番茄红素对镉损伤大鼠氧化应激的影响

目的:观察番茄红素(lycopene,LP)对镉(Cd)损伤大鼠氧化应激的影响。方法:大鼠饲喂氯化镉(Cd-Cl2)和番茄红素,4周后处死,测定血清和肝匀浆的超氧化物歧化酶(SOD)活性、过氧化氢酶(CAT)活性、谷胱甘肽过氧化物酶(GSH—Px)活力、丙二醛(MDA)及还原型谷胱甘肽(GSH)含量。结果:与镉损伤组相比,番茄红素组的大鼠血清和肝组织的SOD活性、GSH—Px活力上升,MDA含量降低,在统计学上差异有显著性(P<0.05)。番茄红素可以拮抗镉的毒性,提高大鼠机体的抗氧化能力,抑制镉中毒所致的氧化应激。     

番茄红素对高脂血症患者血脂的影响

目的研究番茄红素对高脂血症患者血脂的影响。方法34例高脂血症(甘油三酯>1.88mmol/L)患者按血脂水平随机分为试验组和对照组,每组17例。试验组患者每日服用番茄红素18mg,对照组服用安慰剂,疗程为4周。分别于服药前和停药后测定两组患者的总胆固醇(TC)、甘油三酯(TG)和高密度胆固醇(HDL-C)水平。结果服药前试验组与对照组的TC、TG和HDL-C水平均无显著性差异。服药后试验组的TC和TG水平显著低于对照组(P<0.05)。服药后试验组患者的TC和TG水平均显著低于服药前(P<0.05)。结论番茄红素对高脂血症患者具有降血脂作用。     

番茄红素对家兔动脉粥样硬化形成的保护作用

目的:研究番茄红素对高脂饲料诱导的家兔动脉粥样硬化形成的影响。方法:采用含量为90%的番茄红素作为受试物,将40只健康成年雄性家兔,根据总胆固醇(TC)水平随机分为正常对照组,普通饲料喂养;模型组,高脂饲料喂养;番茄红素低、高剂量组[高脂饲料+番茄红素4mg/(kgbw·d);高脂饲料+番茄红素12mg/(kgbw·d)]和阳性药物对照[高脂饲料+氟伐他汀钠10mg/(kgbw·d)]五组。光学显微镜检测HE染色的主动脉壁病理改变,检测家兔血清TC、TG、HDL-C、LDL-C、T-AOC、MDA、NO及IL-1含量,血浆番茄红素、ox-LDL含量。结果:各剂量番茄红素均可在一定程度上抑制高脂饲料诱导的家兔主动脉血管壁病理变化,降低家兔血清TC、TG、LDL-C水平,升高血清T-AOC活力,减少MDA、ox-LDL生成,增加血清中NO含量,血清IL-1水平降低。结论:番茄红素可减轻由高脂饲料引起的家兔主动脉血管壁粥样斑块病变。     

bcl-2及相关基因在番茄红素诱导人胃癌细胞凋亡过程中的作用

目的通过体外试验研究bcl-2及相关基因在番茄红素诱导人胃癌SGC-7901细胞凋亡过程中的作用。方法将番茄红素作用于人胃癌SGC-7901细胞,DAPI染色观察细胞凋亡情况,RT-PCR法检测bcl-2、bax、p53mRNA的表达。结果番茄红素作用于人胃癌SGC-7901细胞后,细胞发生凋亡,凋亡率为78.5%;随番茄红素浓度的增加,bcl-2mRNA的表达明显降低,baxmRNA和p53mRNA的表达均显著增加,并均呈剂量-效应关系。结论番茄红素在体外能诱导人胃癌SGC-7901细胞凋亡,且以促进p53mRNA过表达,从而上调baxmRNA的表达,下调bcl-2mRNA表达,即通过改变bax与bcl-2的比例来促进人胃癌SGC-7901细胞凋亡。     

番茄红素对急性肺损伤大鼠肺氧化损伤影响

目的研究番茄红素对急性肺损伤(ALI)大鼠氧化损伤的保护作用。方法采用不同剂量番茄红素给大鼠连续灌胃35 d,然后腹腔注射脂多糖6.0 mg/(kg.bw)建立ALI模型,正常对照腹腔注射生理盐水,各组动物分别在注射后1,4和6 h摘取右肺,检测肺组织中丙二醛(MDA)和抗氧化酶含量。结果番茄红素能明显降低ALI模型大鼠肺组织中MDA的含量(P<0.01),对超氧化物歧化酶(SOD)无明显作用,但谷胱甘肽过氧化物酶(GSH-PX)含量明显增加(P<0.01)。结论番茄红素能降低脂多糖诱导ALI过程中的氧化损伤,对肺组织具有一定的保护作用。     

番茄红素对苯并(a)芘诱发小鼠前胃组织癌变的影响

目的观察番茄红素对苯并(a)芘[B(a)P]诱发小鼠前胃组织癌变过程的影响及其可能的作用机制。方法昆明小鼠随机分成5组(n=30):正常对照组、B(a)P组、番茄红素高[20mg/kg+B(a)P]、中[10mg/kg+B(a)P]、低[5mg/kg+B(a)P]3个不同剂量的实验组,实验组与B(a)P组给予B(a)P,建立前胃癌模型,观察不同浓度的番茄红素对小鼠前胃癌形成的作用;同时用单细胞凝胶电泳法检测外周血淋巴细胞DNA损伤情况,检测超氧化物岐化酶(SOD)、丙二醛(MDA)及谷胱甘肽过氧化物酶(GSH-Px)的含量。结果正常对照组未见肿瘤形成,其余4组均见肿瘤形成,并经病理证实。番茄红素高、中、低剂量组、B(a)P对照组前胃肿瘤发生率分别为50%、60%、80%、100%。与正常对照组相比,番茄红素高、中、低剂量组和B(a)P对照组MDA含量升高,SOD活性下降,DNA氧化损伤加重,差异有显著性(P<0.05)。与B(a)P对照组相比,番茄红素高剂量组MDA含量降低,高、中剂量组SOD活性升高,DNA氧化损伤减轻,差异有显著性(P<0.05)。番茄红素对GSH-Px影响不显著。结论番茄红素具有抑制肿瘤...     

番茄红素预防脂代谢紊乱的作用及机制探讨

目的探讨番茄红素预防高脂喂饲大鼠脂代谢紊乱的作用及机制。方法用高脂饲料喂养大鼠,同时,给予番茄红素灌胃,检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、肝重、肝指数、脂蛋白脂酶(LPL)和肝脂酶(HL)活性;用蛋白印迹法测定低密度脂蛋白受体(LDL-R)的表达,探讨番茄红素预防高脂血症的可能机制。结果番茄红素各剂量组的血TC、TG、LDL-C肝重及肝指数显著减轻,有效地提高了LPL和HL活性,其中,高剂量组明显。同时,番茄红素可增加LDL-R的表达。结论番茄红素具有预防高脂喂饲大鼠肝组织脂代谢紊乱的作用。其机制可能是通过提高LRL和HL活性,增加LDL-R的表达,减少甘油三酯(TG)和低密度脂蛋白(LDL)在肝组织中的蓄积,从而预防肝组织脂代谢的紊乱。     

Therapeutic effect of iodised serum milk protein,lycopene and their combination on benign prostatic hyperplasia induced in rats

Benign prostatic hyperplasia (BPH) is a common chronic disease in ageing men. Synthetic inhibitors of 5α-reductase commonly used in BPH treatment have limited effectiveness and may cause side effects. Evaluation of iodised serum milk protein and lycopene therapeutic effect in rat BPH model was the aim of the present study. BPH was induced in male Wistar rats by surgical castration and subsequent testosterone administrations (25 mg/kg, 7 injections). Rats with induced BPH received lycopene (5 mg/kg), iodised serum milk protein (200 µg/kg) or their combination for 1 month daily. The efficacy of the treatment was evaluated by the prostate weight, prostatic index and ventral lobe epithelium thickness. In lycopene and iodised serum milk protein-treated rats, prostate weight and prostatic index were significantly reduced compared to control group; and lycopene and iodised serum milk protein used in combination yielded an additive effect. Thus, further investigation of combined supplementation with micronutrients and plant-derived substances in BPH models may help to find new opportunities or its safe and effective treatment.     

Lycopene and male infertility

Excessive amounts of reactive oxygen species （ROS） cause a state of oxidative stress, which result in sperm membrane lipid peroxidation, DNA damage and apoptosis, leading to decreased sperm viability and motility. Elevated levels of ROS are a major cause of idiopathic male factor infertility, which is an increasingly common problem today. Lycopene, the most potent singlet oxygen quencher of all carotenoids, is a possible treatment option for male infertility because of its antioxidant properties. By reacting with and neutralizing free radicals, lycopene could reduce the incidence of oxidative stress and thus, lessen the damage that would otherwise be inflicted on spermatozoa. It is postulated that lycopene may have other beneficial effects via nonoxidative mechanisms in the testis, such as gap junction communication, modulation of gene expression, regulation of the cell cycle and immunoenhancement. Various lycopene supplementation studies conducted on both humans and animals have shown promising results in alleviating male infertility--lipid peroxidation and DNA damage were decreased, while sperm count and viability, and general immunity were increased. Improvement of these parameters indicates a reduction in oxidative stress, and thus the spermatozoa is less vulnerable to oxidative damage, which increases the chances of a normal sperm fertilizing the egg. Human trials have reported improvement in sperm parameters and pregnancy rates with supplementation of 4-8 mg of lycopene daily for 3-12 months. However, further detailed and extensive research is still required to determine the dosage and the usefulness of lycopene as a treatment for male infertility.     

Lycopene,tomato products and prostate cancer‐specific mortality among men diagnosed with nonmetastatic prostate cancer in the Cancer Prevention Study II Nutrition Cohort

While dietary lycopene and tomato products have been inversely associated with prostate cancer incidence, there is limited evidence for an association between consumption of lycopene and tomato products and prostate‐cancer specific mortality (PCSM). We examined the associations of prediagnosis and postdiagnosis dietary lycopene and tomato product intake with PCSM in a large prospective cohort. This analysis included men diagnosed with nonmetastatic prostate cancer between enrollment in the Cancer Prevention Study II Nutrition Cohort in 1992 or 1993 and June 2011. Prediagnosis dietary data, collected at baseline, were available for 8,898 men, of whom 526 died of prostate cancer through 2012. Postdiagnosis dietary data, collected on follow‐up surveys in 1999 and/or 2003, were available for 5,643 men, of whom 363 died of prostate cancer through 2012. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for PCSM. Neither prediagnosis nor postdiagnosis dietary lycopene intake was associated with PCSM (fourth vs. first quartile HR = 1.00, 95% CI 0.78–1.28; HR = 1.22, 95% CI 0.91–1.64, respectively). Similarly, neither prediagnosis nor postdiagnosis consumption of tomato products was associated with PCSM. Among men with high‐risk cancers (T3–T4 or Gleason score 8–10, or nodal involvement), consistently reporting lycopene intake ≥ median on both postdiagnosis surveys was associated with lower PCSM (HR = 0.41, 95% CI 0.17–0.99, based on ten PCSM cases consistently ≥ median intake) compared to consistently reporting intake < median. Future studies are needed to confirm the potential inverse association of consistently high lycopene intake with PCSM among men with high‐risk prostate cancers.