不同炮制方法对化橘红中柚皮苷含量的影响

目的以柚皮苷含量为指标,考察不同炮制方法对化橘红质量的影响.方法采用HPLC法测定柚皮苷含量,色谱柱:Kromasil ODS柱(250 mm×4.6 mm),流动相:甲醇二水-乙酸(35:61:4),流速:1.0 mL/min,检测波长:283 nm,柱温:25℃.结果采用不同的炮制方法,化橘红柚皮苷含量有显著差异,以静电干燥明显高于烘干干燥、自然干燥和真空干燥.结论以静电干燥所得化橘红柚皮苷含量高,是炮制化橘红的较好方法.     

梅州沙田柚的花、果、叶中柚皮苷含量比较研究

目的对梅州沙田柚花、果、叶的柚皮苷进行比较研究,为该植物综合利用提供依据。方法采用薄层色谱法鉴别柚皮苷;采用高效液相色谱法测定柚皮苷含量。结果摘花期柚花的柚皮苷含量高,选果期的柚果于第1次摘果即5月初时含量最高．裁枝期的叶含量较低。结论次花、次果、柚叶均可综合利用,变废为宝。     

RP-HPLC法测定绿衣枳实中柚皮苷的含量

目的建立绿衣枳实中柚皮苷的含量测定方法。方法采用HPLC法,色谱柱为Kromasil C18(250mm×4.6mm,5μm);流动相为乙腈-0.1%磷酸水溶液(30∶70);检测波长为283nm;流速为1.0mL·min-1。结果柚皮苷在0.168~2.016μg呈良好的线性关系,回归方程为Y=1964.8X-2.55(r=0.9998),平均加样回收率为100.9%,RSD为2.12%(n=6)。结论本方法操作简便,结果准确,分离效果好,可用于该药材的质量控制。     

正交实验法优选骨碎补提取工艺的研究

目的：研究骨碎补的提取工艺。方法：以骨碎补总黄酮及柚皮苷含量为指标，采用正交实验法进行优选，并用紫外分光光度法测定总黄酮的含量．HPLC法测定柚皮苷含量。结果：提取次数是骨碎补有效成分提取的关键因素，其次是溶媒用量．乙醇浓度和提取时间为最次要因素。结论：最佳提取工艺为骨碎补用10倍量60％乙醇回流提取3次．1h/次。     

采用自动煎药机制备橘红痰咳液的工艺及稳定性研究

目的:研究自动煎药机制备橘红痰咳液的最佳煎药工艺及稳定性。方法:选定影响煎药的3个主要因素,通过正交试验确定最佳煎药工艺;采用HPLC法测定不同贮存方法和贮存时间橘红痰咳液中苦杏仁苷和柚皮苷的含量及其卫生学检测指标。结果:橘红痰咳液在所测定的7周内,药液微生物含量符合《中国药典》2010版中关于合剂的微生物限度要求;苦杏仁苷和柚皮苷在7周内含量比较稳定。结论:煎药机制备橘红痰咳液最佳煎煮工艺为浸泡40min,100℃煎40min;橘红痰咳液在常温和冰箱能保存4周。     

柚皮苷对糖尿病心肌病大鼠心肌超微结构和缺氧诱导因子1α的影响

目的:观察柚皮苷对糖尿病心肌病大鼠心肌超微结构及缺氧诱导因子1α(HIF-1α)表达的影响,探讨柚皮苷防治糖尿病心肌病的作用机制。方法:将50只雄性Wister大鼠随机分为空白对照组(NC)、模型对照组(DC)和柚皮苷组(NA)。DC组和NA组采用高糖高脂饲料喂养,并且在喂养6周后予链脲佐菌素腹腔注射行糖尿病心肌病造模。NA组给予柚皮苷灌胃,NC组DC组予生理盐水灌胃。各组每2周断尾采血,检测血糖、血脂、肌钙蛋白、B型利钠肽等指标。12周后将各组动物经心脏取血后处死,取心脏测定心重指数。制作标本用电镜观察心肌细胞超微结构,采用免疫组织化学方法检测心肌组织HIF-1α表达情况。结果:柚皮苷有较弱的降糖作用,能有效降低糖尿病心肌病大鼠总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)及心重指数,并明显减轻心肌病变,增加心肌HIF-1α表达。结论:柚皮苷可改善糖尿病心肌病糖、脂代谢,减轻心肌超微结构病变,对心肌具有保护作用,可能与其增加心肌HIF-1α表达有关。     

交锁髓内钉与钢板内同定微创治疗胫腓骨多段骨折的病例对照研究

目的 :采用小鼠气囊模型评价柚皮苷对聚甲基丙烯酸甲酯(Polymethylmethacrylate,PMMA)诱发的破骨细胞性骨溶解的作用。方法:选取48只雌性8~10周龄Balb/c小鼠纳入研究,采用背部注入空气法在其中的32只小鼠中建立气囊模型,植入同种系小鼠颅骨(颅骨源自其余的16只小鼠)。实验共分为4组(150 mg/kg柚皮苷治疗组、30 mg/kg柚皮苷治疗组、PBS空白对照组、DMSO载体对照组),每组8只动物。对两个柚皮苷治疗组和DMSO载体对照组的小鼠使用PMMA颗粒刺激,每组8只相应浓度进行处理,颗粒刺激第7天收集囊膜和囊内植入骨进行抗酒石酸酸性磷酸酶(Tartrate resistant acid phosphatase,TRAP)染色、Ca2+释放以及改良Masson染色病理分析进行评价,观察柚皮苷的治疗作用。结果:与DMSO载体组相比,柚皮苷治疗组降低了TRAP阳性细胞浸润的数量,差异有统计学意义(P<0.01);其中150 mg/kg浓度优于30 mg/kg浓度(8.90±1.75 vs 15.23±1.86)。在气囊模型骨吸收冲洗液中,柚皮苷能降低钙的释放,特别是150 mg/kg浓度组更为明显(P<0.05)。改良的Masson染色显示柚皮苷可减少PMMA刺激所致的骨胶原的丢失,但150 mg/kg浓度组作用大于30 mg/kg浓度组。大体及病理切片显示两种浓度的柚皮苷显著降低PMMA刺激所致的炎性反应,表现为气囊厚度的减低和炎性细胞浸润数量的减少。结论 :柚皮苷抑制PMMA诱导的破骨细胞形成,有效缓解PMMA诱发的炎性反应以及随后发生的急性骨吸收。     

Naringin ameliorates gentamicin-induced nephrotoxicity and associated mitochondrial dysfunction,apoptosis and inflammation in rats: Possible mechanism of nephroprotection

Gentamicin-induced nephrotoxicity has been well documented, although its underlying mechanisms and preventive strategies remain to be investigated. The present study was designed to investigate the protective effect of naringin, a bioflavonoid, on gentamicin-induced nephrotoxicity and to elucidate the potential mechanism. Serum specific renal function parameters (blood urea nitrogen and creatinine) and histopathology of kidney tissues were evaluated to assess the gentamicin-induced nephrotoxicity. Renal oxidative stress (lipid peroxidation, protein carbonylation, enzymatic and non-enzymatic antioxidants), inflammatory (NF-kB [p65], TNF-α, IL-6 and MPO) and apoptotic (caspase 3, caspase 9, Bax, Bcl-2, p53 and DNA fragmentation) markers were also evaluated. Significant decrease in mitochondrial NADH dehydrogenase, succinate dehydrogenase, cytochrome c oxidase and mitochondrial redox activity indicated the gentamicin-induced mitochondrial dysfunction. Naringin (100 mg/kg) treatment along with gentamicin restored the mitochondrial function and increased the renal endogenous antioxidant status. Gentamicin induced increased renal inflammatory cytokines (TNF-α and IL-6), nuclear protein expression of NF-κB (p65) and NF-κB-DNA binding activity and myeloperoxidase (MPO) activity were significantly decreased upon naringin treatment. In addition, naringin treatment significantly decreased the amount of cleaved caspase 3, Bax, and p53 protein expression and increased the Bcl-2 protein expression. Naringin treatment also ameliorated the extent of histologic injury and reduced inflammatory infiltration in renal tubules. U-HPLS-MS data revealed that naringin co-administration along with gentamicin did not alter the renal uptake and/or accumulation of gentamicin in kidney tissues. These findings suggest that naringin treatment attenuates renal dysfunction and structural damage through the reduction of oxidative stress, mitochondrial dysfunction, inflammation and apoptosis in the kidney.     

柚皮苷硬膜外腔注射对髓核致坐骨神经痛大鼠的疼痛行为影响

目的研究柚皮苷硬膜外腔注射对致坐骨神经痛大鼠的疼痛行为学的影响。方法选择雄性SD大鼠28只,制作髓核致坐骨神经痛大鼠模型。随机分为4组,每组7只大鼠。术后第3天开始注药治疗,柚皮苷组每日硬膜外腔注入柚皮苷注射液50μl,地塞米松组每日硬膜外腔注入地塞米松注射液50μl,生理盐水组每日硬膜外腔注入生理盐水50μl,未注药组硬膜外腔无药物注入处理。检测大鼠术前,术后及给药后1、3、7、14d的疼痛行为指标（50％机械性刺激缩足阈值和热刺激缩足反应潜伏期）。结果4组大鼠在术后均对机械刺激产生明显的痛觉过敏,与术前比较差异有显著性（P〈0.05）;柚皮苷组与地塞米松组在提高疼痛行为学指标的作用方面差异无显著性（P〉0.05）。结论硬膜外腔注射柚皮苷可有效改善髓核致坐骨神经痛大鼠的疼痛反应。     

Synthesis,characterization and cytotoxic activity of naturally isolated naringin-metal complexes

High-purity naringin was isolated from the fruit peels of Citrus maxima and characterized by various spectroscopic methods like UV and NMR. The isolated compound ligand (HL) was used as ligand-metal complexes synthesis after using Ag (I), Y (III) and Ru (III) metals. These ligand-metal complexes were characterized by elemental analysis, FT-IR, UV–VIS, TGA, molar conductance and magnetic properties. Cytotoxic activity of the isolated naringin and its metal complexes were investigated against two human cancer cell lines namely, white breast Adenocarcinoma (MCF7) and Lung carcinoma (A549) using cell viability assay. Transition metal increased the cytotoxic activity of naringin when they were conjugated. LC50 of Ag ligand complex demonstrated strong cytotoxicity against MCF-7 and A549 cell line that was found higher active more than three and four times the strength, respectively when compared to LC50 of Adriamycin. While LC50 of Adriamycin compound was slightly more active only about 30% and twice the strength of the Ru ligand complex against MCF-7 and A549 cell line, respectively.