原花青素B1与B2抑制脂多糖诱导的BV-2细胞炎症反应作用的比较

目的:比较原花青素二聚体的2种同分异构体——原花青素B1和B2对脂多糖(lipopolysaccharide,LPS)诱导的BV-2细胞炎症反应的抑制作用。方法:体外培养BV-2细胞,MTT法检测原花青素B1与B2对BV-2细胞活力的影响;以1 mg/L的LPS刺激BV-2细胞12 h建立的细胞炎症模型为研究对象,分别采用ELISA法、Transwell趋化实验和Western blot法比较原花青素B1和B2对LPS诱导的BV-2细胞分泌肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)和白细胞介素1β(interleukin-1β,IL-1β)、趋化行为及核因子κB(NF-κB)磷酸化的抑制作用。结果:原花青素B1和B2对BV-2细胞没有毒性。与LPS组比较,原花青素B1和B2均可显著降低LPS诱导的TNF-α和IL-1β的释放及BV-2细胞的趋化作用,并抑制NF-κB的磷酸化。结论:原花青素B1和B2均能抑制LPS诱导的BV-2细胞炎症反应,其作用强度无显著差异。     

莲房原花青素对高脂血症大鼠脂质过氧化及内皮素1的影响

目的研究莲房原花青素（Proanthocyanidins from Lotus Seedpod，LSPC）对食饵性高脂血症模型大鼠脂质过氧化和内皮素1（ET-1）的调节作用。方法Wistar大鼠随机分成4组，即对照组（C组）、高脂血症模型组（H组）、LSPC高剂量组（HD组）、LSPC低剂量组（LD组），除对照组饲普通饲料外，其余各组喂饲高脂饲料并进行干预实验比较。4周后检测大鼠血脂及血浆超歧物过氧化物酶（SOD）、丙二醛（MDA）、一氧化氮（N0）、ET-1的变化。结果与对照组相比较，H组血清总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）水平显著升高；血浆中MDA和ET-1含量明显增高，而SOD活性和NO含量明显降低。HD组和LD组血浆SOD活性和NO含量显著升高，MDA和ET-1含量明显降低，但对血脂水平无显著性影响。结论LSPC具有心血管保护作用，其作用机制与抗氧化作用和改善血管内皮功能有关。     

原花青素对小鼠视网膜光化学损伤的保护作用

目的观察原花青素对视网膜光化学损伤后感光细胞的保护作用。方法24只昆明小鼠随机分为3组：A组为正常对照组;B组为光化学损伤模型对照组;C组为原花青素给药组。C组在造模前三天开始灌胃给原花青素混悬液（400mg/kg/d）,B和C组先暗适应12小时,然后在自制的光损伤箱内光照12小时,连续光照3天。在造模后第7天,将每组的8只小鼠进行光镜观察视网膜形态学,并采用计算机图像分析技术,对各实验组小鼠视网膜厚度及视网膜外核层厚度进行定量测量。结果光照第7天后,三组视网膜厚度和视网膜外核层厚度相比均具有显著性差异（p〈0.01）。结论原花青素对视网膜光化学损伤具有一定的保护作用。     

Effect of a polyphenol-rich dietary supplement containing Pinus massoniana bark extract on blood pressure in healthy adults: A parallel,randomized placebo-controlled trial

ObjectivesHigh blood pressure (BP) is a major risk factor for cardiovascular disease and prevalence rates continue to rise with ageing populations. Polypharmacy remains a burden among the ageing, thus alternative effective strategies are warranted. This study investigated the effects of a polyphenols rich dietary supplement containing Pinus massoniana bark extract (PMBE) for modulating BP in healthy Australian adults.DesignThis study is a secondary analysis of data from a double-blinded, placebo-controlled clinical trial.MethodsSixty-two healthy adults aged 55–75 years were randomized to receive 50 mL dietary supplement containing placebo (0 mg PMBE) or PMBE (1322 mg PMBE) daily for 12 weeks. Seated systolic BP (SBP) and diastolic (DBP) were measured at baseline, 6 weeks and 12 weeks. Effects of PMBE on modulating BP was also explored in this study stratified for SBP status (optimal v high) as well as by SBP medication status. Mixed effect regression modelling was employed involving fixed categorical effects for elapsed time, treatment assignment and their interaction as well as random subject-level intercept to account for within-subject correlations resulting from repeated measurements. Significant models were further examined by addition of covariates and power calculations were performed since this study was a secondary analysis.ResultsSBP significantly reduced (−3.29 mmHg, p = 0.028) after PMBE at 12 weeks compared to baseline. SBP in individuals with normal-high SBP (>120 mmHg) in the PMBE group reduced by − 6.46 mmHg (p = 0.001) at 12 weeks compared to baseline. No significant changes were reported for individuals with optimal (≤120 mmHg) SBP nor did DBP significantly change in either study groups. In individuals with non-medicated normal-high SBP, SBP significantly reduced by − 7.49 mmHg (p = 0.001) and DBP by − 3.06 mmHg (p = 0.011) at 12 weeks compared to baseline after PMBE. Cross-group comparisons were not statistically different.ConclusionsA polyphenol-rich dietary supplement derived from PMBE led to a clinically and statistically significant reduction in SBP in adults. Future studies to investigate the effects of PMBE-polyphenol supplementation on BP are warranted to confirm and explore optimal dose and impact on hypertension.     

原花青素对STZ致胰岛细胞损伤的保护作用

目的 探讨原花青素(PC)对链脲佐菌素(STZ)损伤大鼠胰岛素瘤细胞(INS-1)的保护作用.方法 INS-1细胞培养24 h后,以链脲佐菌素(STZ)损伤细胞,将细胞分为正常对照组、STZ组、PC保护组(PC +STZ),PC保护组培养液中加入不同浓度的PC干预12h后,用MTT比色法测定细胞存活率,用放免法检测培养细胞上清液胰岛素分泌量的变化,用比色法测定培养细胞上清液丙二醛( MDA)和超氧化物歧化酶(SOD)等指标的变化.结果 PC可以减少STZ对INS-1细胞的损伤,PC保护组的INS-1细胞存活率增加(P＜0.01);与STZ组比较,PC保护组促进了INS-1细胞的胰岛素分泌(P＜0.01),降低了INS-1细胞的MDA含量(P＜0.01),增强了T-AOC的活性(P＜0.01).结论 原花青素对STZ损伤INS-1细胞有一定的保护作用,其机制可能是通过降低MDA生成,提高T-AOC能力有关.     

原花青素缓释片对辐射损伤小鼠机体抗应激功能的影响

目的：观察原花青素缓释片对辐射损伤小鼠应激功能的影响。方法：选取150只健康ICR雄性小鼠,随机分为空白对照组、模型组、人参总皂苷阳性药物组、原花青素缓释片低（100mg·kg-1）、高（500mg·kg-1）剂量组。辐照前各组每天分别以0.9%氯化钠溶液和不同剂量药物连续灌胃14d,灌胃至第7天,除空白对照组外,其余各组小鼠均接受6Gy60Co全身性照射1次,照射后继续灌胃7d。通过抗疲劳和耐缺氧实验,观察原花青素缓释片对辐射损伤小鼠抗应激功能的影响。结果：原花青素缓释片低、高剂量组均可以显著延长辐照损伤小鼠负重游泳持续时间,其中,低剂量组与模型组比较,差异有统计学意义（P〈0.05）,阳性对照组、高剂量组与模型组比较,差异均有显著统计学意义（P〈0.01）。高剂量组小鼠耐缺氧时间明显高于模型组（P〈0.01）;低剂量组虽有延长,但与模型组比较差异无统计学意义（P〉0.05）。原花青素缓释片高、低剂量组及阳性对照组均可显著抑制急性缺氧再暴露后丙二醛（MDA）的升高,其中,低剂量组与模型组比较,差异有统计学意义（P〈0.05）,高剂量组与模型组比较差异有显著统计学意义（P〈0.01）。结论：原花青素缓释片对辐射损伤小鼠的机体具有明显增强抵抗力、抗应激功能作用。     

原花青素对高脂血症大鼠血脂、脂蛋白磷脂酶A2的影响及意义

目的:探讨原花青素(OPC)对高脂血症大鼠血脂的影响及意义。方法:选择96只高脂血症大鼠,随机分成模型组16只、原花青素组80只,原花青素组再随机分为原花青素2,4,6,8,10mg/kg组,每组各16只。另取16只非高脂血症大鼠大鼠作为对照组。原花青素2,4,6,8,10mg/kg组每天给予相应剂量的原花青素灌胃1次,模型组、对照组每天给予与原花青素组相同体积的生理盐水1次,共灌胃2周。分别检测灌胃前后各组血清总胆固醇(TC)、甘油二酯(TG)、高密度脂蛋白(HDL)和脂蛋白磷脂酶A2(Lp-PLA2)水平。结果:随着原花青素浓度增加,血清TC、TG、Lp-PLA2水平显著降低(P<0.05),血清HDL水平显著升高(P<0.05)。8mg/kg和10mg/kg剂量组中TC和TG恢复正常比例显著高于2,4,6mg/kg组(P>0.05),6,8,10mg/kg剂量组中大鼠HDL和Lp-PLA2恢复正常比例显著高于2mg/kg和4mg/kg组(P<0.05)。结论:原花青素具有降低血脂作用,且其效果具有剂量依赖性。     

原花青素在多孔薄膜中实现高效加载和长效释放的研究

目的 探讨了原花青素药物分子通过材料表面介导的方式实现长效扩散型释放行为的可能性。方法 将原花青素分散在水中配制为药物溶液,与三氯甲烷共混后通过超声乳化的方式将混合液制备成为稳定的反相乳液。在高湿度环境条件下,将所制得的乳液浇筑在聚苯乙烯平面膜片上,待有机溶剂和水分挥发后获得表面和本体层均具有多孔结构的聚合物薄膜,并以此一步法实现原花青素在薄膜中的封装加载。最后将所制备得到的药物加载薄膜在磷酸缓冲盐溶液中浸泡进行药物释放实验,分时段取出缓冲液样品进行光谱表征确定原花青素的释放量,以此实现在28天内对原花青素释放行为的跟踪表征。结果 利用反相乳液浇筑致孔的方法,可以制备具有多层多孔结构的载药聚合物薄膜。经过乳液中水油比的调节,可以实现薄膜表层和本体层的多孔结构的调控。利用含水溶性荧光素乳液的浇筑成膜实验,并通过激光共聚焦显微镜结果证实了由反相乳液的乳液水滴所携带的亲水组分可以高效地实现在所形成多孔结构中的选择性分布,证明了原花青素组分在多孔膜当中可以实现有效加载。在这种多孔多层结构的薄膜当中所加载的原花青素可以实现超过28天以上的长效缓释,其释放行为遵循了Fickian扩散式机理。结论 利用聚合物多孔薄膜或者涂层作为药物载体,可以实现有效的药物加载和长效型释放,将能为设计高效灵活的药物释放体系提供有效的参考。     

Proanthocyanidin encapsulation for sustained bioactivity in dentin bioadhesion: A two-year study

ObjectivesTo determine the long-term effect on the stability of dentin-resin interfaces after the addition of polylactide (PLA) capsules containing proanthocyanidin (PAC) to adhesive resin.MethodsSub-micron (SM) and micron (M) size capsules containing PACs were produced using a combination of emulsification and solvent evaporation techniques and characterized. Human dentin surfaces (n = 8) were etched (35% glycolic acid) and primed (15% enriched Vitis vinifera extract solution - VV_e), followed by the application of an experimental adhesive containing 0 (control), 1.5 wt% of SM or M PAC-filled PLA capsules light cured for 40 s. A crown was built using commercial composite. After 24 h-immersion (37 °C) in simulated body fluid, specimens were serially sectioned into resin-dentin beams. Microtensile bond strength (TBS), micro-permeability and fracture pattern were assessed immediately and after 1 and 2 years. Data were statistically analyzed using two-way ANOVA and post-hoc test (α = 0.05).ResultsPolydisperse capsules were manufactured with average diameter of 0.36 µm and 1.08 µm for SM and M, respectively. The addition of capsules did not affect TBS (p = 0.889). After 2 years, TBS significantly decreased in SM (p = 0.006), whereas M showed similar initial values (p = 0.291). Overall, less micro-permeability was found in M than the control and SM group (p < 0.001). After 2 years, fractured surfaces from capsule-containing groups failed within the adhesive layer while control fractured at the bottom of the hybrid layer.SignificanceThe addition of PAC-filled PLA microcapsules in a dental adhesive did not affect the bond strength while increased and sustained the protection against micro-permeability in the interface, likely due to release of PACs.     

The procyanidin-mediated induction of apoptosis and cell-cycle arrest in esophageal adenocarcinoma cells is not dependent on p21(Cip1/WAF1)

Previous studies have shown that the proanthocyanidin-mediated induction of apoptosis and arrest of the cell cycle in cancer cells was associated with up-regulation of p21^Cip1/WAF1 (p21), suggesting that p21 may be the molecular mediator of the observed effects. Here we show that procyanidins induce a rapid and sustained arrest of the cell cycle, and increase apoptosis, concomitant with an increase in p21 expression. However, blocking the PA-induced up-regulation of p21 expression with siRNA did not alter PA-mediated changes in apoptosis and cell cycle, demonstrating that p21 is not responsible for the PA-induced effects.