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The fraction of horse chestnut seeds was named escins, which mainly consists of A, B, C, and D escin. Accumulating evidence suggests that escin exerts potent anti-inflammatory and anti-edematous effects. The effects of escin on inflammation and edema have been confirmed in various models. In a study in 1961, intravenous administration of escin was found to reduce acute edema in a rat paw. In the same study, escin was found to inhibit the increase in vascular permeability induced by egg white injection. Escin dose-dependently reduced the capillary permeability in chlo?roform-induced local inflammation in the abdominal skin surface of rabbits. The anti-inflammatory and anti-edematous effects of external use of escin were studied in carrageenan-induced paw edema and histamine-induced capillary perme?ability in rats. Escin gel decreased the contents of PGE2, TNF-α, and IL-1β, and reduced the raw edema and capillary permeability. The carrageenan-induced paw edema and pleuritis in bilaterally adrenalectomized rats were used to inves?tigate the anti-inflammatory effects of escin and glucocorticoid alone or combined. Co-administration of escin with corti?sone significantly reduced the volume of exudates and the number of white blood cells of exudates. The findings sug?gest escin can synergize with glucocorticoids to enhance their anti-inflammatory effect. The anti-inflammatory effect of escin was investigated in carrageenan-induced paw edema and acetic acid-induced capillary permeability in mice. Escin showed an anti-inflammatory effect, which is similar to that seen with dexamethasone treatment. However, escin showed a longer duration of the anti-inflammatory response than that of dexamethasone. Furthermore, escin had no signif?icant effects on spleen index, thymus index , proliferative capacity of splenocytes, lymphocyte count, and phagocytic rate. The findings suggest that escin is a potent anti-inflammatory drug with long-lasting anti-inflammatory effects without any immunosuppressive effects. Traditionally the mechanism of anti-inflammatory effect of escin is supposed to be rela?tive to release of PGF2α and corticosterone. The early studies showed that escin might promote the release of PGF2αand affect the pituitary adrenal system, stimulate the release of adrenocorticotropic hormone (ACTH) and glucocorticoid, which may explain its anti-inflammatory and anti-edema effects. Escin has glucocorticoid-like anti-inflammatory effect. However, escin did not exhibit an anti-inflammatory effect in low dose. Combination of suboptimal concentrations of escin with corticosterone inhibited the release of inflammatory factors including NO, TNF-αand IL-1βin the LPS-stimulated macrophage cells. Previous studies demonstrate that escin combined with glucocorticoid produced synergistic anti-inflammatory effects. The potential synergistic mechanisms may be associated with the property which escin regulates the glucocorticoid receptor (GR) signaling pathway. Escin can upregulate the expression of GR, promote the combina?tion of glucocorticoid and GR, then promote the activated GR transfer into the nucleus. Activated GR will inhibit the acti?vation of NF-κB directly, thus further inhibiting the expression of TNF-αand IL-1βand other inflammatory factors. Escin could inhibit 11β-HSD2 but not 11β-HSD1, thus decrease the metabolism of glucocorticoid. Escin and glucocorticoids have similar chemical structures. This indicate that one of the anti-inflammatory mechanisms of escin may be due to its stimulating GR by binding to it. Eacin might be a partial agonist of GR. A good many of researches have demonstrated the anti-inflammatory properties of escin, and shed light on the underlying mechanisms by which escin exerts these effects. Escin, as an oral or intravenous formulation, or a topical gel, inhibits inflammation, producing measurable improve?ments in edema and acute lung injury. Further clinical studies of escin are needed to demonstrate these properties in larger patient populations.
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OBJECTIVE To investigate the effect and mechanism of AngongNiuhuang Pill(AGNH) on neurological function and intestinal mucosal barrier in intracerebral hemorrhage (ICH). METHODS Male CD-1 mice were randomly divided into sham, ICH, AGNH 0.1 g·kg-1, AGNH 0.2 g·kg-1, and AGNH 0.4 g·kg-1groups. The ICH mice models were prepared by intrastriatal injection with collage-nase using a stereotaxic frame.Garcia test was used to evaluate the neurological function of mice.The brain water content was measured with dry/wet weight method.The permeability of intestinal mucosa was detected by FITC-D method. H&E staining was used to observe the pathological changes of intestine. The content of endotoxin in blood and the expressions of ZO-1,occludin in intestinewere also investigated.RESULTS After AGNH administration,the neurological score of mice was increased,and the brain water content was decreased(P<0.01).AGNH attenuated the ICH-induced increase of perme-ability of intestinal mucosa(P<0.01).Treatment with AGNHnot only alleviated the pathological changes of the intestine but alsoreduced the endotoxin content in blood (P<0.01).The expressions of ZO-1, occludinin AGNH groups were significantly increased compared with that of ICH group (P<0.05). CONCLUSION AGNH improves the neurological dysfunction in ICH mice and the mechanism of action is implicated in protecting the intestinal mucosa.
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OBJECTIVE Xingnaojing injection(XNJ)is an extracts of Angong Niuhuang Pill that is a well-known traditional Chinese medicine used for the treatment of septicemia and stroke.This study aims to investigate the effect of XNJ on intestinal mucosal barrier in septicemia and intracerebral hem-orrhage(ICH)mice models.METHODS The septicemia mice models were induced by intravenous in-jection with lipopolysaccharide(20 mg·kg-1).And the ICH mice models were made by intrastriatal injec-tion of bacterial collagenase. The septicemia animals were treated intravenously with XNJ at dose of 2.5,5,10,or 15 mL·kg-1.The ICH animals were treated intravenously with XNJ at dose of 10 mL·kg-1. Thereafter, the permeability of intestinal mucosa was assayed by FITC-D method. RESULTS Com-pared with the control group(44.72±4.30),the permeability of intestinal mucosa in the mice in septice-mia group (233.68±28.18) was significantly increased (P<0.01). Treatment with XNJ at dose of 5, 10, and 15 mL·kg-1reduced the permeability of intestinal mucosa (150.45 ± 17.52,139.21 ± 17.05,132.55 ± 18.88,respectively, P<0.01)except 2.5mL·kg-1(240.71±21.42,P>0.01);Compared with sham group (57.88±7.31),the permeability of intestinal mucosa in the mice of ICH(282.25±23.78)was significantly in-creased(P<0.01). Treatment with XNJ (10 mL·kg-1)in the mice of ICH group ameliorated the change of permeability in intestinal mucosa (148.83±15.86, P<0.01). CONCLUSION XNJ exhibits the protec-tive effect on the intestinal mucosal barrier in septicemia and ICH, which will prevent the endotoxin to penetrate the intestinal mucosa and then to enter the circulation in infections and stress.
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OBJECTIVE This work aimed to investigate the anti-rheumatoid arthritic effect of gentio-picroside from Gentiana macrophylla Pall using an animal model of adjuvant induced arthritis. METH-ODS Adjuvant arthritis was induced in fifty SD male rats,which were randomly divided into five groups (n=10):control(0.5% CMC-Na)group,AIA(rats with CFA)group,dexamethasone(1 mg·kg-1)group, gentiopicroside(50 mg·kg-1)group,and gentiopicroside(100 mg·kg-1)group.Rats were administered intragastrically with drugs or CMC-Na once a day for a period of 2 weeks.Paw swelling,arthritic index, histological changes were assessed to evaluate the anti-arthritic effect.Weight growth,spleen and thymus indexes were also investigated in.RESULTS Gentiopicroside at dose of 100 mg·kg-1significantly inhibited the secondary paw swelling(P<0.05)and arthritis index(P<0.05),decreased synovial inflammatory infil-tration, synovial hyperplasia and bone erosion. Furthermore, gentiopicroside showed no immunosup-pressive adverse effects in body weight, index of spleen and thyums compared with dexamethasone administration (P<0.05, P<0.01). CONCLUSION Gentiopicroside possessed anti-arthritic efficacy in AIA rats without immunosuppressive effects.
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OBJECTIVE To explore the effects and underlying mechanism of Jieyu Anshen granule (JY) in chronic unpredictable mild stress (CUMS)-treated rats after ischemic stroke. METHODS A rat model of post-stroke depression(PSD)was developed by additional CUMS procedures after middle cere-bral artery occlusion(MCAO).Sprague-Dawley rats were given 1 g·kg-1and 3 g·kg-1of JY by gastrogavage for 4 weeks.Escitalopram(10 mg·kg-1)served as a reference drug.Behavioral tests including sucrose preference test, forced swim test and open-field test were performed to evaluate the antidepressant effects. Levels of norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) in rat brain were assayed. The anti-inflammatory activity was evaluated by measuring TNF-α and IL-1β in brain. Serum adrenocorticotropic hormone (ACTH) and corticosterone (CORT) were estimated as indices of hypothalamic-pituitary-adrenal (HPA) axis activity. Western blot analysis was used to evaluate hippo-campal expression of the 5-HT1A receptor (5-HT1AR) and brain-derived neurotrophic factor (BDNF). RESULTS PSD rats exhibited decreased sucrose consumption and motor activity, increased immobility time (P<0.01). JY treatment reversed the depressive behaviors in PSD rats (P<0.05, P<0.01). Treat-ment with JY resulted in significantly increased levels of NE, DA and 5-HT in the hippocampus and prefrontal cortex (P<0.05, P<0.01), and increased expression of 5- HT1AR and BDNF in the hippocampus(P<0.01). JY treatment significantly down-regulated the levels of TNF-α and IL-1β in hippocampus andprefrontal cortex (P<0.05). Treatment with JY also resulted in significantly decreased ACTH and CORTin serum which had been increased (P<0.05). CONCLUSION These findings suggest that JY treat-ment could ameliorate PSD, and the effects are likely ascribed to inhibiting HPA axis hyperfunction andinflammatory, up-regulating the levels of neurotransmitters (NE, DA and 5-HT), and the expression ofhippocampal 5-HT1AR and BDNF.
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<p><b>AIM</b>To investigate the protective effect of hydroxysafflor yellow A (HSYA), a soluble element extracted from Carthamus tinctorius L., on focal cerebral ischemia in rats.</p><p><b>METHODS</b>Focal cerebral ischemia in male Wistar-Kyoto (WKY) rats were induced by permanent middle cerebral artery occlusion (MCAO). Three doses of 1.5, 3.0 and 6.0 mg x kg(-1) of HSYA were administrated to three groups of rats, separately, via sublingular vein injection 30 min after the onset of ischemia. 24 h after ischemia in rats, neurological deficit scores were evaluated and the infarction area of brain was assessed by quantitative image analysis. The in vitro neuroprotective effect of HSYA was tested in cultured fetal cortical neurons exposed to glutamate and sodium cyanide (NaCN).</p><p><b>RESULTS</b>HSYA at doses of 3.0 and 6.0 mg x kg(-1) exerted significant neuroprotective effects on rats with focal cerebral ischemic injury as expressed by neurological deficit scores and reduced the infarct area as compared with saline group, and the potency of HSYA at dose of 6.0 mg x kg(-1) was similar to that of 0.2 mg x kg(-1) of nimodipine. In vitro studies, HSYA significantly inhibited neurons damage induced by exposure to glutamate and NaCN in cultured fetal cortical cells.</p><p><b>CONCLUSION</b>HSYA has potential neuroprotective action against focal cerebral ischemia in rats and cultured rat fetal cortical neurons as well.</p>
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Animais , Masculino , Ratos , Comportamento Animal , Encéfalo , Patologia , Isquemia Encefálica , Patologia , Carthamus tinctorius , Química , Células Cultivadas , Córtex Cerebral , Biologia Celular , Chalcona , Farmacologia , Ácido Glutâmico , Infarto da Artéria Cerebral Média , L-Lactato Desidrogenase , Metabolismo , Neurônios , Biologia Celular , Metabolismo , Fármacos Neuroprotetores , Farmacologia , Plantas Medicinais , Química , Quinonas , Farmacologia , Ratos Endogâmicos WKY , Cianeto de SódioRESUMO
<p><b>OBJECTIVE</b>To study the protective effect of ligusticum chuanxiong phthalides on cerebral ischemia in rats and its related mechanism of action.</p><p><b>METHOD</b>Middle cerebral artery occlusion (MCAO) model, thrombosis formation, platelet aggregation and hemorrheological parameters were measured to evaluate the protective effect of ligusticum chuanxiong phthalides.</p><p><b>RESULT</b>Ligusticum chuanxiong phthalides could markedly decrease the infarct size and behavior deficits score, inhibit the thrombus formation and platelet aggregation, ameliorate hemorrheological parameters with a dose-dependent manner in rats.</p><p><b>CONCLUSION</b>Ligusticum chuanxiong phthalides has protective effects on focal cerebral ischemia in rats, and its mechanism may be relevant to its inhibition of platelet-dependent thrombosis and amelioration of hemorrheological parameters.</p>
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Animais , Masculino , Ratos , Benzofuranos , Farmacologia , Viscosidade Sanguínea , Isquemia Encefálica , Sangue , Patologia , Relação Dose-Resposta a Droga , Hematócrito , Infarto da Artéria Cerebral Média , Sangue , Patologia , Ligusticum , Química , Fármacos Neuroprotetores , Farmacologia , Plantas Medicinais , Química , Agregação Plaquetária , Ratos Wistar , Trombose VenosaRESUMO
<p><b>AIM</b>To study the effects of hydroxysafflor yellow A (HSYA) on the mitochondrial function of cortex mitochondrial during cerebral ischemia in rats.</p><p><b>METHODS</b>Rat focal cerebral ischemia model in rats was established by ligation of middle cerebral central artery. Cortex mitochondria were isolated and prepared for the measurement of membrane fluidity, swelling, respiratory function, activities of mitochondrial respiratory enzymes and superoxide dismutase (SOD), contents of phospholipid, malondial dehyde (MDA) and Ca2+ to evaluate the function of mitochondria.</p><p><b>RESULTS</b>Focal cerebral ischemia resulted in severe neuronal mitochondrial injuries, which could be alleviated by i.v. HSYA (10, 20 mg x kg(-1)), and nimodipine (Nim, 1.0 mg x kg(-1)). The swelling of mitochondria was ameliorated, the decomposability of membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased, HSYA also significantly inhibited the decrease in the activities of respiratory enzymes and SOD of mitochondria, and the increase in MDA and Ca2+ levels caused by cerebral ischemia in rats.</p><p><b>CONCLUSION</b>HSYA showed a protective action against the cortex mitochondrial injuries in rats induced by cerebral ischemia. The mechanisms may be derived from reducing lipid peroxides, inhibiting Ca2+ overload, scavenging free radicals and improving the energy metabolism.</p>
