Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.     

Antibacterial potential of Forsythia suspensa polysaccharide against resistant Enterobacter cloacae with SHV‐12 extended‐spectrum β‐lactamase (ESBL)

In this study, a homogenous polysaccharide (FSP), with an average molecular weight of 9.08 × 10⁴ Da, was isolated from Forsythia suspense and its antibacterial potential against Enterobacter cloacae producing SHV‐12 ESBL was investigated. Growth kinetics, in vitro competition and biofilm formation experiments demonstrated that SHV‐12 ESBL contributed to a fitness benefit to E cloacae strain. The antibacterial activity of FSP (2.5, 5.0 and 10.0 μg/mL) was tested against E cloacae bearing SHV‐12 ESBL gene using bacterial sensitivity, agar bioassay and agar well diffusion assays. It was found that the addition of FSP demonstrated potent antibacterial activities against this bacterial as showed by the decrease of bacterial growth and the increase of the inhibition zone diameter. Furthermore, SHV‐12 ESBL gene expression was decreased in E cloacae strain following different FSP treatment in a concentration‐dependent manner. In conclusion, these data showed that FSP exhibited potent good antibacterial activity against E cloacae producing SHV‐12 ESBL via inhibition of SHV‐12 ESBL gene expression, which may promote the development of novel natural antibacterial agents to treat infections caused by this drug‐resistant bacterial pathogen.     

Neutrophil extracellular traps activate lung fibroblast to induce polymyositis‐related interstitial lung diseases via TLR9‐miR‐7‐Smad2 pathway

Excessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)‐associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ILD and promoted pulmonary fibrosis (PF) in vivo. miR‐7 expression was down‐regulated in lung tissue of PM group than control group, and NETs further decreased miR‐7 expression. TLR9 and Smad2 were up‐regulated in lung tissue of PM group than control group, and NETs further increased TLR9 and Smad2 expressions. In vitro experiments showed that PMA‐treated NETs accelerated the proliferation of LF and their differentiation into myofibroblast (MF), whereas DNase I decreased the promotion effect of NETs. Neutrophil extracellular trap components myeloperoxidase (MPO) and histone 3 also promoted the proliferation and differentiation of LF. In addition, we demonstrated that TLR9 involved in the regulation of NETs on LF proliferation and differentiation, and confirmed the interaction between miR‐7 and Smad2 in LF. Finally, miR‐7‐Smad2 pathway was confirmed to be involved in the regulation of TLR9 on LF proliferation and differentiation. Therefore, NETs promote PM‐related ILD, and TLR9‐miR‐7‐Smad2 signalling pathway is involved in the proliferation of LFs and their differentiation into MFs.     

A novel lncRNA PLK4 up‐regulated by talazoparib represses hepatocellular carcinoma progression by promoting YAP‐mediated cell senescence

A growing number of studies recognize that long non‐coding RNAs (lncRNAs) are essential to mediate multiple tumorigenic processes, including hepatic tumorigenesis. However, the pathological mechanism of lncRNA‐regulated liver cancer cell growth remains poorly understood. In this study, we identified a novel function lncRNA, named polo‐like kinase 4 associated lncRNA (lncRNA PLK4, GenBank Accession No. RP11‐50D9.3), whose expression was dramatically down‐regulated in hepatocellular carcinoma (HCC) tissues and cells. Interestingly, talazoparib, a novel and highly potent poly‐ADP‐ribose polymerase 1/2 (PARP1/2) inhibitor, could increase lncRNA PLK4 expression in HepG2 cells. Importantly, we showed that talazoparib‐induced lncRNA PLK4 could function as a tumour suppressor gene by Yes‐associated protein (YAP) inactivation and induction of cellular senescence to inhibit liver cancer cell viability and growth. In summary, our findings reveal the molecular mechanism of talazoparib‐induced anti‐tumor effect, and suggest a potential clinical use of talazoparib‐targeted lncRNA PLK4/YAP‐dependent cellular senescence for the treatment of HCC.     

Reduction of SOST gene promotes bone formation through the Wnt/β-catenin signalling pathway and compensates particle-induced osteolysis

The increase in bone resorption and/or the inhibition of bone regeneration caused by wear particles are the main causes of periprosthetic osteolysis. The SOST gene and Sclerostin, a protein synthesized by the SOST gene, are the characteristic marker of osteocytes and regulate bone formation and resorption. We aimed to verify whether the SOST gene was involved in osteolysis induced by titanium (Ti) particles and to investigate the effects of SOST reduction on osteolysis. The results showed osteolysis on the skull surface with an increase of sclerostin levels after treated with Ti particles. Similarly, sclerostin expression in MLO-Y4 osteocytes increased when treated with Ti particles in vitro. After reduction of SOST, local bone mineral density and bone volume increased, while number of lytic pores on the skull surface decreased and the erodibility of the skull surface was compensated. Histological analyses revealed that SOST reduction increased significantly alkaline phosphatase- (ALP) and osterix-positive expression on the skull surface which promoted bone formation. ALP activity and mineralization of MC3T3-E1 cells also increased in vitro when SOST was silenced, even if treated with Ti particles. In addition, Ti particles decreased β-catenin expression with an increase in sclerostin levels, in vivo and in vitro. Inversely, reduction of SOST expression increased β-catenin expression. In summary, our results suggested that reduction of SOST gene can activate the Wnt/β-catenin signalling pathway, promoting bone formation and compensated for bone loss induced by Ti particles. Thus, this study provided new perspectives in understanding the mechanisms of periprosthetic osteolysis.     

Two New Abietane Diterpenoids from Selaginella moellendorffii Hieron.

Two new abietane diterpenoids, (3S,5R,10S)‐3‐hydroxy‐12‐O‐demethyl‐11‐deoxy‐19(4→3)‐abeo‐cryptojaponol, 12,19‐dihydroxyabieta‐8,11,13‐trien‐7‐one, were isolated from Selaginella moellendorffii Hieron., together with one known abietane diterpenoid and four known tetracyclic triterpenoids. Their structures were characterized by their 1D‐ and 2D‐NMR, ECD and mass spectral studies. All compounds were tested for their inhibitory effects on proliferation of three human cancer cells (human non‐small‐cell lung carcinoma cell lines A549 and human breast adenocarcinoma cell lines MDA‐MB‐231 and MCF‐7) in vitro. Among them, three compounds displayed modest cytotoxic activities against the above three human cancer cell lines with IC₅₀ values ranging from 16.28 to 40.67 μM.     

Enabling Deformable and Stretchable Batteries

Deformable energy storage devices are needed to power next‐generation wearable electronics that interface intimately with human skin. Currently, deformable energy storage devices demonstrate poor performance compared to their rigid lithium‐ion counterparts, forcing wearable manufacturers to design their devices around bulky battery compartments. However, technological advances to create deformable batteries at the component and device level have yielded continuous improvement in stretchable batteries over the last five years. In this Essay, the major strategies at the component and device level that have been successfully employed to create stretchable batteries are reviewed. The outstanding challenges facing deformable energy storage are also discussed, namely, energy density, packaging, delamination, device integration, and manufacturing. This Essay will give researchers who are interested in contributing to the development of deformable batteries a cursory understanding of the most successful strategies to date, and provide insights into the most important directions to pursue in the future.     

白蛋白静脉滴注联合茵栀黄颗粒治疗新生儿黄疸血清 AKP、TBA、 FFA、γ-GT、HS-CRP的影响

目的:研究白蛋白静脉滴注联合茵栀黄颗粒对新生儿黄疸血清碱性磷酸酶(alkaline phosphatase,AKP)、总胆汁酸(totalbileacids,TBA)、游离脂肪酸(free fatty acid,FFA)、γ-谷氨酰基转移酶(γ-glutamyltransferase,γ-GT)、超敏C-反应蛋白(hypersensitive C-reactive protein, HS-CRP)的影响。方法:选择2016年1月～2019年1月我院收治的95例新生儿病理性黄疸患儿,随机分为两组。对照组服用茵栀黄颗粒治疗,观察组在服用茵栀黄的基础上静脉滴注白蛋白治疗。检测两组的血清间接胆红素(indirectreacting bilirubin,,IBIL)、总胆红素(total bilirubin,TBIL)和AKP、TBA、FFA、y-GT、HS-CRP水平。结果:观察组的有效率明显高于对照组(P0.05);两组治疗后的血清IBIL、TBIL水平明显降低(P0.05),观察组的IBIL、TBIL水平明显低于对照组(P0.05);两组治疗后的血清AKP、TBA、FFA、γ-GT、HS-CRP水平明显降低(P0.05),观察组的血清AKP、TBA、FFA、γ-GT、HS-CRP水平明显低于对照组(P0.05)。结论:白蛋白静脉滴注联合茵栀黄颗粒对新生儿黄疸的治疗效果良好,有助于促进血清胆红素和其他血清学相关指标恢复正常,且安全性好。     

门冬胰岛素联合甘精胰岛素对新诊断2型糖尿病患者炎性因子、血糖及血脂水平的影响

目的:探讨门冬胰岛素联合甘精胰岛素对新诊断2型糖尿病患者血清炎性因子、血糖及血脂水平的影响。方法:选取我院2017年3月～2019年3月收治的100例新诊断2型糖尿病患者,将其随机分为研究组和对照组,每组50例患者。对照组患者给予门冬胰岛素治疗,研究组患者给予门冬胰岛素联合甘精胰岛素治疗,对比两组患者治疗前后血清炎性因子、血糖及血脂水平的变化。结果:治疗后,两组患者糖化血红蛋白(hemoglobin A1c,HbA1c)、空腹血糖(fasting plasma glucose,FPG)、餐后2h血糖(2h postprandial blod glucose,2hPBG)、血清肿瘤坏死因子(Tumor necrosis factor,TNF-α)、高敏C反应蛋白(high-sensitive C-reactive protein,hs-CRP)水平均较治疗前明显降低(P0.05),且研究组患者以上指标均显著低于对照组(P0.05);两组患者治疗后总胆固醇(Total Cholesterol,TC)、甘油三酯(Triglyceride,TG)、低密度脂蛋白胆固醇(Low-density lipoprotein cholesterol,LDL-C)水平均较治疗前明显降低,高密度脂蛋白胆固醇(High-density lipoprotein cholesterol,HDL-C)明显升高(P0.05),且研究组以上指标的改善程度均优于对照组(P0.05)。研究组患者的胰岛素用量明显少于对照组(P0.05),患者血糖首次达标时间明显短于对照组(P0.05)。结论:门冬胰岛素联合甘精胰岛素适用于新诊断2型糖尿病患者,可有效降低血糖、血脂、血清TNF-α和hs-CRP水平。