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4-Amino-3-hydroxy-1-naphthalenesulfonic acid

$58

  • Brand : BIOFRON

  • Catalogue Number : BN-O1152

  • Specification : 98%(HPLC)

  • CAS number : 116-63-2

  • Formula : C10H9NO4S

  • Molecular Weight : 239.25

  • PUBCHEM ID : 8316

  • Volume : 5mg

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Catalogue Number

BN-O1152

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

239.25

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=CC=C2C(=C1)C(=CC(=C2N)O)S(=O)(=O)O

Synonyms

1-Amino-2-naphthol-4-sulfonic Acid/4-amino-3-hydroxynaphthalene-1-sulfonic acid/1,2,4-Acid/1-Naphthalenesulfonic acid, 4-amino-3-hydroxy-/4-Amino-3-hydroxy-1-naphthalenesulfonic acid

IUPAC Name

4-amino-3-hydroxynaphthalene-1-sulfonic acid

Density

1.6±0.1 g/cm3

Solubility

Flash Point

Boiling Point

466ºC

Melting Point

295ºC

InChl

InChl Key

RXCMFQDTWCCLBL-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:116-63-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

27428957

Abstract

Methylsulfonylmethane (MSM) is an organic sulfur-containing compound which has been used as a dietary supplement for osteoarthritis. MSM has been shown to reduce oxidative stress and inflammation, as well as exhibit apoptotic or anti-apoptotic effects depending on the cell type or activating stimuli. However, there are still a lot of unknowns about the mechanisms of actions of MSM. In this study, MSM was tested on colon cancer cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis revealed that MSM inhibited cell viability and increased apoptotic markers in both HCT-116 p53 +/+ and HCT-116 p53 −/− colon cancer cells. Increased poly (ADP-ribose) polymerase (PARP) fragmentation and caspase-3 activity by MSM also supported these findings. MSM also modulated the expression of various apoptosis-related genes and proteins. Moreover, MSM was found to increase c-Jun N-terminal kinases (JNK) phosphorylation in both cell lines, dose-dependently. In conclusion, our results show for the first time that MSM induces apoptosis in HCT-116 colon cancer cells regardless of their p53 status. Since p53 is defective in >50% of tumors, the ability of MSM to induce apoptosis independently of p53 may offer an advantage in anti-tumor therapy. Moreover, the remarkable effect of MSM on Bim, an apoptotic protein, also suggests its potential use as a novel chemotherapeutic agent for Bim-targeted anti-cancer therapies.

KEYWORDS

MSM, HCT-116, apoptosis, Bim, colon cancer, JNK

Title

Methylsulfonylmethane Induces p53 Independent Apoptosis in HCT-116 Colon Cancer Cells

Author

Arzu Zeynep Karabay,1,* Asli Koc,2,* Tulin Ozkan,3,* Yalda Hekmatshoar,3 Asuman Sunguroglu,3 Fugen Aktan,1 and Zeliha Buyukbingol1 Atsushi Matsuzawa, Academic Editor

Publish date

2016 Jul;

PMID

30244686

Abstract

Background
There is a lack of large-scale epidemiological data on the clinical practice of enteral nutrition (EN) feeding in China. This study aimed to provide such data on Chinese hospitals and to investigate factors associated with EN delivery.

Methods
This cross-sectional study was launched in 118 intensive care units (ICUs) of 116 mainland hospitals and conducted on April 26, 2017. At 00:00 on April 26, all patients in these ICUs were included. Demographic and clinical variables of patients on April 25 were obtained. The dates of hospitalization, ICU admission and nutrition initiation were reviewed. The outcome status 28 days after the day of investigation was obtained.

Results
A total of 1953 patients were included for analysis, including 1483 survivors and 312 nonsurvivors. The median study day was day 7 (IQR 2-19 days) after ICU entry. The proportions of subjects starting EN within 24, 48 and 72 h after ICU entry was 24.8% (84/352), 32.7% (150/459) and 40.0% (200/541), respectively. The proportion of subjects receiving > 80% estimated energy target within 24, 48, 72 h and 7 days after ICU entry was 10.5% (37/352), 10.9% (50/459), 11.8% (64/541) and 17.8% (162/910), respectively. Using acute gastrointestinal injury (AGI) 1 as the reference in a Cox model, patients with AGI 2-3 were associated with reduced likelihood of EN initiation (HR 0.46, 95% CI 0.353-0.599; p < 0.001). AGI 4 was significantly associated with lower hazard of EN administration (HR 0.056; 95% CI 0.008-0.398; p = 0.004). In a linear regression model, greater Sequential Organ Failure Assessment scores (coefficient - 0.002, 95% CI - 0.008 to − 0.001; p = 0.024) and male gender (coefficient - 0.144, 95% CI - 0.203 to − 0.085; p < 0.001) were found to be associated with lower EN proportion. As compared with AGI 1, AGI 2-3 was associated with lower EN proportion (coefficient - 0.206, 95% CI - 0.273 to − 0.139; p < 0.001). Conclusions The study showed that EN delivery was suboptimal in Chinese ICUs. More attention should be paid to EN use in the early days after ICU admission.

KEYWORDS

Enteral feeding, Intensive care units, Cross-sectional study

Title

Enteral nutrition feeding in Chinese intensive care units: a cross-sectional study involving 116 hospitals

Author

Juan Xing,1 Zhongheng Zhang,2 Lu Ke,1 Jing Zhou,1 Bingyu Qin,3 Hongkai Liang,4 Xiaomei Chen,5 Wenming Liu,6 Zhongmin Liu,7 Yuhang Ai,8 Difeng Wang,9 Qiuhui Wang,10 Qingshan Zhou,11 Fusen Zhang,12 Kejian Qian,13 Dongpo Jiang,14 Bin Zang,15 Yimin Li,16 Xiaobo Huang,17 Yan Qu,18 Yinguang Xie,19 Donglin Xu,20 Zhiqiang Zou,21 Xiangde Zheng,22 Jianbo Liu,23 Feng Guo,24 Yafeng Liang,25 Qiang Sun,26 Hongmei Gao,27 Yang Liu,28 Ping Chang,29 Aibin Ceng,30 Rongli Yang,31 Gaiqi Yao,32 Yun Sun,33 Xiaorong Wang,34 Yi Zhang,35 Yichao Wen,36 Jian Yu,37 Rongqing Sun,38 Zhiwei Li,39 Shiying Yuan,40 Yunlin Song,41 Peiyang Gao,42 Haiyan Liu,43 Zhaohui Zhang,44 Yunfu Wu,45 Biao Ma,46 Qiang Guo,47 Feng Shan,48 Mingshi Yang,49 Hailing Li,50 Yuanfei Li,51 Weihua Lu,52 Lei Wang,53 Chuangyun Qian,54 Zhiyong Wang,55 Jiandong Lin,56 Rumin Zhang,57 Peng Wan,58 Zhiyong Peng,59 Yuqiang Gong,60 Linxi Huang,61 Guobao Wu,62 Jie Sun,63 Yijun Deng,64 Dongwu Shi,35 Lixin Zhou,65 Fachun Zhou,66 Qindong Shi,67 Xiaodong Guo,68 Xueyan Liu,69 Weidong Wu,70 Xiangzhong Meng,71 Liandi Li,72 Weiwei Chen,73 Shusheng Li,74 Xianyao Wan,75 Zhixin Chao,76 An Zhang,77 Liming Gu,78 Wei Chen,79 Jinglan Wu,80 Lihua Zhou,81 Zhenhuan Zhang,82 Yibing Weng,83 Yongshun Feng,84 Chunli Yang,85 Yongjian Feng,86 Sumin Zhao,87 Fei Tong,88 Dong Hao,89 Hui Han,90 Baocai Fu,91 Chuanyong Gong,92 Zhiping Li,93 Kunlin Hu,94 Qiuye Kou,95 Han Zhang,96 Jie Liu,97 Chuming Fan,98 Xin Zhou,99 Xiumei Chen,100 Junli Sun,101 Xuejun Zhou,102 Bin Song,103 Cheng Sun,104 Liyun Zhao,105 Xinglu Dong,106 Linlin Zhang,107 Dafei Tong,108 Zhiguo Pan,109 Chuangjie Cai,110 Donghao Wang,111 Yingjun Dong,112 Yuanqi Gong,113 Zhisong Wu,114 Xinke Meng,115 Ping Wang,116 and Weiqin Licorresponding author1

Publish date

2018;

PMID

26859847

Abstract

Flavokawain C (FKC) is a naturally occurring chalcone which can be found in Kava (Piper methysticum Forst) root. The present study evaluated the effect of FKC on the growth of various human cancer cell lines and the underlying associated mechanisms. FKC showed higher cytotoxic activity against HCT 116 cells in a time- and dose-dependent manner in comparison to other cell lines (MCF-7, HT-29, A549 and CaSki), with minimal toxicity on normal human colon cells. The apoptosis-inducing capability of FKC on HCT 116 cells was evidenced by cell shrinkage, chromatin condensation, DNA fragmentation and increased phosphatidylserine externalization. FKC was found to disrupt mitochondrial membrane potential, resulting in the release of Smac/DIABLO, AIF and cytochrome c into the cytoplasm. Our results also revealed that FKC induced intrinsic and extrinsic apoptosis via upregulation of the levels of pro-apoptotic proteins (Bak) and death receptors (DR5), while downregulation of the levels of anti-apoptotic proteins (XIAP, cIAP-1, c-FlipL, Bcl-xL and survivin), resulting in the activation of caspase-3, -8 and -9 and cleavage of poly(ADP-ribose) polymerase (PARP). FKC was also found to cause endoplasmic reticulum (ER) stress, as suggested by the elevation of GADD153 protein after FKC treatment. After the cells were exposed to FKC (60μM) over 18hrs, there was a substantial increase in the phosphorylation of ERK 1/2. The expression of phosphorylated Akt was also reduced. FKC also caused cell cycle arrest in the S phase in HCT 116 cells in a time- and dose-dependent manner and with accumulation of cells in the sub-G1 phase. This was accompanied by the downregulation of cyclin-dependent kinases (CDK2 and CDK4), consistent with the upregulation of CDK inhibitors (p21Cip1 and p27Kip1), and hypophosphorylation of Rb.

Title

Flavokawain C Inhibits Cell Cycle and Promotes Apoptosis, Associated with Endoplasmic Reticulum Stress and Regulation of MAPKs and Akt Signaling Pathways in HCT 116 Human Colon Carcinoma Cells

Author

Chung-Weng Phang,1 Saiful Anuar Karsani,1 Gautam Sethi,2 and Sri Nurestri Abd Malek1,* Michel M Ouellette, Editor

Publish date

2016;


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