Kappa-晒化卡拉胶对实验动物的抗心律失常作用

Kappa-硒化卡拉胶是一含硒有机化合物。ip 9 mg·kg^-1·d^-1×5d或单次ig 35,70,140mg·kg^-1能显著提高乌头碱致大鼠HA的阈剂量,此作用可与Na₂SeO₃ 1 mg·kg^-1·d^-1×5d ip比拟.随着Kappa-硒化卡拉胶ig剂量增加,尚可提高乌头碱所致VE,VT和VF的阈剂量。ip 9mg·kg^-1·d^-1×5 d或ig 70mg·kg^-1能提高BaCl₂致大鼠或哇巴因致豚鼠HA的阈剂量。对BaCl₂致大鼠VF或哇巴因致豚鼠VE的阈剂量,分别在ig70mg·kg^-1与140mg·kg^-1时有提高,而ipNa₂SeO₃ 1 mg·kg^-1·d^-1×5d无此明显影响。     

香菇多糖的免疫调节作用

研究香菇多糖(LTN)的免疫调节作用。结果表明,LTN1及5mg·kg^-1·d^-1×6,ip可促进正常小鼠由ConA(2.5mg·kg^-1)刺激的脾脏T淋巴细胞增殖反应。1,5及10mg·kg^-1·d^-1×8或5,ip能分别纠正由环磷酰胺(Cy,200mg·kg^-1和80mg·kg^-1,ip)诱导的免疫亢进或低下状态。此外,LTN(1,5和10mg·kg^-1·d^-1×6,ip),促使小鼠胸腺L3T4+(Th)和Lyt2+(Ts)细胞数减少,外周脾脏L3T4+和Lyt2+细胞数增加,腹腔巨噬细胞释出肿瘤坏死因子(TNF)也明显增加。这些作用均以LTN5mg·kg^-1·d^-1作用最佳。提示LTN可能通过影响T细胞及其亚型,促进TNF活性调节机体的免疫功能。     

重组小鼠β防御素3体内抗甲型流感病毒H1N1作用

目的 观察重组小鼠β防御素3(rMBD3)对甲型流感病毒感染小鼠的保护作用。方法 以10 mg·kg^-1·d^-1rMBD3腹腔注射3月,观察小鼠的一般状态,以及对主要脏器的影响。BALB/c小鼠,♀,分为正常对照组、模型对照组、rMBD3高剂量组(10 mg·kg^-1·d^-1)、rMBD3低剂量组(5 mg·kg^-1·d^-1)和利巴韦林组(100 mg·kg^-1·d^-1)。采用流感病毒液滴鼻感染建立甲型流感病毒H1N1感染小鼠模型,感染病毒12 h后分别腹腔注射给药。每日观察小鼠一般情况和死亡情况。于攻毒第3天检测肺泡灌洗液流感病毒滴度、血清γ干扰素含量、肺指数和肺组织病理变化。结果 小鼠腹腔注射10?mg·kg^-1·d^-1 rMBD3 3月,未发现明显异常反应或死亡,各重要脏器的未见明显病理改变。rMBD3各剂量组肺泡灌洗液中的病毒滴度、肺指数抑制率均降低,肺组织病理改变减少。结论 rMBD3对小鼠无明显毒性作用,在体内具有抗流感病毒、保护流感小鼠的活性。     

(+),(-)和(±)棉酚在雌大鼠抗早孕作用的研究

妊娠第6～9天大鼠,分别ig(±)和(-)棉酚80mg·kg^-1·d^-1和40mg·kg^-1·d^-1,结果有明显的抗早孕作用。然而(+)棉酚40mg·kg^-1·d^-1对大鼠生育无明显影响。(-)棉酚30μg·ml^-1能抑制体外培养黄体细胞孕酮的分泌。(+)棉酚10μg·ml^-1能促进黄体细胞分泌孕酮。hCG1IU·ml^-1能明显刺激体外培养颗粒细胞孕酮的分泌。(±)棉酚10和30μg·ml^-1皆能明显降低颗粒细胞对hCG的反应性。     

阿魏酸对小鼠脑缺血再灌注损伤及大鼠血液流变性的影响

目的观察阿魏酸对小鼠脑缺血再灌注损伤、大鼠血液流变性的影响。方法用结扎双侧颈总动脉法,造成小鼠脑缺血再灌注模型;观察阿魏酸(0.8,1.6 g·kg^-1·d^-1)对小鼠全脑缺血30m in及再灌注60m in后超氧化物歧化酶(SOD)活性、乳酸脱氢酶(LDH)活性、MDA含量的影响。大鼠皮下注射肾上腺素(0.8mg·kg^-1),共2次,间隔4h,在第一次注射后2h将大鼠浸入4℃冰水5m in,造成血瘀模型,观察阿魏酸(50～200mg·kg^-1·d^-1)对血黏度的影响。结果阿魏酸(0.8g·kg^-1·d^-1)可显著提高脑组织LDH活性、可明显降低MDA含量、可显著提高SOD活性;阿魏酸(1.6g·kg^-1·d^-1)可显著降低MDA/SOD比值;对大鼠血黏度无明显影响。结论预防性应用阿魏酸对小鼠脑缺血再灌注损伤有一定程度的保护作用,对大鼠血液流变性无明显影响。     

乳癖消合剂抗实验性大鼠乳腺增生作用研究

目的观察乳癖消合剂对大鼠实验性乳腺增生的治疗作用。方法10周龄雌性SD大鼠肌肉注射苯甲酸雌二醇0.5 mg·kg^-1·d^-1,连续20 d,继而肌注黄体酮5 mg·kg^-1·d^-1,连续5 d,造模后灌胃给予乳癖消合剂2.5,5,10 g(生药)·kg^-1·d^-1,连续35 d后检查血清雌、孕激素水平,测定第2,3对乳头高度及直径,并取第2对乳腺进行病理切片,在镜下评价乳腺增生程度。结果乳癖消合剂能抑制雌二醇+黄体酮所致乳腺增生大鼠的乳头高度及直径的增加,降低造模大鼠血清垂体促乳素、雌二醇含量,增加孕酮含量,并明显抑制乳腺增生程度。结论乳癖消合剂对大鼠实验性乳腺增生具有明显的治疗作用。     

氧化苦参碱对病毒性心肌炎小鼠心肌细胞凋亡及相关因子的影响

目的 探讨氧化苦参碱(oxymatrine,OMT)对病毒性心肌炎小鼠心肌细胞凋亡及其凋亡相关因子蛋白表达的影响。方法 42只BALB/c小鼠随机分为正常对照组(NC)、病毒性心肌炎模型组(VM)、OMT高剂量组(OMT-H,25?mg·kg^-1·d^-1)、OMT中剂量组(OMT-M,12.5 mg·kg^-1·d^-1)、OMT低剂量组(OMT-L,6.25 mg·kg^-1·d^-1)、OMT极低剂量组(OMT-EL,3.125 mg·kg^-1·d^-1)、利巴韦林对照组(RB,100 mg·kg^-1·d^-1)。病毒性心肌炎小鼠由柯萨奇病毒B3型腹腔注射感染所致,各治疗组从末次给予病毒24 h后开始,腹腔注射,每日1次。于治疗第12天,每组处死小鼠6只,留取心肌标本。TUNEL法检测心肌细胞凋亡情况,免疫印迹法和免疫组织化学法检测Bcl-2和Bax蛋白的表达情况。结果 OMT治疗显著降低了病毒性心肌炎小鼠凋亡心肌细胞的数量,与病毒性心肌炎模型组比较,OMT-L组效果最佳(P<0.01)。与病毒性心肌炎模型组小鼠比较,OMT治疗组的小鼠心肌组织中Bax蛋白表达降低,而Bcl-2蛋白表达没有明显改变。结论 氧化苦参碱可减少病毒性心肌炎小鼠心肌细胞的凋亡,该作用与下调Bax蛋白表达有关。     

甘草类黄酮对四氯化碳致小鼠急性肝损伤的影响

甘草类黄酮(GF)是从甘草根中提得。本文结果表明,预先ig GF 200,400,600mg·kg^-1·d^-1×2d能显著降低CCl₄所致血清谷丙转氨酶,乳酸脱氢酶活性的升高以及肝内丙二醛含量的增加,其作用呈剂量依赖性。GF可减轻CCl₄所致的肝脏坏死,但对血清内酶的活性没有抑制作用,也不减少正常小鼠血清中酶的活性。GF的肝保护作用可能与其抗脂质过氧化作用有关。     

异黄酮genistein对小鼠恶性黑色瘤转移的实验性治疗

目的:研究异黄酮genistein 对肿瘤转移的治疗作用。方法:B16-BL6 细胞由尾静脉注入C57BL/6 小鼠体内,于d 15 观察动物肺转移灶。genistein 混悬于2% 卵磷脂中,从接种瘤细胞前1 天开始ip,剂量为100 和200mg·kg^-1·d^-1 。结果:genistein 可抑制肺转移灶形成,200 mg·kg^-1 用药组小鼠转移灶数目明显减少;作为对照,腹腔给予环磷酰胺100 mg·kg^-1 后,形成的转移灶数目无明显变化,但形成的转移瘤灶体积减小。当genistein 和环磷酰胺合用时,转移小鼠的存活时间明显延长。结论:genistein 可抑制肿瘤转移,其作用与细胞毒药物不同, 与细胞毒药物合用可提高其抗肿瘤转移的作用。     

嵩乙醚的抗血吸虫作用

实验感染日本血吸虫的小鼠,用蒿乙醚或蒿甲醚100～200mg·kg^-1·d^-1×2d灌胃治疗,显示两药对小鼠体内不同发育期血吸虫的减虫率相仿。特别是d7童虫和d35成虫组的减虫率较高,分别达77.5～87.2%和51.7～61.3%。经蒿乙醚作用后,d7童虫和d35成虫的糖原明显减少或消失,虫的皮层和实质组织中的碱性磷酸酶活力亦明显受抑制,表明蒿乙醚具有抗日本血吸虫童虫和成虫的作用。     

Astragalus polysaccharide attenuates isoproterenol-induced cardiac hypertrophy by regulating TNF-α/PGC-1α signaling mediated energy biosynthesis

We previously reported that Astragalus polysaccharide (APS) extracted from Chinese medicine Astragalus membranaceus (Fisch.) Bge, attenuates hypertrophy of neonatal rat ventricular myocytes (NRVMs) induced by isoproterenol (Iso). The present study was designed to investigate the effects and the possible mechanism of APS on Iso-induced hypertrophy in rats and NRVMs with focus on tumor necrosis factor α (TNF-α)/peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) signaling mediated energy biosynthesis. 36-Week old rats were randomly divided into 3 groups: (1) Control, rats received vehicle; (2) Iso, rats received isoproterenol injections; (3) Iso+APS, rats received isoproterenol injections and APS. NRVMs were divided into similar groups as rats. The results showed that combination of APS with Iso significantly attenuated the pathological changes, reduced the ratios of heart weight/body weight (HW/BW) and left ventricular weight/BW (LVW/BW), improved the cardiac hemodynamics, down-regulated mRNA and protein expression of atrial natriuretic peptide (ANP), increased the ratios of ATP/ADP and ATP/AMP, and decreased the content of free fatty acid (FFA) in heart tissue of rats compared with Iso alone. In addition, pretreatment with APS significantly decreased the surface area and protein content, down-regulated mRNA and protein expression of ANP, increased the ratios of ATP/ADP and ATP/AMP, and decreased the content of FFA in NRVMs compared with Iso alone. Furthermore, APS increased the protein expressions of ATP5D, the σ subunit of ATP synthase, PGC-1α and pyruvate dehydrogenase kinase 4 (PDK4) in tissue and NRVMs respectively and inhibited the production of TNF-α in serum and culture medium compared with Iso alone. The results suggested that APS attenuates Iso-induced cardiac hypertrophy through regulating TNF-α/PGC-1α signaling mediated energy biosynthesis.     

黄芪多糖对腹主动脉缩窄致大鼠心肌肥厚能量代谢紊乱的抑制作用

目的探讨黄芪多糖(APS)对腹主动脉缩窄(AAC)致大鼠心肌肥厚的抑制作用及其机制。方法大鼠采用结扎腹主动脉的方法制备AAC模型,1周后ig给予大鼠APS 200,400和800 mg.kg-1,每天1次,共11周。计算心脏质量指数(HMI)和左心室质量指数(LVMI);测定左心室收缩压(LVSP)、左心室舒张末压(LVEDP)和左心室内压最大升降速率(±dp/dtmax),HE染色观察大鼠左室心肌形态学改变;测定左心室乳酸(LAC)、游离脂肪酸(FFA)含量;采用逆转录-聚合酶链反应(RT-PCR)测定心肌心钠素mRNA(ANPmRNA)表达;测定心肌细胞线粒体膜电位(MMP)。结果与假手术组相比,AAC模型组的大鼠,MMP明显降低,其他指标均显著增高。与模型组相比,APS 800 mg.kg-1组HMI,LVMI,LVSP,LVEDP和±dp/dtmax均显著降低(P<0.05);APS 400和800 mg.kg-1组ANP mRNA表达明显下降,MMP明显升高(P<0.05);APS200,400和800 mg.kg-1组LAC水平明显降低(<0.05)。结论 APS能够有效抑制AAC大鼠心肌肥厚并改善其能量代谢紊乱,提高线粒体的活力。     

当归多糖对辐射损伤小鼠血液中microRNA作用的研究

目的探讨当归多糖对60 Coγ-射线辐射损伤小鼠血液中microRNA的影响及意义。方法将35只SPF级C57BL/6J小鼠随机分为未照射组、2Gy照射未干预组、2Gy照射APS 4mg·kg~(-1)组、2Gy照射APS 8mg·kg~(-1)组、10Gy照射未干预组、10Gy照射APS 4mg·kg~(-1)组和10Gy照射APS 8mg·kg~(-1)组,共7组。照射组接受60 Coγ-射线2Gy、10Gy(剂量率为10Gy·h~(-1))全身照射后,连续3d注射APS 4mg·kg~(-1)和APS 8mg·kg~(-1),于照射后72h采集外周血。应用Agilent microRNA生物芯片筛选小鼠血液中差异表达microRNA。结果与未照射组比较,2Gy照射未干预组差异表达microRNA 30个,10Gy照射未干预组差异表达microRNA 31个,且与未照射组比较差异有统计学意义(P<0.05)。2Gy照射APS 4mg·kg~(-1)组和2Gy照射APS 8mg·kg~(-1)组之间差异表达microRNA无统计学意义(P>0.05)。10Gy照射APS 4mg·kg~(-1)组和10Gy照射APS 8mg·kg~(-1)组治疗差异表达microRNA均有所降低,除microRNA-455、microRNA-9和let-7外,10Gy照射APS 8mg·kg~(-1)组治疗降低更加显著,与10Gy照射APS 4mg·kg~(-1)组比较差异有统计学意义(P<0.05)。结论 APS通过改变血液中microRNA的表达,促进辐射小鼠的损伤修复。     

双环醇对扑热息痛引起小鼠肝脏能量代谢和线粒体功能障碍的影响

目的　研究双环醇对扑热息痛(对乙酰氨基酚)引起小鼠肝能量代谢紊乱和线粒体功能障碍的保护作用。方法　小鼠ip扑热息痛120mg·kg^-1 引起急性肝损伤,观察血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平、肝活体磷谱、肝线粒体膜流动性及线粒体ATPase活性的改变。结果　双环醇可显著抑制扑热息痛中毒小鼠PME/ATP及PME/PDE的升高。双环醇(200mg·kg^-1)可显著降低扑热息痛导致的线粒体膜流动性下降,并对线粒体ATPase活性降低有显著保护作用。结论　双环醇可保护扑热息痛导致的急性肝损伤,使肝脏能量代谢和磷脂代谢趋于正常,并对损伤的线粒体功能有显著的保护作用     

Effect of indomethacin on the blood pressure and plasma catecholamine responses to acute endotoxaemia

Injection of E. coli endotoxin (7 mg kg-1 i.v.) to pentobarbitone anaesthetized cats resulted in prolonged decrease of systemic blood pressure and increases in plasma concentrations of adrenaline, noradrenaline and 6-ketoprostaglandin (PG) F 1 alpha. Indomethacin pretreatment (10 mg kg-1 i.v.) attenuated the decrease in blood pressure following endotoxin injection. Plasma adrenaline, noradrenaline and 6-keto-PG F1 alpha were significantly lower in the indomethacin-treated cats. These data indicate that the superior haemodynamic status of the indomethacin pretreated animals exposed to endotoxic shock is not the result of potentiation of the peripheral sympathetic response.     

6,7-二乙酰黄芩素对四氯化碳和D-氨基半乳糖所致的急性肝损伤的保护作用

目的:研究6,7-二乙酰黄芩素对四氯化碳(CCl4)和D-氨基半乳糖(D-GalN)所致急性肝损伤的保护作用。方法:分别用CCl4和D-GalN诱导化学性急性肝损伤模型,测定血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)水平;并用苏木素-伊红(HE)染色处理肝脏组织切片,光镜观察病理学改变;用试剂盒测定肝线粒体中AST,SOD和GSH-PX的活性及脂质过氧化产物MDA含量。结果:在CCl4和D-GalN诱导和的小鼠肝急性损伤模型中,6,7-二乙酰黄芩素给药(50,100 mg.kg-1,ig)明显降低血清ALT,AST水平;明显改善肝脏病理组织状况;6,7-二乙酰黄芩素给药(25,50,100 mg.kg-1,ig)明显降低CCl4诱导的肝急性损伤小鼠的肝线粒体中AST活性和MDA的含量,显著增加SOD和GSH-PX的活性。结论:6,7-二乙酰黄芩对CCl4和D-GalN诱导和的小鼠肝急性损伤均具有保护作用,该作用与其增加线粒体中抗氧化酶的酶的活性、降低脂质过氧化水平有关。     

黄芪皂苷甲对血浆cAMP及再生肝DNA合成的影响

Astragalus saponin 1, one of the components isolated from Astragalus membranaceus Bge was found to induce accumulation of cAMP in rabbit plasma at the ip dose of 10mg/kg. The increase of cAMP started at 30 rain and reached maximum in 0.5～4h after a single injection. The effect of the component on DNA biosynthesis in partially hepatectomized mice seemed to be significant. The component was also shown to enhance the incorporation of [³H] TdR into the regenerating liver in mice.     

Role of nitric oxide in maintaining vascular integrity in endotoxin-induced acute intestinal damage in the rat.

1. The role of endogenous nitric oxide (NO) in maintaining intestinal vascular integrity following acute endotoxin (E. coli. lipopolysaccharide) challenge was investigated in the anaesthetized rat by use of NG-monomethyl-L-arginine (L-NMMA), a selective inhibitor of NO synthesis. 2. L-NMMA (10-50 mg kg-1, i.v.) pretreatment enhanced both the macroscopic and histological intestinal damage and the increases in vascular permeability, measured as the leakage of [125I]-labelled human serum albumen, induced after 15 min by endotoxin (50 mg kg-1, i.v.). 3. The effects of L-NMMA (50 mg kg-1, i.v.) were enantiomer specific, as D-NMMA had no effect. Furthermore, these effects were reversed by L-arginine (300 mg kg-1, i.v.), the precursor of NO synthesis but not by D-arginine (300 mg kg-1, i.v.). 4. L-NMMA (10-50 mg kg-1, i.v.) increased mean systemic arterial blood pressure but this does not appear to be the mechanism by which endotoxin-induced intestinal damage was enhanced, since similar systemic pressor responses induced by phenylephrine (10 micrograms kg-1 min-1, i.v.), had no such effect. 5. The results suggest that synthesis of NO from L-arginine has a role in maintaining the microvascular integrity of the intestinal mucosa following acute endotoxin challenge.     

黄芪皂苷抗实验性肝损伤作用

两种黄芪苷ASI和SK能对抗D-半乳糖胺,醋氨酚引起的肝损伤。表现为减轻肝毒引起的病变,SGPT降低,肝MDA下降,GSH升高;且三项指标变化呈明显相关。从离体大鼠肝细胞制备法也证明ASI和SK在0.75μmol/L～0.18 nmol/L浓度范围内,可对抗CCl₄引起的GPT升高。给小鼠连续灌服ASI 12,50 mg/kg或SK 6,20 mg/kg能提高肝微粒体细胞色素P—450活性。此结果表明,黄芪苷是黄芪抗肝毒损伤的有效成分。其机理除抗生物氧化外,尚与代谢调节作用有关。