凤丹籽饼粕化学成分研究

目的 研究凤丹Paeonia ostii籽饼粕的化学成分。方法 采用硅胶、凝胶柱色谱及制备高效液相色谱等多种方法进行分离纯化,根据波谱数据分析鉴定化合物结构。结果 从凤丹籽饼粕的70%乙醇提取物中分离得到5个化合物,分别鉴定为对羟基苯甲酸-β-D-葡萄糖基-(1→6)-β-D-葡萄糖苷（1）、虎杖苷（2）、木犀草素-7-O-β-D-葡萄糖苷（3）、齐墩果酸（4）、白桦脂酸（5）。结论 化合物1为新化合物,命名为凤丹苷A。化合物2～3为首次从芍药科植物中分离得到,化合物4～5为首次从该植物中分离得到。     

UPLC法同时测定金欣口服液中8种指标成分

目的 建立UPLC法同时测定金欣口服液中芥子碱硫氰酸盐、虎杖苷、野黄芩苷、白藜芦醇、黄芩苷、大黄素-8-O-β-葡萄糖苷、黄芩素、汉黄芩素8种指标成分的量.方法 采用UPLC法,Acquity UPLC BEH C18色谱柱(100 mm×2.1mm,1.7 μm),乙腈-0.1％甲酸水溶液为流动相,体积流量0.4 mL/min,梯度洗脱,检测波长280 nm,柱温35℃;分别对线性关系、精密度、重复性、稳定性及加样回收率进行考察.结果 被测定的8种指标成分分别在选定的范围内线性关系良好,平均加样回收率99％～102％,RSD均小于3.1％.结论 本方法操作简便,测定结果准确可靠,可用于金欣口服液的质量控制.     

HPLC同时测定虎贞痛风胶囊中大车前苷、虎杖苷、特女贞苷、白藜芦醇的含量

目的:建立同时测定虎贞痛风胶囊中大车前苷、虎杖苷、特女贞苷、白藜芦醇含量的HPLC方法。方法:采用高效液相法测定,色谱条件为Agilent SB-C18色谱柱(4.6 mm×250 mm,5μm),流动相乙腈-0.1%甲酸溶液梯度洗脱,检测波长280 nm,流速1.0 m L·min-1,柱温30℃。结果:大车前苷、虎杖苷、特女贞苷、白藜芦醇分别在0.099 6~1.992(r=0.999 9),0.123~2.46(r=0.999 9),0.145~2.90(r=0.999 9),0.025~0.50μg(r=0.999 8)与峰面积呈良好的线性关系,平均回收率分别为99.27%,99.43%,98.83%,98.07%。结论:该方法快速简便,重复性好,专属性强,可作为虎贞痛风胶囊的质量控制方法。     

星点设计-效应面法优选妇雅净泡腾片提取工艺

目的:采用星点设计-效应面法优选妇雅净泡腾片的提取工艺。方法:以乙醇量、乙醇体积分数和提取时间为主要影响因素,以虎杖苷含量、蛇床子素含量和浸膏得率为评价指标,用星点设计-效应面法选择提取工艺的最佳条件。结果:最佳提取工艺为加入10倍量60%乙醇、提取2次、每次2 h。结论:星点设计-效应面法优选妇雅净泡腾片的提取工艺方法简便,预测性好。     

白藜芦醇苷降血脂作用的实验研究

目的 研究白藜芦醇苷的降血脂活性.方法 通过饲喂高脂饲料建立高脂血症大鼠和家兔动物模型,分别连续给药7d和14 d,观察白藜芦醇苷对2种动物模型血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)水平的影响.结果 白藜芦醇苷显著降低高血脂家兔血清TC、TG和LDL水平,能明显对抗大鼠升高的血清TG含量.结论 白藜芦醇苷具有降血脂的作用.     

Polydatin protects hepatocytes against mitochondrial injury in acute severe hemorrhagic shock via SIRT1-SOD2 pathway

Objective: The aim of the study was to determine whether hepatocyte mitochondrial injury instigates severe shock and to explore effective therapy.

Methods: Wistar rats were randomly divided into five groups: Control (sham) group, shock + normal saline, shock + cyclosporine A, shock + resveratrol (Res) and shock + polydatin (PD) group. Mitochondrial morphology and function in hepatocytes following treatment were determined.

Results: Hepatocytes following severe shock exhibited mitochondrial dysfunction characterized with opening of mitochondrial permeability transition pores, mitochondrial swelling, decreased mitochondrial membrane potential (ΔΨm) and reduced ATP levels. Moreover, severe shock induced oxidative stress with increased lipid peroxidation and reactive oxygen species, decreased SOD₂ (Superoxide Dismutase 2) and GSH/GSSG, which resulted in increased lysosomal membrane permeabilization and hepatocyte mitochondrial injury. Additionally, Res and PD restored decreased deacetylase sirtuin1 activity and protein expression in liver tissue following severe shock, suppressed oxidative stress-induced lysosomal unstability and mitochondrial injury by increasing the protein expression of SOD₂, and thereby contributed to the prevention of hepatocyte mitochondria dysfunction and liver injury.

Conclusions: PD effectively preserved hepatocytes from mitochondrial injury via SIRT1-SOD₂ pathway and may be a new approach to treatment of irreversible shock.     

Polydatin attenuates renal fibrosis in diabetic mice through regulating the Cx32-Nox4 signaling pathway

We previously found that polydatin could attenuate renal oxidative stress in diabetic mice and improve renal fibrosis. Recent evidence shows that NADPH oxidase 4 (Nox4)-derived reactive oxygen species (ROS) contribute to inflammatory and fibrotic processes in diabetic kidneys. In this study we investigated whether polydatin attenuated renal fibrosis by regulating Nox4 in vitro and in vivo. In high glucose-treated rat glomerular mesangial cells, polydatin significantly decreased the protein levels of Nox4 by promoting its K48-linked polyubiquitination, thus inhibited the production of ROS, and eventually decreasing the expression of fibronectin (FN) and intercellular adhesion molecule-1 (ICAM-1), the main factors that exacerbate diabetic renal fibrosis. Overexpression of Nox4 abolished the inhibitory effects of polydatin on FN and ICAM-1 expression. In addition, the expression of Connexin32 (Cx32) was significantly decreased, which was restored by polydatin treatment. Cx32 interacted with Nox4 and reduced its protein levels. Knockdown of Cx32 abolished the inhibitory effects of polydatin on the expression of FN and ICAM-1. In the kidneys of streptozocin-induced diabetic mice, administration of polydatin (100 mg·kg⁻¹·d⁻¹, ig, 6 days a week for 12 weeks) increased Cx32 expression and reduced Nox4 expression, decreased renal oxidative stress levels and the expression of fibrotic factors, eventually attenuating renal injury and fibrosis. In conclusion, polydatin promotes K48-linked polyubiquitination and degradation of Nox4 by restoring Cx32 expression, thereby decreasing renal oxidative stress levels and ultimately ameliorating the pathological progress of diabetic renal fibrosis. Thus, polydatin reduces renal oxidative stress levels and attenuates diabetic renal fibrosis through regulating the Cx32-Nox4 signaling pathway.     

虎杖苷对脓毒症致急性肾损伤小鼠的保护作用

目的观察虎杖苷对盲肠结扎穿孔(cecal ligation and puncture,CLP)所致脓毒症诱导的急性肾损伤小鼠的影响,并初步探讨其作用机制。方法建立小鼠CLP诱导的脓毒症致急性肾损伤模型,随后用不同剂量的虎杖苷(50、100、300 mg/kg)干预,观察小鼠一般情况,并于手术24 h后,用试剂盒方法测定血清尿素氮(BUN)、肌酐(Cr)水平,ELISA法测定血清白细胞介素-6(IL-6)表达量,Western blotting法检测肾脏诱导型一氧化氮合酶(iNOS)蛋白水平,并取肾脏组织进行病理分析。结果与模型组相比,虎杖苷明显改善小鼠一般情况,同时降低血清BUN、Cr、IL-6及肾脏中iNOS蛋白水平,缓解肾脏组织损伤,并呈一定的剂量依赖关系。结论虎杖苷对脓毒症致急性肾损伤具有保护作用,其作用机制可能与其抑制血清IL-6及肾脏中iNOS蛋白表达有关。     

虎杖甙在兔肺缺血再灌注损伤中的保护作用

目的:探讨虎杖甙(polydatin,PD)对兔肺缺血再灌注损伤的保护作用.方法:采用在体兔单肺原位缺血再灌注损伤模型.30只日本大耳兔,随机均分为三组:假手术组(S组),缺血再灌注组(I/R组)和缺血再灌注 PD组(PD组).实验末测血清SOD活力和MDA含量,肺湿干重比和肺泡损伤数比值,观察肺超微结构变化.结果:①I/R组与S组相比,SOD活力下降,MDA含量、湿干重比及肺泡损伤数比值增加(P均＜0.01).PD组与I/R组相比,S0D活力增加,MDA含量降低,湿干重比及肺泡损伤数比值下降(P均＜0.01).②电镜显示I/R组有明显的肺超微结构损伤,而PD组损伤不明显.结论:PD对肺缺血再灌注损伤有明显的保护作用.     

HPLC法测定藜芦中虎杖苷和白藜芦醇的含量

目的:建立HPLC法测定由甲醇加热回流和甲醇超声两种方法提取的藜芦中虎杖苷和白藜芦醇的含量的方法.方法:采用Spherigel C18色谱柱(150mm×4.6mm,5μm),流动相为四氢呋喃-乙腈-水(40:40:220),流速1.0mL·min-1,检测波长303nm.结果:虎杖苷在0～50mg·L-1内成良好线性关系,平均回收率甲醇加热回流提取102.4%,RSD1.1%;甲醇超声提取97.2%,RSD1.1%.白藜芦醇在0～100mg·L-1内成良好线性关系,平均回收率甲醇加热回流提取96.6%,RSD1.5%;甲醇超声提取96.6%,RSD1.2%.结论:本法可作为藜芦质量控制的手段之一.