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。     

Abstracts of Articles on Vitamins

Background: Carotenoids are mainly carried by lipoproteins in blood, however little is known about the influence of polymorphisms of apolipoproteins (apo), cholesterol ester transfer protein (CETP) and lipoprotein lipase (LPL) involved in serum lipid metabolism.

Objective: We aimed to analyze whether serum concentrations of 5 carotenoids (lutein-zeaxanthin, β-cryptoxanthin, lycopene, α-carotene, β-carotene) are associated with common polymorphisms of Apo E, Apo B, Apo CIII, CETP, and LPL.

Methods: Serum concentrations of lutein-zeaxanthin, β-cryptoxanthin, lycopene, α-carotene, and β-carotene were measured and polymorphisms of Apo E (cys112arg and arg158cys), Apo B (thr71ile), Apo CIII [C(?482)T, Apo CIII T(?455)C, Apo CIII C1100T, Apo CIII C3175G, Apo CIII T3206G], CETP (ile405val), and LPL (S447X) were determined in a sample of 447 children and adults drawn from the Stanislas Study.

Results: After adjustment for age, sex, smoking, physical activity, oral contraceptive use, BMI, serum cholesterol and triglyceride concentrations, and fruit and vegetable intakes, carriers vs. non carriers of the lipoprotein lipase X447 allele had significant lower concentrations of lutein-zeaxanthin, β-cryptoxanthin, α-carotene and β-carotene; differences vs. S447S genotype being the largest for X447X: ?18.8%, ?50.5%, ?54.8% and ?47.1%, for the four carotenoid fractions, respectively. No significant association was noticed for lycopene concentration. None of the other tested polymorphisms was significantly related to the serum carotenoid concentrations.

Conclusions: Our investigation for the first time demonstrates that LPL S447X polymorphism could alter serum concentrations of carotenoids in healthy individuals, independently of serum cholesterol and triglyceride concentration. These data indicate that genetic factors could be involved in the variability of carotenoid bioavailability and bioconversion.     

Spectroscopic Characterization of Lycopene Extract from Lycopersicum esculentum (Tomato) and Its Evaluation as a Chemopreventive Agent Against Experimental Hepatocarcinogenesis in Mice

The present study was designed to characterize the lycopene extract (LycT) prepared from tomatoes (Lycopersicum esculentum) and then to evaluate its chemopreventive efficacy in N‐diethylnitrosamine (NDEA)‐induced experimental hepatocarcinogenesis in female Balb/c mice. The extraction of lycopene was carried out using hexane/acetone/ethanol as an extracting medium and then characterized by ultraviolet–visible, nuclear magnetic resonance and Fourier transform infrared spectroscopy. Chemopreventive efficacy of characterized LycT in vivo was evaluated in terms of hepatic tumour incidence, multiplicity, burden, hepatosomatic index and animal survival rate. Results indicated that average lycopene content of the tomato was 11.6–14 mg/kg tomato weight. Spectroscopic data confirmed the structural characteristics of lycopene in the extract. In the animal study, reduction in tumour incidence (42.05%), tumour burden (1.39) and tumour multiplicity (3.42) was observed upon LycT pretreatment to NDEA‐treated animals. Histopathological analysis unravelled that the increased survival rate in LycT + NDEA‐treated animals was due to the delay in the formation of aggressive tumour nodules. These observations indicate that lycopene seems to be an able candidate for chemoprevention in hepatocarcinogenesis resulting from NDEA insults. Copyright © 2012 John Wiley & Sons, Ltd.     

Lycopene and prostate cancer: emerging evidence

Prostate cancer has the third highest incidence of all cancers in men worldwide and is the most common neoplasm diagnosed among men beyond middle age in many developed countries. Mounting evidence surrounding the consumption of tomato products has shown promise for the prevention of prostate cancer. This protective effect has more recently been linked to lycopene, the most abundant carotenoid in tomatoes. Lycopene is a natural pigment that gives the red color to many foods. In Western countries, 85% of dietary lycopene can be attributed to the consumption of tomato-based products. This article reviews emerging evidence from epidemiologic studies for the role of lycopene in prostate cancer prevention. The majority of evidence currently comes from observational studies, but recent human clinical trials and animal studies have provided additional support. Growing evidence on the biologic mechanisms of lycopene in prostate cancer prevention also confirm the epidemiologic findings.     

番茄红素对紫外线诱导人晶状体上皮细胞氧化损伤的保护作用

目的：探讨番茄红素对紫外线诱导的人晶状体上皮细胞(hulan lens epithelial cells,HLEC)氧化损伤的保护作用及可能机制。
　　方法：HLEC传代培养,分为阴性对照组、氧化损伤组、番茄红素低剂量组和番茄红素高剂量组, MTT比色法检测细胞存活率,电子显微镜观察细胞形态学改变,DCFH-DA荧光探针检测胞内ROS变化,分光光度计检测上清液中超氧化物歧化酶( superoxide dislutase,SOD)、谷胱甘肽过氧化物酶( glutathione peroxidase, GSH )活性及丙二醛( lalondialdehyde,MDA)的含量。
　　结果：番茄红素能明显抑制紫外线诱导的细胞活性的下降,减少紫外线所致HLEC内ROS的生成,引起HLEC内SOD和GSH-Px水平的升高及MDA水平的下降。
　　结论：番茄红素通过提高细胞内SOD和GSH-Px含量,降低细胞内MDA含量,发挥其较强的抗氧化作用,从而为其用于白内障防治提供可靠的实验依据。     

Anti‐proliferative and apoptosis‐inducing activity of lycopene against three subtypes of human breast cancer cell lines

Although lycopene, a major carotenoid component of tomatoes, has been suggested to attenuate the risk of breast cancer, the underlying preventive mechanism remains to be determined. Moreover, it is not known whether there are any differences in lycopene activity among different subtypes of human breast cancer cells. Using ER/PR positive MCF‐7, HER2‐positive SK‐BR‐3 and triple‐negative MDA‐MB‐468 cell lines, we investigated the cellular and molecular mechanism of the anticancer activity of lycopene. Lycopene treatment for 168 consecutive hours exhibited a time‐dependent and dose‐dependent anti‐proliferative activity against these cell lines by arresting the cell cycle at the G₀/G₁ phase at physiologically achievable concentrations found in human plasma. The greatest growth inhibition was observed in MDA‐MB‐468 where the sub‐G₀/G₁ apoptotic population was significantly increased, with demonstrable cleavage of PARP. Lycopene induced strong and sustained activation of the ERK1/2, with concomitant cyclin D1 suppression and p21 upregulation in these three cell lines. In triple negative cells, lycopene inhibited the phosphorylation of Akt and its downstream molecule mTOR, followed by subsequent upregulation of proapoptotic Bax without affecting anti‐apoptotic Bcl‐xL. Taken together, these data indicate that the predominant anticancer activity of lycopene in MDA‐MB‐468 cells suggests a potential role of lycopene for the prevention of triple negative breast cancer.