sedentary) mice groups. Synphilin protein is the substance that manifestly reacts with ${\alpha}$-synuclein. In this study, we used Synphilin as a manifest sign of recovery from neurodegeneration. We analyze the brain stems of the substantia nigra and striatum region using the western blotting technique. Results : There were no expression of synphilin in the saline-induced groups. The addition of MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) greatly accelerated synphilin expression which meant an aggregation of ${\alpha}$-synuclein. But, the MPTP-induced treadmill exercise group showed significantly lower expression than the MPTP-induced sedentary group. This means treadmill exercise has a definite effect on the decrease of ${\alpha}$-synuclein aggregation. Conclusions : In this study, our results suggest that treadmill exercise promoted the removal of the aggregation of ${\alpha}$-synuclein, resulting in protection against disease development and blocks the apoptotic process in the chronic parkinsonian mice brain with severe neurodegeneration.
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