Autophagy Inhibition Promotes Gambogic Acid-induced Suppression of Growth and Apoptosis in Glioblastoma Cells

Luo, Guo-Xuan,Cai, Jun,Lin, Jing-Zhi,Luo, Wei-Shi,Luo, Heng-Shan,Jiang, Yu-Yang,Zhang, Yong Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.12

Objective: To investigate the effects of gambogic acid (GA) on the growth of human malignant glioma cells. Methods: U251MG and U87MG human glioma cell lines were treated with GA and growth and proliferation were investigated by MTT and colony formation assays. Cell apoptosis was analyzed by annexin V FITC/PI flow cytometry, mitochondrial membrane potential assays and DAPI nuclear staining. Monodansylcadaverine (MDC) staining and GFP-LC3 localisation were used to detect autophagy. Western blotting was used to investigate the molecular changes that occurred in the course of GA treatment. Results: GA treatment significantly suppressed cell proliferation and colony formation, induced apoptosis in U251 and U87MG glioblastoma cells in a time- and dose-dependent manner. GA treatment also lead to the accumulation of monodansylcadaverine (MDC) in autophagic vacuoles, upregulated expressions of Atg5, Beclin 1 and LC3-II, and the increase of punctate fluorescent signals in glioblastoma cells pre-transfected with GFP-tagged LC3 plasmid. After the combination treatment of autophagy inhitors and GA, GA mediated growth inhibition and apoptotic cell death was further potentiated. Conclusion: Our results suggested that autophagic responses play roles as a self-protective mechanism in GA-treated glioblastoma cells, and autophagy inhibition could be a novel adjunctive strategy for enhancing chemotherapeutic effect of GA as an anti-malignant glioma agent.

Effect of notch position on creep damage for brazed joint

Luo, Yun,Jiang, Wenchun,Zhang, Qian,Zhang, Weiya,Woo, Wanchuck,Tu, Shan-Tung,Hao, Muming Elsevier Applied Science 2016 Advances in engineering software Vol.100 No.-

<P><B>Abstract</B></P> <P>In this paper, we investigated the effect of notch position on creep damage for Hastelloy C276-BNi2 brazed joint. Three different types of notches locate in edge of base metal (base notch), edge of filler metal (surface notch) and center of filler metal (inside notch) were compared, and the influence of notch geometric parameters on creep damage was also investigated. The results show that the different notch position and dimension generate different creep damage distributions and have a great influence on creep life. The creep failure is the easiest to occur in surface notch, then the base notch, and the last is inside notch. The brazed joint with higher maximum principal stress and von Mises stress generates creep failure easier. For the base notch, the failure time increases with the increase of base notch distance and the creep failure location moves gradually from the center of filler metal to notch tip. The notch locating away from filler metal is beneficial to reduce the creep damage in filler metal and enhance the creep life. For the inside notch, the failure time decreases with notch length increases and the maximum creep damage locates at notch tip. With the increase of inside notch width, the failure time increases first and then keep steadiness, and the failure location moves away from notch tip. The effects of notch position and dimension should be fully considered in creep failure analyses and life assessments of brazed joints.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The creep failure is easy generate in surface notch. </LI> <LI> The far away notch is helpful to reduce the creep damage of filler metal. </LI> <LI> As H increases, the failure location moves from filler metal to base metal. </LI> <LI> As H increases, the failure time increases first then keeps stable. </LI> <LI> The failure time decreases with L increases while it increases with W increases. </LI> </UL> </P>

Effect of Argon Gas Pressure on Residual Stress, Microstructure Evolution and Electrical Resistivity of Beryllium Films

Bing-Chi Luo,Kai Li,Ji-Qiang Zhang,Jiang-Shan Luo,Wei-Dong Wu,Yong-Jian Tang 한국물리학회 2016 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.68 No.4

The residual stress in beryllium films fabricated on K9 substrates by using magnetron sputtering deposition is measured by using a curvature method and is theoretically estimated by using the Nix and Clemens (NC) model. The experimental results indicate that the 1.3-μm-thick film is always in a tensile state for pressure variations in the range from 0.4 to 1.2 Pa. When the sputtering gas pressure is increased, the average stress increases at first, after which it decreases by a remarkable amount. The observed descending trend of the tensile stress when the sputtering gas pressure is beyond 0.6 Pa is mainly attributed to the grain size in the film being larger than that in the film when the pressure is below 0.6 Pa. The maximal residual stress of 552 MPa at a sputtering gas pressure of 0.6 Pa is close to the tensile strength (550 MPa) of the corresponding beryllium bulk material and is about 8 times smaller than that calculated by using the N-C model. In addition, the surface morphologies of the as-fabricated films reveal fibrous grains while the cross-sectional morphologies are characterized by a coarsening of columnar grains. The measured electric resistivity of each film strongly depends on its porosity and the sizes of its grains.

Enteric dysbiosis-linked gut barrier disruption triggers early renal injury induced by chronic high salt feeding in mice

Jingjuan Hu,Haihua Luo,Jieyan Wang,Wenli Tang,Junqi Lu,Shan Wu,Zhi Xiong,Guizhi Yang,Zhenguo Chen,Tian Lan,Hongwei Zhou,Jing Nie,Yong Jiang,Peng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loadinginduced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.

Differentiated miRNA expression and validation of signaling pathways in apoE gene knockout mice by cross-verification microarray platform

Hui Han,Wei Jiang,Yu-Hong Wang,Guang-Jin Qu,Ting-Ting Sun,Feng-Qing Li,Shan-Shun Luo 생화학분자생물학회 2013 Experimental and molecular medicine Vol.45 No.3

The microRNA (miRNA) regulation mechanisms associated with atherosclerosis are largely undocumented. Specific selection and efficient validation of miRNA regulation pathways involved in atherosclerosis development may be better assessed by contemporary microarray platforms applying cross-verification methodology. A screening platform was established using both miRNA and genomic microarrays. Microarray analysis was then simultaneously performed on pooled atherosclerotic aortic tissues from 10 Apolipoprotein E (apoE) knockout mice (apoE/) and 10 healthy C57BL/6 (B6) mice. Differentiated miRNAs were screened and cross-verified against an mRNA screen database to explore integrative mRNA–miRNA regulation. Gene set enrichment analysis was conducted to describe the potential pathways regulated by these mRNA–miRNA interactions. High-throughput data analysis of miRNA and genomic microarrays of knockout and healthy control mice revealed 75differentially expressed miRNAs in apoE/ mice at a threshold value of 2. The six miRNAs with the greatest differentiation expression were confirmed by real-time quantitative reverse-transcription PCR (qRT–PCR) in atherosclerotic tissues. Significantly enriched pathways, such as the type 2 diabetes mellitus pathway, were observed by a gene-set enrichment analysis. The enriched molecular pathways were confirmed through qRT–PCR evaluation by observing the presence of suppressor of cytokine signaling 3 (SOCS3) and SOCS3-related miRNAs, miR-30a, miR-30e and miR-19b. Cross-verified highthroughput microarrays are optimally accurate and effective screening methods for miRNA regulation profiles associated with atherosclerosis. The identified SOCS3 pathway is a potentially valuable target for future development of targeted miRNA therapies to control atherosclerosis development and progression.

Different fates of oocytes with DNA double-strand breaks in vitro and in vivo

Lin, Fei,Ma, Xue-Shan,Wang, Zhen-Bo,Wang, Zhong-Wei,Luo, Yi-Bo,Huang, Lin,Jiang, Zong-Zhe,Hu, Meng-Wen,Schatten, Heide,Sun, Qing-Yuan Taylor Francis 2014 Cell Cycle Vol.13 No.17

Facile Synthesis of Flower-Like AgI/BiOBr Z-Scheme Nanocomposite with Enhanced Photocatalytic Activity for Degradation of 17α-Estradiol (EE2)

Lingxin Li,Han Li,Yanju Long,Shan Wang,Yu Chen,Sifeng Zhang,Lulu Wang,Lijun Luo,Fengzhi Jiang 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2019 NANO Vol.14 No.1

In the present work, a direct Z-scheme AgI/BiOBr heterojunction displaying improved photocatalytic activity was designed by a chemical bath deposition method. The obtained photocatalysts were systematically characterized through XRD, SEM, XPS, BET and UV-Vis diffuse reflectance spectroscopy. The synthesized AgI/BiOBr photocatalyst displayed superior photocatalytic performance in the case of 17α-ethinylestradiol (EE2), where 97.0% compound has been removed within 9 min of irradiation. The rate constant using AgI/BiOBr photo-catalyst was 16.0 and 138.7 times more than that of pure AgI and BiOBr, respectively. Furthermore, the photocatalytic mechanism was investigated. The results of this study indicated that AgI/BiOBr was a stable and efficient photocatalyst, with promising practical applications.

Intestine epithelial cell-derived extracellular vesicles alleviate inflammation induced by Clostridioides difficile TcdB through the activity of TGF-β1

Wan Shuangshuang,Song Guangzhong,Hu Hui,Xu Yaqing,Zeng Peng,Lin Shan,Yang Jun,Jiang Jinqin,Song Xiaojun,Luo Yongneng,Jin Dazhi 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.3

Background Clostridioides diffi cile infection (CDI) has been primarily associated with the toxin B (TcdB), one of the three known protein toxins secreted by C. diffi cile , which can activate the intestinal immune system and lead to pathological damage. Even though the biological functions of intestine epithelial cell-derived extracellular vesicles (I-Evs) have been well documented, the role of I-Evs in the process of CDI is still unknown. Objectives The protective eff ect of I-Evs against C. diffi cile TcdB was investigated both in cultured murine colon carcinoma MC38 cells and a mouse model used in this study. Results Mouse I-Evs with mean diameter ranging from 100 to 200 nm and a density of 1.09–1.17 g/mL were obtained and confi rmed containing the Ev-associated specifi c surface markers CD63 and TSG101 as well as high level of TGF-β1. In MC38 cells, I-Evs were able to decrease the gene expression of IL-6, TNF-α, IL-1β, and IL-22 induced by C. diffi cile TcdB, but to increase both the gene expression and protein levels of TGF-β1. I-Evs treatment via intraperitoneal administration alleviates C. diffi cile TcdB-induced local colon infl ammation in mice and increased their survival rate from 50% up to 80%. Furthermore, I-Evs induced an increase in the proportion of CD4 + Foxp3 + Tregs in vitro and in vivo through a TGF-β1-dependent mechanism by activating the TGF-β1 pathway and prompting phosphorylation of the downstream proteins Smad 2/3. Conclusion For the fi rst time, our study demonstrated that I-Evs originated from intestine epithelial cells can alleviate infl ammation induced by C. diffi cile TcdB both in vitro and in vivo. Therefore, I-Evs might be potentially a novel endogenous candidate for eff ective treatment of CDI.

Triterpenoid saponins from Clinopodium chinense (Benth.) O. Kuntze and their biological activity

Yin-Di Zhu,Jing-Yi Hong,Feng-Da Bao,Na Xing,Ling-Tian Wang,Zhong-Hao Sun,Yun Luo,Hai Jiang,Xudong Xu,Nai-Liang Zhu,Hai-Feng Wu,Gui-Bo Sun,Jun-Shan Yang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.12

Four new ursane-type triterpenoid saponins, clinopoursaponins A–D (1–4), six new oleanane-type triterpenoid saponins, clinopodiside VII–XII (5–10), as well as eight known triterpene analogues (11–18), were isolated from the aerial parts of Clinopodium chinense (Benth.) O. Kuntze. The structures of the new compounds were determined based on extensive spectral analyses, including 1D (1H and 13C) and 2D NMR experiments (COSY, NOESY, HSQC, 2D TOCSY, HSQC-TOCSY and HMBC), HR-ESI-MS and chemical methods. Compounds 1–18 were evaluated for their protective effects against anoxia/reoxygenation-induced apoptosis in H9c2 cells and cytotoxicities against murine mammary carcinoma cell line 4T1. Compounds 8, 9 and 18 exhibited significant protective effects, while compound 1 exhibited cytotoxic activity with IC50 value of 7.4 μm compared to 7.6 μm for the positive control 10-hydroxycamptothecin.