吸附树脂AB—8对甘草酸的吸附性能及其在提取纯化中的应用

考察了大孔吸附树脂AB-8对甘草酸的吸附性能和原液浓度pH值、流速、洗脱剂的种类对树脂吸附性能的影响。结果表明,AB-8树脂对甘草酸吸附量高,易于洗脱,分离效果较好,回收率较一般方法高,达70％～80％,纯度达90％以上。     

蚂蚁光顾云南紫胶虫对其天敌紫胶黑虫种群的影响

为了弄清蚂蚁光顾云南紫胶虫Kerria yunnanensis Ouet Hong对其天敌紫胶黑虫Holcocera pulverea Meyr种群的影响,于云南紫胶虫成虫期,对有无蚂蚁光顾的胶被抽样,调查胶被上紫胶黑虫的为害率及种群数量变化。结果显示,紫胶黑虫对有无蚂蚁光顾的胶被的为害率均很高,并逐月增加;其中有蚂蚁光顾的胶被紫胶黑虫的为害率略小于无蚂蚁光顾的胶被。蚂蚁光顾能明显减少紫胶黑虫的种群数量(︱t︱=2.764,df=356,P<0.01),其原因可能是蚂蚁光顾能干扰紫胶黑虫的产卵行为、破坏卵、取食卵和幼虫并且这种保护主要发生在云南紫胶虫幼虫期;云南紫胶虫进入成虫期后,由于紫胶黑虫生活于胶被内,并且产卵于胶被的凹陷处或雄虫胶壳内或雌虫肛突孔处,蚂蚁很少与紫胶黑虫相遇,故蚂蚁光顾对紫胶黑虫每月增长量没有显著影响(︱t︱=0.970,df=161,P>0.05)。紫胶黑虫和蚂蚁相遇的行为反应存在显著差异(χ2=4.781,df=1,P<0.05),蚂蚁对紫胶黑虫有捕食作用。蚂蚁与云南紫胶虫之间存在互利关系。蚂蚁取食云南紫胶虫的蜜露,能降低紫胶黑虫的为害率,并减少紫胶黑虫的种群数量,从而保护云南紫胶虫。     

Nigericin inhibits epithelial ovarian cancer metastasis by suppressing the cell cycle and epithelial−mesenchymal transition

Epithelial ovarian cancer (EOC) has the highest mortality among various types of gynecological malignancies. Most patients die of metastasis and recurrence due to cisplatin resistance. Thus, it is urgent to develop novel therapies to cure this disease. CCK-8 assay showed that nigericin exhibited strong cytotoxicity on A2780 and SKOV3 cell lines. Flow cytometry indicated that nigericin could induce cell cycle arrest at G0/G1 phase and promote cell apoptosis. Boyden chamber assay revealed that nigericin could inhibit migration and invasion in a dose-dependent manner by suppressing epithelial–mesenchymal transition (EMT) in EOC cells. These effects were mediated, at least partly, by the Wnt/β-catenin signaling pathway. Our results demonstrated that nigericin could inhibit EMT during cell invasion and metastasis through the canonical Wnt/β-catenin signaling pathway. Nigericin may prove to be a novel therapeutic strategy that is effective in patients with metastatic EOC.     

黑木耳胶质铁配合物的制备及其性质研究

利用黑木耳提取多糖后的料渣(主要为胶质物质),与铁(Ⅲ)合成黑木耳胶质铁配合物(AGIC),并测定AGIC的理化性质.结果表明AGIC为无定形棕色粉末,易溶于水,其水溶液中不存在游离的铁(Ⅲ),表明铁(Ⅲ)与黑木耳胶质形成了稳定的配合物.采用抗坏血酸还原,AGIC中的铁(Ⅲ)易被抗坏血酸还原成铁(Ⅱ),说明黑木耳胶质铁配合物有望开发成理想的口服补铁剂.     

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.     

Sestrin 2 attenuates sepsis‐associated encephalopathy through the promotion of autophagy in hippocampal neurons

Sepsis‐associated encephalopathy (SAE) has typically been associated with a poor prognosis. Although sestrin 2 (SESN2) plays a crucial role in metabolic regulation and the stress response, its expression and functional roles in SAE are still unclear. In the present study, SAE was established in mice through caecal ligation and puncture (CLP). The adeno‐associated virus 2 (AAV2)‐mediated SESN2 expression (ie overexpression and knockdown) system was injected into the hippocampi of mice with SAE, and subsequently followed by electron microscopic analysis, the Morris water maze task and pathological examination. Our results demonstrated an increase of SESN2 in the hippocampal neurons of mice with SAE, 2‐16 hours following CLP. AAV2‐mediated ectopic expression of SESN2 attenuated brain damage and loss of learning and memory functions in mice with SAE, and these effects were associated with lower pro‐inflammatory cytokines in the hippocampus. Mechanistically, SESN2 promoted unc‐51‐like kinase 1 (ULK1)‐dependent autophagy in hippocampal neurons through the activation of the AMPK/mTOR signalling pathway. Finally, AMPK inhibition by SBI‐0206965 blocked SESN2‐mediated attenuation of SAE in mice. In conclusion, our findings demonstrated that SESN2 might be a novel pharmacological intervention strategy for SAE treatment through promotion of ULK1‐dependent autophagy in hippocampal neurons.