GPR12 Selections of the Metabolites from an Endophytic Streptomyces sp. Asociated with Cistanches deserticola

Zhen-Jian Lin,Xiao-Ming Lu,Tian-Jiao Zhu,Yu-Chun Fang,Qian-Qun Gu,Weiming Zhu 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.9

An endophytic Streptomyces sp. (AC-2) was isolated from the root of Cistanches deserticola Y.C.Ma..Chemical investigations of the culture broth of AC-2 afforded fifteen compounds including K1115 A (1), tyrosol (2), phenylethylamine derivatives (3, 4), cyclic dipeptides (5-8), nucleosides and their aglycones (9-13), N-acetyltryptamine (14), and pyrrole-2-carboxylic acid (15). Only tyrosol can promote an increase of intracellular cAMP special on GPR12 transfected cells, such as CHO and HEK293, which means it may be a possible ligand for GPR12.

GPR12 Selections of the Metabolites from an Endophytic Streptomyces sp. Asociated with Cistanches deserticola

Lin, Zhen-Jian,Lu, Xiao-Ming,Zhu, Tian-Jiao,Fang, Yu-Chun,Gu, Qian-Qun,Zhu, Weiming 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.9

An endophytic Streptomyces sp. (AC-2) was isolated from the root of Cistanches deserticola Y.C.Ma.. Chemical investigations of the culture broth of AC-2 afforded fifteen compounds including K1115 A (1), tyrosol (2), phenylethylamine derivatives (3, 4), cyclic dipeptides (5-8), nucleosides and their aglycones (9-13), N-acetyltryptamine (14), and pyrrole-2-carboxylic acid (15). Only tyrosol can promote an increase of intracellular cAMP special on GPR12 transfected cells, such as CHO and HEK293, which means it may be a possible ligand for GPR12.

Atom Transfer Radical Polymerization of Hexadecyl Acrylate Using CuSCN as the Catalyst

Wen Jian Xu,Xiu Lin Zhu,Zhen Ping Cheng,Jian Ying Chen,Jian Mei Lu 한국고분자학회 2004 Macromolecular Research Vol.12 No.1

Crocin alleviates neurotoxicity induced by bupivacaine in SH-SY5Y cells with inhibition of PI3K/AKT signaling

Lin Lili,Chen Zhen,Li Jun,Peng Jianye,Wang Jian,Feng Mingjun,Liu Tiancheng,Zhang Mengli,Wu Xian,Ai Fen,Shen Caijie 한국유전학회 2024 Genes & Genomics Vol.46 No.1

Background Bupivacaine, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Crocin has been widely reported as a potential neuroprotective agent in neural injury models. Objective The aim of this study was to investigate the role and regulatory mechanism of crocin underlying bupivacaine-induced neurotoxicity. Method Human neuroblastoma SH-SY5Y cells were treated with bupivacaine and/or crocin for 24 h, followed by detecting cell viability using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. The effect of crocin or bupivacaine on SH-SY5Y cell proliferation was measured by Ki67 immunofluorescence assay. The levels of apoptosis-related proteins and the markers in the PI3K/Akt signaling pathway were examined using western blot analysis. The activities of caspase 3, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were tested using respective commercial assay kits. Flow cytometry analysis was executed for detecting SH-SY5Y cell apoptosis. Result Crocin attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells. Meanwhile, crocin inhibited SH-SY5Y cell apoptosis induced by bupivacaine via repressing the activity of caspase-3, reducing Bax expression, and elevating Bcl-2 expression. Moreover, crocin mitigated oxidative stress in SH-SY5Y cells by increasing the content of CAT, SOD, GSH-Px and reducing the content of MDA. Additionally, crocin protected against bupivacaine-induced dephosphorylation of Akt and GSK-3β. The protective effects of crocin against bupivacaine-induced neurotoxicity in SH-SY5Y cells were counteracted by the Akt inhibitor. Conclusion These results suggested that crocin may exert a neuroprotective function by promoting cell proliferation and suppressing apoptosis and oxidative stress in SH-SY5Y cells. Thus, crocin might become a promising drug for the treatment of bupivacaine-induced neurotoxicity. Background Bupivacaine, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Crocin has been widely reported as a potential neuroprotective agent in neural injury models. Objective The aim of this study was to investigate the role and regulatory mechanism of crocin underlying bupivacaine-induced neurotoxicity. Method Human neuroblastoma SH-SY5Y cells were treated with bupivacaine and/or crocin for 24 h, followed by detecting cell viability using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. The effect of crocin or bupivacaine on SH-SY5Y cell proliferation was measured by Ki67 immunofluorescence assay. The levels of apoptosis-related proteins and the markers in the PI3K/Akt signaling pathway were examined using western blot analysis. The activities of caspase 3, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were tested using respective commercial assay kits. Flow cytometry analysis was executed for detecting SH-SY5Y cell apoptosis. Result Crocin attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells. Meanwhile, crocin inhibited SH-SY5Y cell apoptosis induced by bupivacaine via repressing the activity of caspase-3, reducing Bax expression, and elevating Bcl-2 expression. Moreover, crocin mitigated oxidative stress in SH-SY5Y cells by increasing the content of CAT, SOD, GSH-Px and reducing the content of MDA. Additionally, crocin protected against bupivacaine-induced dephosphorylation of Akt and GSK-3β. The protective effects of crocin against bupivacaine-induced neurotoxicity in SH-SY5Y cells were counteracted by the Akt inhibitor. Conclusion These results suggested that crocin may exert a neuroprotective function by promoting cell proliferation and suppressing apoptosis and oxidative stress in SH-SY5Y cells. Thus, crocin might become a promising drug for the treatment of bupivacaine-induced neurotoxicity.

Upregulation and biological function of transmembrane protein 119 in osteosarcoma

Zhen-Huan Jiang,Jun Peng,Hui-Lin Yang,Xing-Li Fu,Jin-Zhi Wang,Lei Liu,Jian-Nong Jiang,Yong-Fei Tan,Zhi-Jun Ge 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Osteosarcoma is suggested to be caused by genetic and molecular alterations that disrupt osteoblast differentiation. Recent studies have reported that transmembrane protein 119 (TMEM119) contributes to osteoblast differentiation and bone development. However, the level of TMEM119 expression and its roles in osteosarcoma have not yet been elucidated. In the present study, TMEM119 mRNA and protein expression was found to be up-regulated in osteosarcoma compared with normal bone cyst tissues. The level of TMEM119 protein expression was strongly associated with tumor size, clinical stage, distant metastasis and overall survival time. Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA, which revealed that downregulation of TMEM119 could inhibit the proliferation of osteosarcoma cells by inducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and invasion, and decreased the expression of TGF-β pathway-related factors (BMP2, BMP7 and TGF-β). TGF-β application rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion. Further in vitro experiments with a TGF-β inhibitor (SB431542) or BMP inhibitor (dorsomorphin) suggested that TMEM119 significantly promotes cell migration and invasion, partly through TGF-β/BMP signaling. In conclusion, our data support the notion that TMEM119 contributes to the proliferation, migration and invasion of osteosarcoma cells, and functions as an oncogene in osteosarcoma.

MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1

Liang, Zhen,Li, Shiqi,Xu, Xin,Xu, Xianglai,Wang, Xiao,Wu, Jian,Zhu, Yi,Hu, Zhenghui,Lin, Yiwei,Mao, Yeqing,Chen, Hong,Luo, Jindan,Liu, Ben,Zheng, Xiangyi,Xie, Liping Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.2

MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3'-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3'-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.

MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1

Liping Xie,Zhen Liang,Shiqi Li,Xin Xu,Xianglai Xu,Xiao Wang,Jian Wu,Yi Zhu,Zhenghui Hu,Yiwei Lin,Yeqing Mao,Hong Chen,Jindan Luo,Ben Liu,Xiangyi Zheng 한국분자세포생물학회 2015 Molecules and cells Vol.38 No.2

MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3 -UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3 -UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.

Plasma Macrophage Migration Inhibitory Factor and CCL3 as Potential Biomarkers for Distinguishing Patients with Nasopharyngeal Carcinoma from High-Risk Individuals Who Have Positive Epstein-Barr Virus Capsid Antigen-Specific IgA

Ning Xue,Jian-Hua Lin,Shan Xing,Dan Liu,Shi-Bing Li,Yan-Zhen Lai,Xue-Ping Wang,Min-Jie Mao,Qian Zhong,Mu-Sheng Zeng,Wan-Li Liu 대한암학회 2019 Cancer Research and Treatment Vol.51 No.1

Purpose The purpose of this study was to identify novel plasma biomarkers for distinguishing nasopharyngeal carcinoma (NPC) patients from healthy individuals who have positive Epstein-Barr virus (EBV) viral capsid antigen (VCA-IgA). Materials and Methods One hundred seventy-four plasma cytokines were analyzed by a Cytokine Array in eight healthy individuals with positive EBV VCA-IgA and eight patients with NPC. Real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry were employed to detect the expression levels of macrophage migration inhibitory factor (MIF) and CC chemokine ligand 3 (CCL3) in NPC cell lines and tumor tissues. Plasma MIF and CCL3 were measured by ELISA in 138 NPC patients, 127 EBV VCA-IgA negative (VN) and 100 EBV VCA-IgA positive healthy donors (VP). Plasma EBV VCA-IgA was determined by immunoenzymatic techniques. Results Thirty-four of the 174 cytokines varied significantly between the VP and NPC group. Plasma MIF and CCL3 were significantly elevated in NPC patients compared with VN and VP. Combination of MIF and CCL3 could be used for the differential diagnosis of NPC from VN cohort (area under the curve [AUC], 0.913; sensitivity, 90.00%; specificity, 80.30%), and combination of MIF, CCL3, and VCA-IgA could be used for the differential diagnosis of NPC from VP cohort (AUC, 0.920; sensitivity, 90.00%; specificity, 84.00%), from (VN+VP) cohort (AUC, 0.961; sensitivity, 90.00%; specificity, 92.00%). Overexpressions of MIF and CCL3 were observed in NPC plasma, NPC cell lines and NPC tissues. Conclusion Plasma MIF, CCL3, and VCA-IgA combination significantly improves the diagnostic specificity of NPC in high-risk individuals.

A rapid modeling method and accuracy criteria for common-cause failures in Risk Monitor PSA model

Zhang, Bing,Chen, Shanqi,Lin, Zhixian,Wang, Shaoxuan,Wang, Zhen,Ge, Daochuan,Guo, Dingqing,Lin, Jian,Wang, Fang,Wang, Jin Korean Nuclear Society 2021 Nuclear Engineering and Technology Vol.53 No.1

In the development of a Risk Monitor probabilistic safety assessment (PSA) model from the basic PSA model of a nuclear power plant, the modeling of common-cause failure (CCF) is very important. At present, some approximate modeling methods are widely used, but there lacks criterion of modeling accuracy and error analysis. In this paper, aiming at ensuring the accuracy of risk assessment and minimizing the Risk Monitor PSA models size, we present three basic issues of CCF model resulted from the changes of a nuclear power plant configuration, put forward corresponding modeling methods, and derive accuracy criteria of CCF modeling based on minimum cut sets and risk indicators according to the requirements of risk monitoring. Finally, a nuclear power plant Risk Monitor PSA model is taken as an example to demonstrate the effectiveness of the proposed modeling method and accuracy criteria, and the application scope of the idea of this paper is also discussed.

Estimation and compensation for deviation of contour in slow tool servo precision turning for complicated curved surface

Feng-Ze Qin,Jian-Wei Ma,Zhen-Yuan Jia,Guan-Lin Li,Jian-Zhou Zhang 대한기계학회 2022 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.36 No.8

In the presence of extremely high precision turning the complicated curved surface with geometry features of large slope gradient and multi convex-concave characteristics, the micron-scale deviation of contour resulting from the tracking deviation of the feed axis becomes non-negligible. To diminish the micron-scale contouring deviation, this study presents a valid contouring error estimation and pre-compensation method for slow tool servo (STS) precision turning. Aiming at estimating the tracking deviation of the axis of the turning machine tool in the machining process, the steady-state tracking deviation model of the axis is first constructed. The proposed multiply tangential estimation method is derived from the Taylor series of the foot point. Since the rotation feed movement of the C axis is the main movement in cutting forming movement for STS turning machining, the monotonicity of the displacement for the C axis is ensured. The compensation value for the axis position is derived through the Jacobi matrix of the STS turning machine. With the presented approach, the tool tip location deviation induced by the tracking deviation of the feed axis reduces from 1.087 μm to 0.025 μm. The measurement results of the comparison experiments indicate that with the presented method in this study, the contouring error of the machined part reduces from 5.72 μm to 4.36 μm. The micron-scale contouring error resulting from the tracking deviation of the feed axis is effectually compensated.