芒果苷对慢性炎症MAPK信号通路的影响

目的:探讨芒果苷调控MAPK信号通路而抑制脂多糖(LPS)诱导慢性炎症的机制.方法:60只SD大鼠随机分为正常组、模型组、阳性药泼尼松5 mg·kg-1·d-1组与芒果苷200,100,50 mg·kg-1·d-1组.以LPS间断尾静脉注射建立慢性炎症模型,进行大鼠全血白细胞计数,ELISA测定血清肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)、可溶性细胞间黏附分子1(sICAM-1);RT-PCR检测白细胞MAPK信号通路p8,ERK,JNK基因表达.结果:与模型组比较,芒果苷200 mg·kg-1组全血白细胞总数与血清TNF-α,IL-6,sICAM-1水平明显降低(P＜0.05),白细胞ERK,JNK基因表达下调(P＜0.05),p38基因表达无统计学差异.结论:芒果苷显著抑制LPS诱导慢性炎症的作用机制与其下调MAPK信号通路中ERK,JNK基因表达而降低炎症因子水平有关.     

基于NF-κB通路的芒果苷干预脂多糖诱导的细胞炎症作用机制研究

目的研究芒果苷对小鼠巨噬细胞RAW 264.7的保护作用,并探讨其可能的作用机制。方法采用脂多糖(LPS)诱导RAW 264.7细胞炎症模型。实验分四步:(1)细胞存活率实验分5组,即:空白组、LPS组、LPS+不同浓度(50、100、150μg/mL)芒果苷组。MTT法检测细胞存活率。(2)一氧化氮(NO)、白介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)及白介素6(IL-6)分泌实验分6组,即:空白组、LPS组、LPS和不同浓度芒果苷(50、100、150μg/mL)组、LPS+BAY 11-7082[核因子κB(NF-κB)抑制剂]组。Griess法检测NO分泌量,ELISA法检测IL-1β、TNF-α及IL-6分泌量。(3)诱导型一氧化氮合酶(iNOS)与环氧化酶-2(COX-2)mRNA及蛋白表达实验分组同细胞存活率实验。实时荧光定量PCR检测iNOS及COX-2 mRNA水平变化,Western blot检测iNOS及COX-2蛋白表达水平。(4)细胞质、细胞核中NF-κB表达实验分3组,即:空白组、LPS组、LPS+150μg/mL(终末浓度)芒果苷共处理组, Western blot检测细胞质、细胞核中NF-κB p65蛋白表达量。结果 (1)与空白组比较,LPS组显著降低RAW264.7细胞存活率(P0.05);与LPS组比较,50～150μg/mL芒果苷预处理对RAW264.7细胞增殖无显著影响(P0.05)。(2)与空白组比较,LPS组NO、IL-1β、TNF-α、IL-6分泌量显著升高(P0.05);与LPS组比较,除50μg/mL芒果苷预处理组NO、TNF-α分泌量无显著变化外(P0.05),其余各组NO、IL-1β、TNF-α、IL-6分泌量均显著降低(P0.05)。(3)与空白组比较,LPS组iNOS、COX-2 mRNA及蛋白表达量均显著升高(P0.05);与LPS组比较,50～150μg/mL芒果苷预处理组iNOS、COX-2 mRNA及蛋白表达显著下降(P0.05)。(4)与空白组比较,LPS组细胞质中NF-κB p65蛋白量减少,细胞核中则增多(P0.05);与LPS组比较,150μg/mL芒果苷预处理组细胞质中NF-κB p65蛋白量升高,细胞核中蛋白量减少(P0.05)。结论芒果苷可能通过抑制NF-κB信号通路,而抑制iNOS、COX-2表达及相关炎症因子的分泌,干预LPS诱导的RAW264.7细胞炎症。     

CIA模型大鼠关节滑膜细胞NF-κB信号表达及姜酚胶丸的调控作用研究

目的探讨姜酚胶丸对胶原诱导性关节炎大鼠关节滑膜细胞NF-κB信号表达及炎症因子TNF-α、IL-1和IL-1β影响的研究。方法将6周龄雌性Wistar大鼠随机分为空白对照组、模型组、姜酚胶丸治疗组和雷公藤多苷对照组,每组10只。制备CIA模型,采用Western blot法检测关节滑膜细胞NF-κB/P65、IκBα表达,ELISA法检测大鼠血清TNF-α、IL-1、IL-1β表达情况。结果 1姜酚胶丸治疗组及雷公藤多苷对照组可下调CIA大鼠滑膜细胞NF-κB/P65、IκBα的表达,与模型组比较均有显著性差异(P0.01);2姜酚胶丸治疗组及雷公藤多苷对照组可下调CIA大鼠血清TNF-α、IL-1、IL-1β的表达,与模型组比较均有显著性差异(P0.01)。结论姜酚胶丸可通过降低CIA大鼠关节滑膜细胞NF-κB/P65、IκBα信号蛋白表达,显著下调CIA大鼠血清致炎因子TNF-α、IL-1、IL-1β表达,达到缓解炎症的作用。     

复方银花解毒颗粒对脂多糖致幼龄大鼠急性肺炎模型的抗炎作用及TLR4/NF-κB/NLRP3信号通路的影响

目的研究复方银花解毒颗粒(Compound Yinhua Jiedu Granule)对脂多糖(lipopolysaccharide,LPS)致幼龄大鼠急性肺炎模型的抗炎作用及Toll样受体4(Tolllikereceptor4,TLR4)/核转录因子-κB(nuclearfactor-κB,NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)信号通路的影响。方法将120只幼龄大鼠随机分为6组,分别为对照组、模型组、布洛芬颗粒组(0.8g/kg)及复方银花解毒颗粒低、中、高剂量(1.25、2.5、5 g/kg)组,ig给药1周,末次给药1 h后尾iv LPS(1 mg/kg)制备急性肺炎模型,6 h后采用麻醉后颈椎脱臼处死。采用ELISA试剂盒检测各组大鼠肺泡灌洗液及血清中炎症因子白细胞介素-1β(interleukin-1β,IL-1β)、IL-17、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)水平的变化;HE染色观察肺组织形态学变化;运用免疫组化染色法检测肺组织TLR4,入核NF-κB和NLRP3蛋白的表达,Westernblotting法检测肺组织中TLR4、磷酸化NF-κB(p-NF-κB)、磷酸化核转录因子-κB抑制蛋白α(nuclear factor-κB inhibitor proteinα,p-IκBα)和NLRP3蛋白的表达。结果复方银花解毒颗粒预处理对LPS诱导幼龄大鼠急性肺损伤具有较强的保护作用,可降低模型大鼠肺泡灌洗液及血清中炎症因子IL-1β、IL-17、TNF-α的水平,减少肺组织中TLR4、NF-κB的激活和NLRP3蛋白的表达。结论复方银花解毒颗粒对LPS致幼龄大鼠急性肺炎模型具有抗炎作用,其机制可能与下调TLR4/NF-κB/NLRP3炎症信号通路有关。     

藿朴夏苓汤对HBZY-1细胞及DN大鼠NF-κB炎症通路的影响

目的研究藿朴夏苓汤(HPXLT)对体内外核转录因子-κB(NF-κB)炎症通路的影响,探讨HPXLT对糖尿病肾病(DN)的作用机制。方法体外研究:采用脂多糖(LPS)刺激大鼠肾小球系膜细胞(HBZY-1)及Hep G2细胞,观察HPXLT对细胞炎症因子包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)含量及p-p65蛋白表达的影响,以免疫荧光法观察Hep G2细胞的NF-кB p65转核作用。体内研究:采用腹腔注射链脲佐菌素(STZ,65 mg·kg~(-1))方法制备DN大鼠模型。将大鼠随机分为对照组,模型组,HPXLT高、中、低剂量组(2,1,0.5 g·kg~(-1))和格列本脲组(5 mg·kg~(-1)),连续灌胃给药6周。采用ELISA法测定细胞上清液或大鼠血清TNF-α、IL-1β和IL-6的水平;Western Blot法测定HBZY-1细胞或大鼠肾脏p65、p-p65、TNF-α和IL-1β的蛋白表达水平。结果体外结果:与对照组比较,LPS组的p-p65蛋白表达显著增强,炎症因子TNF-α、IL-1β和IL-6的含量显著升高(P0.01);与LPS组比较,HPXLT各剂量组的p-p65蛋白表达水平显著下调,炎症因子TNF-α、IL-1β和IL-6的含量显著降低(P0.05,P0.01);免疫荧光显示LPS诱导的炎症能促进NF-кB p65的转核,而HPXLT可显著抑制NF-кB p65转核作用。体内结果:与对照组比较,模型组大鼠血清的TNF-α、IL-1β、IL-6炎症因子水平及肾脏的IL-1β、TNF-α、p-p65蛋白表达水平均显著升高(P0.01)。与模型组比较,各给药组大鼠血清的TNF-α、IL-1β和IL-6炎症因子水平均显著降低(P0.05,P0.01),HPXLT高、中剂量组的IL-1β、TNF-α及p-p65蛋白表达水平均明显下调(P0.05,P0.01),各组之间的总NF-кB p65蛋白表达水平无明显改变,差异无统计学意义(P0.05)。结论 HPXLT可能通过抑制NF-κB炎症通路的表达,从而降低DN肾脏的炎症。     

芒果苷对脂多糖诱导的慢性炎症大鼠MAPK通路及血清细胞因子的影响

目的 探讨芒果苷对脂多糖(LPS)诱导慢性炎症大鼠模型中MAPK通路的调控作用及其对血清细胞因子表达谱的影响.方法 以间断尾iv小剂量LPS(200 μg/kg)制备慢性炎症大鼠模型.模型大鼠随机分为模型组,泼尼松(5 mg/kg)组与芒果苷高、中、低剂量(200、100、50 mg/kg)组,每天ig给药1次,共给药4周.第4周给药末,分别以RT-PCR、蛋白免疫印迹法检测白细胞MAPK通路p38、ERK、JNK基因表达与蛋白磷酸化水平,以抗体微阵列蛋白质芯片检测血清细胞因子表达谱.结果 与模型组比较,芒果苷高剂量组白细胞ERK、JNK基因表达以及ERK蛋白磷酸化受到明显抑制,血清细胞间黏附分子1 (ICAM-1)、单核细胞趋化蛋白1(MCP-1)、中性粒细胞趋化因子1(INC-1)与血小板源性生长因子(PDGF)水平显著降低.结论 芒果苷通过调控白细胞MAPK通路ERK、JNK基因表达以及ERK蛋白磷酸化,降低血清趋化细胞因子水平,从而发挥抗LPS诱导的慢性炎症作用.     

左归降糖解郁方对糖尿病并发抑郁症大鼠海马趋化因子CX3C受体1和炎症因子的影响

目的探讨左归降糖解郁方治疗糖尿病并发抑郁症的可能作用机制。方法 40只SD大鼠随机分为正常组,模型组,西药组及中药高、低剂量组,每组8只。除正常组外,其余各组通过高脂乳剂灌胃、尾静脉注射链脲佐菌素和慢性应激建立糖尿病并发抑郁症模型。应激造模的同时西药组给予二甲双胍0.18 g/(kg·d)+氟西汀1.8 mg/(kg·d)灌胃;中药高、低剂量组分别给予左归降糖解郁方20.53、10.26 g/(kg·d)灌胃,正常组和模型组给予等体积蒸馏水灌胃,均每日1次。灌胃28天后,检测大鼠海马中炎症因子白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的含量,小胶质细胞的标记物离子钙接头蛋白分子1(Iba-1)、趋化因子CX3C受体1(CX3CR1)、核转录因子κB(NF-κB)及磷酸化核转录因子κB(p NF-κB)蛋白表达。结果与正常组比较,模型组大鼠海马IL-1β、TNF-α表达及其小胶质细胞Iba-1、CX3CR1、p NF-κB表达均显著升高(P0.01)。与模型组比较,西药组及中药高剂量组大鼠海马IL-1β和TNF-α表达及其小胶质细胞Iba-1、CX3CR1、p NF-κB表达均显著下降,中药低剂量组IL-1β、TNF-α、CX3CR1和p NF-κB表达亦下降(P0.05或P0.01)。与中药高剂量组比较,中药低剂量组CX3CR1及p NF-κB表达显著升高(P0.05或P0.01)。结论左归降糖解郁方可显著降低糖尿病并发抑郁症大鼠的海马炎症水平,该作用可能与其抑制小胶质细胞激活并下调CX3CR1和NF-κB表达有关。     

苓桂术甘汤对慢性心衰模型大鼠心肌组织TNF-α及血清NF-κB和IL-1β的影响

目的 观察苓桂术甘汤对慢性心力衰竭模型大鼠心肌组织肿瘤坏死因子-α(TNF-α)蛋白及mRNA表达、血清核因子-κB (NF-κB)、白细胞介素-1β(IL-1β)水平的影响,探讨苓桂术甘汤防治慢性心衰的作用机制.方法 采用冠状动脉结扎法制备慢性心衰大鼠模型,造模4周后将模型大鼠随机分为模型组,卡托普利(4.375 mg/kg)阳性对照组,苓桂术甘汤低、中、高剂量(生药2.1、4.2、8.4 g/kg)组,另设假手术组,每天给药1次,连续给药4周.Westem blotting、RT-PCR法分别检测各组大鼠心肌组织TNF-α蛋白及mRNA的表达,ELISA法检测血清中NF-κB、IL-1β水平.结果 与假手术组相比,模型组大鼠心肌组织TNF-α蛋白及mRNA表达增强,血清NF-κB、IL-1β水平显著升高(P＜0.01);与模型组相比,苓桂术甘汤及卡托普利均能显著抑制模型大鼠心肌组织TNF-α蛋白及mRNA表达、降低模型大鼠血清NF-κB、IL-1β水平(P＜0.05、0.01).结论 苓桂术甘汤干预慢性心衰的机制与其调节细胞因子网络有关.     

黄芪甲苷通过TLR4/NF-κB通路改善脂多糖诱导的急性血管内皮损伤

目的:研究黄芪甲苷对脂多糖(LPS)诱导的急性血管内皮损伤的保护作用并探讨其可能分子机制。方法:在动物实验中,黄芪苷治疗组经连续灌胃给药14天后,除正常组外,其余各组均通过腹腔注射脂多糖(10mg/kg)以建立急性血管内皮损伤模型,DMT系统记录张力以评估血管舒张功能,ELISA法检测大鼠血清TNF-α和IL-6的含量,免疫组化法检测大鼠血管NF-κB p65蛋白的表达和分布,Western-blot法检测主动脉TLR4蛋白的表达;细胞水平采用CCK-8试剂盒检测人脐静脉内皮细胞(HUVEC)的增殖能力;ELISA法检测HUVEC上清液TNF-α和IL-6的含量;硝酸还原酶法检测HUVEC上清液一氧化氮(NO)的含量;Western-blot法检测HUVEC TLR4和核NF-κB p65蛋白的表达。结果:在动物水平,与模型组相比,40mg/kg和80mg/kg黄芪甲苷均能显著改善血管的舒张功能;40mg/kg以上组黄芪苷降低血清TNF-α和IL-6的含量、下调TLR4和NF-κB p65的表达水平。在细胞水平,与模型组相比,50μM和100μM黄芪甲苷能显著促进HUVEC的增殖能力,降低HUVEC上清液中TNF-α和IL-6的含量,增加上清液中NO的释放量,下调TLR4和核NF-κB p65蛋白的表达,而且,黄芪甲苷对LPS诱导的HUVEC损伤作用与NF-κB p65抑制剂相似。结论:黄芪甲苷对LPS诱导的急性血管内皮损伤具有保护作用,其可能通过TLR4/NF-κB p65信号通路发挥作用。     

从细胞因子风暴探讨热毒宁注射液抗大鼠急性肺损伤作用机制

目的通过细胞因子风暴探讨热毒宁注射液对脂多糖(LPS)致大鼠急性肺损伤(ALI)的治疗作用及机制。方法采用LPS按6 mg/kg对SD大鼠气管内滴注制备ALI模型,观察热毒宁注射液3个剂量(10.16、5.08、2.54 g/kg)组和阳性对照药地塞米松注射液(0.5 mg/kg)iv给药后对大鼠肺组织匀浆白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、IL-4、IL-6、IL-8、IL-10、细胞间黏附分子-1(ICAM-1)、核转录因子-κB(NF-κB)水平及肺组织形态学的影响。结果热毒宁注射液能够降低ALI模型大鼠肺脏IL-1β、TNF-α、IL-4、IL-6、IL-8、IL-10、ICAM-1、NF-κB水平,改善大鼠肺组织形态学变化。结论热毒宁注射液可改善肺组织病理变化,减轻LPS致ALI过程中炎性介质的生成和释放可能是治疗ALI的重要机制。     

Effect of mangiferin on hyperglycemia and atherogenicity in streptozotocin diabetic rats

In the present study, the effect of mangiferin (a xanthone glucoside, isolated from the leaves of Mangifera indica) on the atherogenic potential of streptozotocin (STZ)-diabetes was investigated. In addition, the effect of mangiferin on oral glucose tolerance in glucose-loaded normal rats was also determined. The chronic intraperitoneal (i.p.) administration of mangiferin (10 and 20 mg/kg) once daily (o.d.) for 28 days exhibited antidiabetic activity by significantly lowering fasting plasma glucose level at different time intervals in STZ-diabetic rats. Further, mangiferin (10 and 20 mg/kg, i.p.) showed significant antihyperlipidemic and antiatherogenic activities as evidenced by significant decrease in plasma total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C) levels coupled together with elevation of high-density lipoprotein cholesterol (HDL-C) level and diminution of atherogenic index in diabetic rats. In addition, the chronic administration of mangiferin (10 and 20 mg/kg, i.p.) for 14 days significantly as well as markedly improved oral glucose tolerance in glucose-loaded normal rats suggesting its potent antihyperglycemic activity. The accumulating evidences suggest that both pancreatic and extrapancreatic mechanisms might be involved in its antidiabetic or antihyperglycemic action. In conclusion, the present study demonstrates that mangiferin possesses significant antidiabetic, antihyperlipidemic and antiatherogenic properties thus suggesting its beneficial effect in the treatment of diabetes mellitus associated with hyperlipidemia and related cardiovascular complications.     

Mangiferin Attenuates Renal Fibrosis Through Down‐Regulation of Osteopontin in Diabetic Rats

This study was designed to investigate the effects of mangiferin on renal fibrosis, osteopontin production, and inflammation in the kidney of diabetic rats. Diabetes was induced through the single administration of streptozotocin (55 mg/kg, i.p.). Diabetic rats were treated with mangiferin (15, 30, and 60 mg/kg/day, i.g.) for 9 weeks. The kidney was fixed in 10% formalin for glomerulus fibrosis examination using Masson trichrome staining. Kidney and blood were obtained for assays of the associated biochemical parameters. Chronic mangiferin treatment prevented renal glomerulus fibrosis evidenced by decreases in Mason‐stained positive area of glomeruli, protein expression of type IV collagen, and α‐smooth muscle actin in the kidney of diabetic rats, in comparison with decreases in mRNA and protein expression of osteopontin as well as protein expression of cyclooxygenase 2 and NF‐кB p65 subunit in the renal cortex of diabetic rats. Moreover, mangiferin reduced the levels of interleukin 1β in both the serum and the kidney of diabetic rats. Our findings demonstrate that mangiferin prevents the renal glomerulus fibrosis of diabetic rats, which is realized through the suppression of osteopontin overproduction and inflammation likely via inactivation of NF‐кB. Copyright © 2014 John Wiley & Sons, Ltd.     

Experimental pharmacokinetics of biologically active plant phenolic compounds. I. Pharmacokinetics of mangiferin in the rat

The pharmacokinetics of mangiferin (the main component of the drug ‘Alpizarin’) was studied by HPLC in rats after intravenous injection of the drug in a single dose of 0.3, 1, 3, 10 and 30 mg/kg and after its oral administration in a single dose of 50–500 mg/kg. It was shown that the mangiferin pharmacokinetics for the above dose levels was nonlinear, and within each dose could be described by a two-compartmental model. Its nonlinearity might be associated with saturated binding and metabolism of the compound.     

Synergistic antiinflammatory effects of pinitol and glucosamine in rats

This study evaluated the antiinflammatory activities of pinitol and glucosamine either alone or in combination against carrageenan- and cotton pellet-induced acute and subacute inflammation in rats. Five groups were included in each of the acute and subacute inflammation studies: the vehicle control group, positive control group (aminopyrine 100 mg/kg), pinitol group (20 mg/kg), glucosamine group (25 mg/kg) and a pinitol (20 mg/kg) and glucosamine (25 mg/kg) combination group. When 20 mg/kg of pinitol was administered to the rats, paw edema induced by the carrageenan injection was significantly suppressed and the level of granuloma formation induced by the cotton pellet implantation was slightly reduced. When 25 mg/kg of glucosamine was administered, paw edema caused by the acute inflammation was slightly reduced and the level of granuloma formation caused by the subacute inflammation was strongly suppressed. Although the combined application of pinitol and glucosamine did not have an additional antiinflammatory effect on the paw edema caused by acute inflammation, it did have an increased antiinflammatory effect on the formation of granuloma induced by subacute inflammation. Therefore, pinitol and glucosamine have an antiinflammatory effect on acute and subacute conditions. Moreover, a synergistic antiinflammatory effect against subacute inflammation was observed when the two chemicals were administered in combination.     

Role of mangiferin on biochemical alterations and antioxidant status in isoproterenol-induced myocardial infarction in rats

The current study dealt with the protective role of mangiferin, a polyphenol from Mangifera indica Linn. (Anacardiaceae), on isoproterenol (ISPH)-induced myocardial infarction (MI) in rats through its antioxidative mechanism. Subcutaneous injection of ISPH (200 mg/kg body weight in 1 ml saline) to rats for 2 consecutive days caused myocardial damage in rat heart, which was determined by the increased activity of serum lactate dehydrogenase (LDH) and creatine phosphokinase isoenzymes (CK-MB), increased uric acid level and reduced plasma iron binding capacity. The protective role of mangiferin was analyzed by triphenyl tetrazolium chloride (TTC) test used for macroscopic enzyme mapping assay of the ischemic myocardium. The heart tissue antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase and glutathione reductase activities, non-enzymic antioxidants such as cerruloplasmin, Vitamin C, Vitamin E and glutathione levels were altered in MI rats. Upon pretreatment with mangiferin (100 mg/kg body weight suspended in 2 ml of dimethyl sulphoxide) given intraperitoneally for 28 days to MI rats protected the above-mentioned parameters to fall from the normal levels. Activities of heart tissue enzymic antioxidants and serum non-enzymic antioxidants levels rose significantly upon mangiferin administration as compared to ISPH-induced MI rats. From the present study it is concluded that mangiferin exerts a beneficial effect against ISPH-induced MI due to its antioxidant potential, which regulated the tissues defense system against cardiac damage.     

芒果苷抑制哮喘小鼠气道炎症的机制

目的:观察芒果苷对哮喘小鼠气道炎症的影响,探讨芒果苷平喘的作用机制.方法:将72只4～5周SPF级BALB/c雌性小鼠随机分为正常对照组、模型对照组、地塞米松阳性对照组(0.001 25 g·kg-1)、芒果苷高、中、低剂量组(0.4,0.2,0.1 g·kg-1).采用卵白蛋白(OVA)致敏和激发构建小鼠哮喘模型,收集支气管肺泡灌洗液(BALF)进行细胞计数及分类;肺组织病理切片HE染色观察炎性细胞浸润情况;采用ELISA法检测小鼠血清中OVA特异性IgE( OVA-sIgE)和BALF中白三烯C4(LTC4),前列腺素D2(PGD2)的含量.结果:芒果苷高、中、低剂量组BALF中嗜酸性粒细胞(EOS)比例由模型组(6.57±1.44)％降低为(1.63±0.43,2.72±0.83,4.11 ±1.08)％(P＜0.01～P＜0.05);芒果苷高、中剂量组BALF中白细胞总数由模型组( 83.25±10.19)×105/mL减少为(25.66±6.16,53.38±9.19)×105/mL(P ＜0.01);芒果苷各剂量均可不同程度的改善肺组织的病理学改变,减轻气道炎症;芒果苷高、中、低剂量组血清中OVA-sIgE含量由模型组(0.26±0.04) ng·mL-1降低为(0.10±0.04,0.12 ±0.02,0.18 ±0.03) ng·mL-1(P＜0.01);芒果苷高剂量组BALF中PGD2水平由模型组(74.36±22.72) ng·mL-1降低为(60.30±12.19)ng·mL-1(P＜0.05),而芒果苷中、低剂量组对PGD2的降低无统计学差异;芒果苷各剂量对LTC4水平有降低趋势.结论:芒果苷可通过减少EOS浸润、小鼠体内OVA-sIgE和PGDz含量,抑制哮喘小鼠的气道炎症,在治疗哮喘方面有潜在的应用前景.     

生 盐知母水煎液中芒果苷在大鼠体内的组织分布

目的:考察生、盐知母水煎液中芒果苷在大鼠体内的组织分布情况,探讨盐知母引药入肾的作用机制。方法:将40只大鼠随机分为对照组、生知母(10 g·kg^-1)组、盐知母(10 g·kg^-1)组、芒果苷(200 mg·kg^-1)组,灌胃给药2 h后处死,立即解剖采集心、肝、脾、肺、肾组织,采用高效液相色谱法(HPLC)测定组织样品中的芒果苷含量。结果:方法专属性、日内和日间精密度、稳定性及提取回收率均符合生物样品分析要求;各组织样本在检测浓度范围内呈良好线性关系;生、盐知母及芒果苷组大鼠给药2 h内芒果苷主要集中在肺、肾组织中,含量从高到低的顺序为肺>肾>脾>肝>心。结论:生、盐知母和芒果苷组大鼠体内芒果苷均集中分布在肺、肾组织中,与知母的归经特点相符。生、盐知母组大鼠体内芒果苷在肺、肾组织中的含量明显高于芒果苷组,但生、盐知母组大鼠各组织中芒果苷含量差异无统计学意义。     

角黄素对脂多糖诱导急性肺损伤小鼠模型免疫功能的影响

目的:研究角黄素对脂多糖(LPS)所致小鼠急性肺损伤(ALI)免疫功能的保护作用。方法:将雄性昆明种小鼠60只,随机分为正常对照组、ALI模型组、地塞米松阳性对照组(15mg/kg)以及角黄素低、中、高剂量组(10mg/kg、15mg/kg、20mg/kg)共6组。不同剂量角黄素给大鼠连续灌胃30d后,腹腔注射脂多糖6.0mg/kg建立ALI模型。在注射后6h,收集腹主动脉血并进行左侧支气管肺泡原位灌洗以收集灌洗液,测定血中淋巴细胞亚群(CD3+、CD4+、CD8+)、肿瘤坏死因子α(TNF-α)、白细胞介素8(IL-8)及丙二醛(MDA)及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性;测定各组的肺湿重/干重比、肺组织中性粒细胞髓过氧化物酶(MPO)含量及肺组织匀浆TNF-α、白细胞介素10(IL-10)含量。结果:角黄素各剂量组均能降低因LPS诱发的血TNF-α、IL-8、MPO、MDA含量与肺组织湿重/干重比的升高,同时抑制肺组织IL-10含量、血SOD与GSH-Px活性的降低,改善血中淋巴细胞亚群分布。结论:角黄素对LPS所致急性肺损伤小鼠免疫功能具有预防性保护作用。     

Mechanism of protective action of mangiferin on suppression of inflammatory response and lysosomal instability in rat model of myocardial infarction

Lysosomal instability has been suggested as a major factor in the development of cellular injury during myocardial necrosis through the formation of inflammatory mediators. The present study was designed to investigate the effect of mangiferin on lysosomal hydrolases and TNF‐α production during isoproterenol (ISPH) induced myocardial necrosis in rats. The rats given ISPH (200 mg/kg body weight twice, subcutaneous) for 2 days showed a significant increase in plasma TNF‐α production, serum and heart lysosomal hydrolases activity. ISPH administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin‐D and β‐glucuronidase in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with mangiferin (100 mg/kg body weight, intraperitoneally) for 28 days, significantly prevented the alterations and restored the enzyme activities to near‐normal status. These findings demonstrate that mangiferin could preserve lysosomal integrity through decrease in the inflammatory process and hence establish the cardioprotective effect of mangiferin. Copyright © 2009 John Wiley & Sons, Ltd.