Bacterial Biofilm Formation Using PCL/Curcumin Electrospun Fibers and Its Potential Use for Biotechnological Applications

Electrospun nanofibers are used for many applications due to their large surface area, mechanical properties, and bioactivity. Bacterial biofilms are the cause of numerous problems in biomedical devices and in the food industry. On the other hand, these bacterial biofilms can produce interesting metabolites. Hence, the objective of this study is to evaluate the efficiency of poly (Ɛ- caprolactone)/Curcumin (PCL/CUR) nanofibers to promote bacterial biofilm formation. These scaffolds were characterized by scanning electron microscopy (SEM), which showed homogeneous fibers with diameters between 441–557 nm; thermogravimetric analysis and differential scanning calorimetry (TGA and DSC) demonstrated high temperature resilience with degradation temperatures over >350 °C; FTIR and ¹H-NMR serve as evidence of CUR incorporation in the PCL fibers. PCL/CUR scaffolds successfully promoted the formation of Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa biofilms. These results will be valuable in the study of controlled harvesting of pathogenic biofilms as well as in metabolites production for biotechnological purposes.     

姜黄素烟酸酯对辐射诱导的巨噬细胞IL-1β、IL-18表达的影响*

目的 研究姜黄素烟酸酯对巨噬细胞受射线照射产生的炎症因子白细胞介素-1β（IL-1β）、白细胞介素-18（IL-18）的影响。方法 将巨噬细胞分为空白对照组、单纯照射组及不同浓度姜黄素烟酸酯组（1.0、3.0和9.0?μmol/L）,应用Western blotting检测IL-1β、IL-18的表达。结果 1.0、3.0和9.0?μmol/L的姜黄素烟酸酯组与单纯照射组比较,差异有统计学意义（P?<0.05）,各浓度姜黄素烟酸酯组IL-1β、IL-18的蛋白表达量较单纯照射组下降;单纯照射组IL-1β、IL-18的蛋白表达量较对照组升高（P?<0.05）。结论 姜黄素烟酸酯可抑制辐射诱导巨噬细内炎症因子IL-1β、IL-18的产生。     

姜黄素预处理对急性缺血再灌注模型大鼠肝脏的保护作用

目的：建立姜黄素预处理的大鼠急性肝脏缺血再灌注模型,初步探讨姜黄素对急性缺血再灌注后大鼠肝脏的保护作用。方法：10只SD大鼠随机分为假手术组（n=3）、溶剂对照组（n=3）和实验组（n=4）。实验组和溶剂对照组大鼠在进行急性肝脏缺血再灌注前分别腹腔注射姜黄素和1%羧甲基纤维素钠（CMC）进行预处理。假手术组大鼠不进行急性肝脏缺血再灌注。采用超高效液相色谱-质谱（UPLC-MS）联用法分析各组大鼠血清中姜黄素水平,胆管导管术和荧光分析法检测各组大鼠胆汁流量,丙二醛（MDA）试剂盒检测各组大鼠肝脏组织中MDA水平。结果：腹腔注射200mg·kg^-1姜黄素1h后大鼠血清中姜黄素水平达到（0.17±0.05）mg·L^-1,并在注射3h后降到检测线以下。实验组大鼠肝脏组织中MDA水平为（9.18±1.78）mmol·g^-1,低于溶剂对照组（527.54mmol·g^-1±237.38mmol·g^-1）和假手术组（162.73mmol·g^-1±90.50 mmol·g^-1）。实验组大鼠在缺血再灌注后胆汁流量恢复到基线的40%左右,与溶剂对照组比较差异无统计学意义（P>0.05）,假手术组大鼠胆汁流量则保持在基线水平。结论：姜黄素腹腔注射给药后能迅速进入大鼠血液循环,并在体内较快代谢,其水平在给药3h后降到检测线以下。姜黄素预处理能有效降低缺血再灌注后肝脏组织中MDA水平,对肝脏起到保护作用,但对恢复胆汁流量的效果不明显。     

姜黄素通过NLRP3/Caspase-1/IL-1β轴对低氧性肺动脉高压的干预作用

目的：探讨姜黄素对低氧性肺动脉高压（HPH）的作用及其机制。方法：同时研究肺动脉平滑肌细胞（PASMCs）和SD大鼠肺组织,PASMCs和SD大鼠都设置为常氧组（N）、低氧组（H）、低氧+姜黄素组（HC）3组。CCK-8法测3组PASMCs细胞活力,Western blot法检测3组PASMCs和肺匀浆中NLRP3、Caspase-1及IL-1β蛋白表达差异。血流动力学检测3组大鼠的平均肺动脉压（mPAP）及右心肥大程度,HE染色观察3组大鼠肺血管重塑程度。结果：与N组比,H组PASMCs的数量有明显增加（P＜0.05）,H组PASMCs和肺匀浆中NLRP3、Caspase-1、IL-1β蛋白表达均上升（均P＜0.05）,H组大鼠的mPAP及右心肥大指数明显升高（均P＜0.05）,发生明显肺血管重塑;与H组比,HC组PASMCs的数量明显降低（P＜0.05）,PASMCs和肺匀浆中NLRP3、Cas-pase-1、IL-1β蛋白表达均下降（均P＜0.05）,HC组大鼠的mPAP及右心肥大指数明显降低（均P＜0.05）,肺血管重塑改善。结论：姜黄素可能通过抑制NLRP3/Caspase-1/IL-1β轴,改善低氧PASMCs异常增殖、HPH大鼠肺血管重塑和右心肥大,降低肺动脉压力。     

Curcumin inhibits inflammatory response and bone loss during experimental periodontitis in rats

Abstract

Objective. Curcumin, an active ingredient of turmeric, is proved to be a potential candidate of controlling inflammation and bone resorption, but few reports are on the periodontitis. The purpose of this study was to evaluate whether the intra-gastric administration of curcumin could inhibit the in?ammation and alveolar bone resorption in rats following ligature-induced experimental periodontitis. Materials and method. Male Wistar rats were randomly divided into three groups: no ligature placement and administration of vehicle, ligature placement and administration of vehicle, ligature placement and administration of curcumin. After the animals were sacrificed, their mandibles were collected for morphological, histological and immunohistochemical analysis; their gingival tissues were collected for cytokine measurements. Results. Bone resorption was significantly higher in the experimental periodontitis animals treated with vehicle compared with the curcumin-treated group or the control group. Furthermore, receptor activator of nuclear factor-κB ligand (RANKL), receptor activator of nuclear factor-κB (RANK), osteoprotegerin (OPG), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) expression levels were higher in the experimental periodontitis animals treated with vehicle compared with the curcumin treated group or the control group. Conclusions. Curcumin may decrease alveolar bone loss in the experimental periodontitis rats via suppressing the expression of RANKL/RANK/OPG and its anti-inflammatory properties.     

Curcumin attenuates endothelial cell fibrosis through inhibiting endothelial–interstitial transformation

Curcumin (Cur) has various pharmacological activities, including anti-inflammatory, antiapoptotic and anticancer effects. However, there is no report on the effect of Cur on endothelial cell fibrosis. This study was designed to investigate the effect and mechanism of Cur on endothelial cell fibrosis. An endothelial cell fibrosis model was established by using transforming growth factor (TGF) induction. Proliferation assays, qRT-PCR, western blotting and immunostaining were performed to investigate the effects and mechanism of Cur on endothelial cell fibrosis. We found that in human umbilical vein endothelial cells (HUVECs), TGF-β1 treatment significantly decreased the expression of nuclear factor erythroid-2-related factor 2 (NRF-2), dimethylarginine dimethylaminohydrolase-1 (DDAH1), and VE-cadherin, the secretion of cellular nitric oxide (NO) and the activity of nitrous oxide synthase (NOS), while asymmetric dimethylarginine (ADMA) and the release of inflammatory factors were elevated. Immunofluorescence showed decreased CD31 and increased α-smooth muscle actin (α-SMA). Overexpression of NRF-2 significantly attenuated the effects of TGF-β1, while downregulation of DDAH1 potently counteracted the effect of NRF-2. In addition, ADMA treatment resulted in similar results to those of TGF-β1, and Cur significantly attenuated the effect of TGF-β1, accompanied by increased VE-cadherin, DDAH1 and NRF-2 and decreased matrix metalloproteinase-9 (MMP-9) and extracellular regulated protein kinases 1/2 (ERK1/2) phosphorylation. The NRF-2 inhibitor ML385 had the opposite effect as that of Cur. These results demonstrated that Cur inhibits TGF-β1-induced endothelial-to-mesenchymal transition (EndMT) by stimulating DDAH1 expression via the NRF-2 pathway, thus attenuating endothelial cell fibrosis.     

姜黄素对小鼠皮肤移植排斥反应的影响

目的 探讨姜黄素对小鼠皮肤移植排斥反应的免疫抑制作用。方法 BALB/c小鼠作为供体,C57BL/6小鼠作为受体,建立背-背皮肤移植模型。术后分为假手术组、模型组、姜黄素（50 mg/kg）组、环孢素A （10 mg/kg）组、姜黄素+环孢素A （50 mg/kg+5 mg/kg）组,每组10只,每天1次,ip给药10 d。记录各只小鼠移植皮片的存活天数,术后第4、8天采用ELISA法检测血浆白细胞介素-2（IL-2）浓度。结果 姜黄素组、环孢素A组、姜黄素+环孢素A组的小鼠移植皮片存活时间分别为14.77、16.81、19.96 d,与模型组（12.10 d）比较差异显著（P<0.01）;姜黄素+环孢素A组的小鼠移植皮片存活时间与姜黄素或环孢素A组比较显著延长（P<0.05、0.01）;姜黄素组、环孢素A组、姜黄素+环孢素A组术后第4天血浆IL-2水平分别为3.68、2.05、2.70 ng/mL,与模型组（4.76 ng/mL）比较差异显著（P<0.05、0.01）;姜黄素组、环孢素A组、姜黄素+环孢素A组术后第8天血浆IL-2水平分别为4.06、2.11、2.95 ng/mL,与模型组（5.85 ng/mL）比较差异显著（P<0.01）。结论 姜黄素具有抑制皮肤移植小鼠免疫排斥反应的作用。     

姜黄素对乳腺癌细胞顺铂敏感性的影响

目的 探讨姜黄素(curcumin)对乳腺癌细胞中顺铂(Cisplatin,CDDP)治疗敏感性的影响及其可能机制.方法 CCK-8检测、Hoechst染色观察CDDP、姜黄素单独及联合用药48 h对MCF7细胞增殖抑制和细胞凋亡的影响;Western blot分析MCF7细胞在CDDP(0、1.25、2.5、5、10、20 μg/mL)、姜黄素(0、1、5、20、30、50、100 μmol/L)单独及联合处理后FEN1(flap endonuclease 1)表达水平的变化;CCK-8检测沉默FEN1对MCF7细胞中CDDP敏感性的影响.结果 CDDP、姜黄素均可以剂量依赖方式抑制MCF7细胞增殖,其IC50分别为5、30 μmol/L;与单独2μg/mLCDDP处理组比较,2μg/mL CDDP联合20-μmol/L姜黄素、30 μmol/L姜黄素处理组对细胞增殖的抑制效应明显增强[分别为(84.1±0.8)％、(51.1±0.5)％、(29.4±0.3)％,P＜0.05];与单独20μmol/L姜黄素处理组比较,20 μmol/L姜黄素联合2μg/mL CDDP、5μg/mL CDDP处理组对细胞增殖的抑制效应也明显增强[分别为(76.9±0.7)％、(42.4±0.3)％、(31.6±0.4)％,P＜0.05];2μg/mL CDDP联合20 μmol/L姜黄素组的细胞凋亡明显增强(P＜0.05);与Control siRNA组比较,FEN1 siRNA+CDDP组可显著增强CDDP抑制MCF7细胞增殖的敏感性[(25.4±0.3)％vs(18.7±0.2)％,P＜0.05];CDDP增殖抑制无效浓度或低浓度时,FEN1蛋白的表达随CDDP的处理剂量依赖性上调,而姜黄素可剂量依赖性下调FEN1蛋白表达;与单独CDDP和姜黄素处理组比较,2μg/mL CDDP联合20 μmol/L姜黄素组可显著降低FEN1蛋白表达(P＜0.05).结论 姜黄素可增强CDDP对乳腺癌细胞的敏感性,其机制与降低细胞FEN1的表达有关.