海洋贝类提取物的药理作用研究

目的 通过观察海洋贝类提取物(EMS)抗血小板聚集和抗氧化的药理作用,探讨EMS抗动脉粥样硬化(AS)作用机理。方法1.采用二磷酸腺苷(ADP)和胶原作诱导剂进行体内及体外血小板聚集实验,观察EMS对大鼠血小板聚集功能的影响。2.检测EMS对血清总超氧化物歧化酶(T-SOD)及脂质过氧化物丙二醛(MDA)含量的影响。结果 1.EMS体外用药(9.76,29.27,48.78 mg·mL~(-1))可显著降低胶原诱导的家兔血小板最大聚集率;在体内实验中,EMS(5,10,20g·kg~(-1))ig对ADP诱导的大鼠血小板聚集率无明显影响。2.EMS(5,10,20g·kg~(-1),ig,qd)可显著升高大鼠血清T-SOD的活性,并降低MDA含量。结论EMS具有抑制血小板聚集功能和抗氧化作用。     

妊娠高血压疾病患者氧化应激状态的改变

目的探讨妊娠高血压疾病患者氧化应激状态的改变情况。方法选取妊娠高血压疾病患者60例,其中妊娠高血压患者15例,轻度子痫前期患者15例,重度子痫前期患者30例。另取同期住院分娩的正常孕妇30例作为对照组。所有研究对象均测血清同型半胱氨酸、丙二醛、超氧化物歧化酶、谷胱甘肽过氧化物酶水平。结果妊娠高血压疾病组MDA水平为7.02±3.05 nmol/L,显著高于对照组5.16±2.79 nmol/L(P<0.01),妊娠高血压疾病组GSH-PX水平105.41±32.95 U/0.1 ml,明显低于对照组127.52±40.64 U/0.1 ml(P<0.05),两组SOD水平无显著差别。妊娠高血压疾病组Hcy为11.8±3.4μmol/L,显著高于对照组9.7±3.0μmol/L(P<0.01)。并且妊娠高血压疾病组Hcy与MDA呈正相关。结论妊娠高血压疾病患者由于氧化物质增加,抗氧化物质减少,氧化还原系统平衡失调,呈现氧化应激状态。     

大豆黄酮抗热应激作用

目的研究大豆黄酮对热应激小鼠谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量的影响。方法将30只小鼠随机分为正常对照组、热应激组和大豆黄酮热应激组,以(45±1)℃持续20 min的热应激模式,观察热应激后小鼠肝、脾、肾及血清中GSH-Px活力及MDA含量变化。结果与正常对照组相比,热应激后小鼠肝脏、脾脏及肾脏GSH-Px活力升高,其中肝脏酶活力显著升高(P<0.05);大豆黄酮热应激组酶活力显著高于正常对照组(P<0.05或P<0.01),肝脏、脾脏酶活力显著高于应激组(P<0.05)。热应激后2组MDA含量均比正常对照组升高,其中肝脏和血清上升显著(P<0.05);大豆黄酮热应激组比应激组有所下降,但差异无统计学意义(P>0.05)。结论大豆黄酮可增强应激机体的抗氧化能力。     

热毒平抗脂质过氧化及对腹腔巨噬细胞凋亡影响

目的研究热毒平抗脂质过氧化以及对腹腔巨噬细胞(macrophage,Mφ)凋亡的影响,为热毒平治疗重症中暑提供实验依据。方法昆明种小鼠50只,随机分为常温对照组、热毒平组、西黄芪胶组、生理盐水组和中暑模型组。在干球温度(34.5±0.5)℃,相对湿度(60±5)%的条件下建立中暑模型,测定用药组和对照组小鼠肝组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量;提取动物腹腔巨噬细胞DNA并行凝胶电泳;用流式细胞仪检测各组小鼠腹腔Mφ凋亡情况。结果热毒平均小鼠肝组织SOD活力升高,MDA含量降低;DNA电泳图中热毒平组无梯状条带;热毒平组腹腔Mφ凋亡百分率比其他组低且接近正常组。结论热毒平能有效的防止高温所致的脂质过氧化、减少其腹腔Mφ凋亡,对重症中暑有着良好的治疗作用。     

柴胡注射液对小鼠学习记忆功能的影响

目的:探讨柴胡注射液对学习记忆行为影响的机制。方法:每天2次给予小鼠腹腔注射不同剂量的柴胡注射液,连续5天后采用行为观察和生化检测相结合的方法,研究柴胡注射液对小鼠学习记忆行为的影响,包括剂量-效应关系和时间-效应关系以及脑内超氧化物歧化酶(SOD)、丙二醛(MDA)和NO含量的变化。结果:与注射生理盐水的对照组相比,在5种剂量(50、100、200、400和800mg/kg)中除了50mg/kg外,其他4种剂量的柴胡注射液均能显著提高小鼠Y-迷宫分辨学习的能力及24h记忆保持率,其中400mg/kg剂量的效果最好;最佳剂量的柴胡注射液易化记忆的作用在训练后24￣72h均显著增强(P<0.01),以24h最为显著;最佳剂量的柴胡注射液可显著提高行为训练后小鼠脑内SOD的活性(P<0.01)、降低脂质过氧化产物MDA水平(P<0.01)以及提高NO含量(P<0.01)。结论:适当剂量的柴胡注射液在一定时间内具有提高小鼠学习记忆能力的功效,该作用可能与伴随的脑组织抗氧化能力提高和NO含量改变有关。     

雪莲花醇提物对大鼠组织和红细胞的抗氧化活性

 目的研究雪莲花醇提物(ESLHM)的抗氧化活性。方法用·HO生成系统Fe²⁺维生素C诱导大鼠心、肝、肾组织匀浆脂质过氧化,用TBA比色法测定MDA含量;用NBT还原法测酵母多糖A刺激大鼠中性粒细胞产生的O₂^-;用分光光度法测H₂O₂诱发的大鼠红细胞溶血度。结果对照组大鼠心、肝、肾匀浆经Fe²⁺+维生素C溶液诱发后MDA含量较空白组升高(P<0.01),中性粒细胞受酵母多糖A刺激后O₂^-生成较空白组升高(P<0.01),红细胞经H₂O₂诱发后溶血度较空白组升高(P<0.01)。而6.3,12.5,25,50,100,200μ·L^-1 ESLHM能不同程度抑制Fe²⁺维生素C诱导的大鼠心、肝、肾脂质过氧化产物MDA生成,其抑制心、肝、肾MDA生成的IC₅₀分别为29.4,32.9,31.4 μg·L^-1,其量效关系均呈负相关,相关系数分别为-0.905, -0.912,-0.908,相关性检验P值均<0.01;能不同程度抑制酵母多糖A刺激中性粒细胞生成O₂^-,其抑制中性粒细胞生成O₂-的IC₅₀为24.6 μg·L^-1,其量效关系呈负相关,相关系数为-0.887(P<0 01);能不同程度抑制H₂O₂诱发的红细胞氧化溶血,其抑制红细胞氧化溶血的IC₅₀为57.6μg·L^-1,其量效关系呈负相关,相关系数为-0.905(P<0.01),.结论雪莲花醇提物通过清除·HO,O₂^-及H₂O₂发挥抗氧化活性。     

Antitumor activity and antioxident role of Bauhinia racemosa against Ehrlich ascites carcinoma in Swiss albino mice

AIM: To study the enzyme activity of CYP2C18 variant with exon 5 skipped. METHODS: A full length CYP2C18 cDNA X1 and an exon 5 skipped variant CYP2C18 X2 were separately subcloned into mammalian expression vector pREP9 to transfect HepG2 cells. The expression of CYP2C18 mRNA in transgenic cells and human liver tissues were determined by RT-PCR. The enzyme activity of CYP2C18 to oxidate tolbutamide in postmitochondrial supernate (S9) fraction was determined by HPLC. The cytotoxicity of ifosfamide to transgenic cells was evaluated by MTT test. RESULTS: HepG2-CYP2C18 X1 cells showed strong expression of the full length CYP2C18 mRNA. On the other hand, HepG2-CYP2C18 X2 cells had only infinitesimal expression of the exon-skipped CYP2C18 as well as the full length CYP2C18, while non-transfected HepG2 cell only demonstrated an infinitesimal expression of the full length CYP2C18. The expression of CYP2C18 exons 2 to 7 was also analyzed by RT-PCR in 7 extratumoral liver tissues. Among them, 3 samples expressed on     

高温胁迫下半夏倒苗前后保护酶活力的变化

目的 :探讨在高温胁迫下半夏倒苗前后保护酶活力的变化 ,从而为防止半夏倒苗提供一定的信息。方法 :待半夏苗高 15cm左右时 ,进行 (30± 1)℃的高温胁迫 ,于不同的胁迫处理天数分别测定半夏叶片、叶柄和块茎中保护酶 (SOD ,POD ,CAT)活性和膜脂过氧化产物丙二醛 (MDA)的含量。结果与结论 :随着高温胁迫时间的延长 ,半夏叶片和叶柄中MDA含量显著增加 ,而块茎中MDA含量增加却不显著。高温胁迫后 ,SOD和CAT活性都逐渐下降。POD活性经高温胁迫后呈现先上升后又迅速下降的趋势。     

山茶花总黄酮对缺血性脑损伤的保护作用

目的研究山茶花总黄酮(TFC)对小鼠急性脑缺血和大鼠局灶性脑缺血的保护作用。方法结扎小鼠双侧颈总动脉建立脑缺血模型,观察TFC对小鼠死亡率及死亡时间的影响。建立局灶性脑缺血(MCAO)模型,观察TFC大鼠对行为学、脑梗死面积的影响,并测定缺血侧脑组织中乳酸脱氢酶(LDH)活性、丙二醛(MDA)及一氧化氮(NO)含量。结果TFC80、40mg·kg-1组可降低缺血小鼠的死亡率,延长死亡时间;60、30、15mg·kg-1组可改善行为障碍,降低行为学评分;60、30mg·kg-1组可减少MCAO大鼠脑梗死范围,降低脑组织中MDA、NO含量,抑制LDH活性的下降。结论TFC对缺血性脑损伤有保护作用,其机制可能与抗自由基和抑制NO生成有关。     

The protective effect of zeaxanthin on human limbal and conjunctival epithelial cells against UV-induced cell death and oxidative stress

AIM: To explore the protective effect of zeaxanthin on human limbal and conjunctival epithelial cells against UV-radiation and excessive oxidative stress. METHODS: Human limbal and conjunctival epithelial cells were isolated from cadaver and cultured in vitro. They were challenged with UVB radiation and H2O2 with and without zeaxanthin pretreatment. Cell viability, p38 and c-JUN NH(2)-terminal kinase (JNK) phosphorylation, IL-6, IL-8 and MCP-1 secretion and malondialdehyde (MDA) content were measured. RESULTS: Zeaxanthin had no measurable cytotoxicity on limbal or conjunctival epithelial cells when used at concentrations of 5 μg/mL and below. At 30 mJ/cm2 UVB, the pretreatment of zeaxanthin increased the percentage of live cells from 50% to 69% (P=0.01) and from 66% to 75% (P=0.05) for limbal and conjunctival epithelial cells, respectively. The concentrations of IL-6, IL-8 and MCP-1 in the culture medium reduced to 66% (for IL-6 and MCP-1) and 56% (for IL-8) of the levels without zeaxanthin. This was accompanied by reduced p38 and JNK protein phosphorylation. Pretreatment of zeaxanthin also reduced intracellular MDA content caused by H2O2 stimulation from 0.86 μmol/L to 0.52 μmol/L (P=0.02) in limbal epithelial cells and from 0.96 μmol/L to 0.56 μmol/L in conjunctival epithelial cells (P=0.03). However, zeaxanthin did not have significant effect on H2O2-induced cell death in limbal or conjunctival epithelial cells. CONCLUSION: Zeaxanthin is an effective reagent in reducing the detrimental effect of UV-radiation and oxidative stress on ocular surface epithelial cells.