Two macrocyclic polyamines as modulators of metal-mediated Aβ40aggregation

2015 ◽  
Vol 7 (6) ◽  
pp. 655-662 ◽  
Author(s):  
Yanfei Yang ◽  
Tingting Chen ◽  
Shajun Zhu ◽  
Xuefang Gu ◽  
Xueping Jia ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Intracellular Ros ◽  
Macrocyclic Polyamines ◽  
L1 And L2

L1 and L2 can inhibit the metal-induced Aβ40aggregation, attenuate neurotoxicity, suppress the intracellular ROS and protect against cell apoptosis.

Dinuclear phosphorescent rhenium(i) complexes as potential anticancer and photodynamic therapy agents

2020 ◽  
Vol 49 (33) ◽  
pp. 11583-11590 ◽  
Author(s):  
Zheng-Yin Pan ◽  
Dai-Hong Cai ◽  
Liang He
Keyword(s):  
Photodynamic Therapy ◽  
Cell Apoptosis ◽  
Lysosomal Dysfunction ◽  
Intracellular Ros

Two dinuclear organometallic Re(i) complexes increase intracellular ROS levels, causing lysosomal dysfunction and cell apoptosis.

scholarly journals Regulating intracellular ROS signal by a dual pH/reducing-responsive nanogels system promotes tumor cell apoptosis

2019 ◽  
Vol Volume 14 ◽  
pp. 5713-5728 ◽  
Author(s):  
Kai Dong ◽  
Qiuya Lei ◽  
Runhao Guo ◽  
Xianglong Wu ◽  
Yanni Zhang ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Apoptosis ◽  
Tumor Cell Apoptosis ◽  
Intracellular Ros

Ruthenium polypyridyl complexes as inducer of ROS-mediated apoptosis in cancer cells by targeting thioredoxin reductase

Metallomics ◽  
2014 ◽  
Vol 6 (8) ◽  
pp. 1480-1490 ◽  
Author(s):  
Zuandi Luo ◽  
Lianling Yu ◽  
Fang Yang ◽  
Zhennan Zhao ◽  
Bo Yu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Apoptosis ◽  
Thioredoxin Reductase ◽  
Cancer Growth ◽  
Ros Generation ◽  
Ruthenium Polypyridyl ◽  
Polypyridyl Complexes ◽  
Intracellular Ros ◽  
Ruthenium Polypyridyl Complexes ◽  
Apoptosis In Cancer Cells

Ruthenium polypyridyl complexes inhibit cancer growth by targeting TrxR and promote the intracellular ROS generation, ultimately triggering mitochondria-mediated cell apoptosis.

scholarly journals Gambogic Acid Lysinate Induces Apoptosis in Breast Cancer MCF-7 Cells by Increasing Reactive Oxygen Species

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Zhan Zhen ◽  
Ya-Jun Lin ◽  
Kai-Ji Li ◽  
Xiao-Shan Yang ◽  
Yu-Fang Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Human Cancer ◽  
Signal Pathway ◽  
Gambogic Acid ◽  
Oxygen Species ◽  
Human Cancer Cells ◽  
Intracellular Ros ◽  
Mcf 7

Gambogic acid (GA) inhibits the proliferation of various human cancer cells. However, because of its water insolubility, the antitumor efficacy of GA is limited.Objectives.To investigate the antitumor activity of gambogic acid lysinate (GAL) and its mechanism.Methods.Inhibition of cell proliferation was determined by MTT assay; intracellular ROS level was detected by staining cells with DCFH-DA; cell apoptosis was determined by flow cytometer and the mechanism of GAL was investigated by Western blot.Results.GAL inhibited the proliferation of MCF-7 cells with IC50values 1.46 μmol/L comparable with GA (IC50, 1.16 μmol/L). GAL promoted the production of ROS; however NAC could remove ROS and block the effect of GAL. GAL inhibited the expression of SIRT1 but increased the phosphorylation of FOXO3a and the expression of p27Kip1. At knockdown of FOXO3a, cell apoptosis induced by GAL can be partly blocked. In addition it also enhanced the cleavage of caspase-3.Conclusions.GAL inhibited MCF-7 cell proliferation and induced MCF-7 cell apoptosis by increasing ROS level which could induce cell apoptosis by both SIRT1/FOXO3a/p27Kip1 and caspase-3 signal pathway. These results suggested that GAL might be useful as a modulation agent in cancer chemotherapy.

scholarly journals Aquaporin-3 Attenuates Oxidative Stress-Induced Nucleus Pulposus Cell Apoptosis Through Regulating the P38 MAPK Pathway

2018 ◽  
Vol 50 (5) ◽  
pp. 1687-1697 ◽  
Author(s):  
Yichun Xu ◽  
Hui Yao ◽  
Qiyou Wang ◽  
Wenbin Xu ◽  
Kaihua Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oxidative Damage ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Aquaporin 3 ◽  
P38 Mapk Pathway ◽  
Intracellular Ros ◽  
Cellular Apoptosis

Background/Aims: Previous studies have shown that oxidative damage is a main contributor to disc nucleus pulposus (NP) cell apoptosis. Aquaporin-3 (AQP-3) facilitates reactive oxygen species (ROS) scavenging and thus alleviates oxidative injury in other cells. This study aims to investigate the role and mechanism of AQP-3 in regulating NP cell apoptosis under oxidative damage. Methods: Rat NP cells were treated with H2O2 for 48 hours, while control NP cells were free of H2O2. Recombinant AQP-3 lentiviral vectors were used to investigate the effect of enhanced AQP-3 expression levels in NP cells. NP cell apoptosis was assessed by flow cytometry, caspase-3 activity, gene expression of apoptosis-related molecules (Bax, Bcl-2 and caspase-3), and protein expression of cellular apoptosis markers (cleaved PARP and cleaved caspase-3). Additionally, intracellular ROS content and activity of the p38 MAPK pathway were evaluated. Results: Compared with the control NP cells, oxidative damage in the treatment cells significantly increased cell apoptosis ratios and caspase-3 activity, upregulated gene expression of Bax and caspase-3, downregulated gene expression of Bcl-2, and increased protein expression of cleaved PARP and cleaved caspase-3, as well as increased intracellular ROS content and activity of the p38 MAPK pathway. However, AQP-3 overexpression partly alleviated cell apoptosis, decreased intracellular ROS content, and inhibited the p38 MAPK pathway in NP cells under oxidative damage. Conclusion: Oxidative damage can significantly downregulate AQP-3 expression. Enhancing AQP-3 expression in NP cells partly attenuates cellular apoptosis through regulating the p38 MAPK pathway under oxidative damage.

Facile synthesis of highly uniform selenium nanoparticles using glucose as the reductant and surface decorator to induce cancer cell apoptosis

2016 ◽  
Vol 4 (13) ◽  
pp. 2351-2358 ◽  
Author(s):  
Tianqi Nie ◽  
Hualian Wu ◽  
Ka-Hing Wong ◽  
Tianfeng Chen
Keyword(s):  
Mitochondrial Dysfunction ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Selenium Nanoparticles ◽  
Facile Synthesis ◽  
Cancer Cell Apoptosis ◽  
Intracellular Ros ◽  
Induction Of Apoptosis ◽  
Highly Uniform ◽  
Induce Cancer Cell Apoptosis

Herein, we demonstrated a new and facial synthesis of highly uniformed SeNPs using glucose as the reductant and surface decorator. Glu–SeNPs induced cancer cell apoptosisviainduction of apoptosis by triggering intracellular ROS overproduction and mitochondrial dysfunction.

scholarly journals Scutellarin-induced A549 cell apoptosis depends on activation of the transforming growth factor-β1/smad2/ROS/caspase-3 pathway

2021 ◽  
Vol 16 (1) ◽  
pp. 961-968
Author(s):  
Guang-Yan Zhang ◽  
Wei-Yong Chen ◽  
Xiao-Bo Li ◽  
Hua Ke ◽  
Xue-Lin Zhou
Keyword(s):  
Growth Factor ◽  
Cell Viability ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Transforming Growth Factor ◽  
A549 Cells ◽  
Ros Production ◽  
Intracellular Ros ◽  
Tgf Β1

Abstract Scutellarin plays an anti-tumor role in A549 lung cancer cells, but the underlying mechanism is unclear. In this study, scutellarin was used to treat A549 cells for 12, 24, and 48 h, followed by the addition of Tempo, a selective scavenger of mitochondrial reactive oxygen species (ROS) and SB431542, a transforming growth factor (TGF)-β1 receptor inhibitor. A dihydroethidium fluorescence probe was used to measure the intracellular ROS level, Cell Counting Kit-8 (CCK-8) was used to detect cell viability, and flow cytometry was performed to examine apoptosis. Western blots were used to detect the total protein level of TGF-β1, p-smad2, and cleaved caspase-3 in A549 cells. The results showed that scutellarin significantly inhibited cell viability and increased apoptosis. Scutellarin also promoted intracellular ROS production, TGF-β1/smad2 signaling pathway activation, and cleaved caspase-3 expression, which was partly reversed by Tempo. Moreover, scutellarin-induced intracellular ROS production and cleaved caspase-3 expression were inhibited by blocking the TGF-β1/smad2 pathway with SB431542. In conclusion, scutellarin promoted apoptosis and intracellular ROS accumulation, which could be abrogated by Tempo and SB431542 treatment in A549 cells. Our study indicated that scutellarin induced A549 cell apoptosis via the TGF-β1/smad2/ROS/caspase-3 pathway.

Synergistic effects of piperlongumine and gemcitabine against KRAS mutant lung cancer

2020 ◽  
pp. 030089162093078
Author(s):  
Wu Ye ◽  
Qingdong Huang ◽  
Tingyu Tang ◽  
Guangyue Qin
Keyword(s):  
Lung Cancer ◽  
Cell Apoptosis ◽  
Combination Index ◽  
Synergistic Effects ◽  
Combined Treatment ◽  
Cell Counting ◽  
Cell Growth Inhibition ◽  
Combined Application ◽  
Intracellular Ros ◽  
Promising Treatment

Objective: To determine the combined efficacy of piperlongumine and gemcitabine for treatment of KRAS mutant lung cancer. Methods: The cell growth inhibition of piperlongumine, gemcitabine, and piperlongumine plus gemcitabine was measured by Cell Counting Kit‑8 assay and the combination index was calculated. In addition, the combined effects of piperlongumine and gemcitabine on cell apoptosis, reactive oxygen species (ROS) contents, and microtubule-associated protein 1 light chain 3B (LC3B) expression were examined. Results: Piperlongumine increased ROS contents and LC3B-II expression. Following the combined treatment with piperlongumine and 10 mM N-acetyl-L-cysteine (NAC), intracellular ROS and cell viability returned to normal levels, and the expression of LC3B-II decreased to the predose level. Gemcitabine also induced cell apoptosis, increased ROS contents, and LC3B-II expression. The combination of piperlongumine with gemcitabine exhibited a synergetic anticancer activity with the combination index <1. The combined application of gemcitabine and piperlongumine yielded synergistic effects on cell apoptosis, but failed to synergistically increase ROS levels and LC3B-II expression. Conclusion: Combination therapy with piperlongumine and gemcitabine is a promising treatment option for KRAS mutant lung cancer.

A View of the Lexical–Grammatical Link in Young Latinos With Specific Language Impairment Using Language-Specific and Conceptual Measures

2019 ◽  
Vol 62 (6) ◽  
pp. 1775-1786 ◽  
Author(s):  
Lucía I. Méndez ◽  
Gabriela Simon-Cereijido
Keyword(s):  
Low Income ◽  
Language Impairment ◽  
Specific Language Impairment ◽  
L2 Acquisition ◽  
Cross Sectional ◽  
Specific Language ◽  
Vocabulary Skills ◽  
In The Beginning ◽  
Study Participants ◽  
L1 And L2

Purpose This study investigated the nature of the association of lexical–grammatical abilities within and across languages in Latino dual language learners (DLLs) with specific language impairment (SLI) using language-specific and bilingual measures. Method Seventy-four Spanish/English–speaking preschoolers with SLI from preschools serving low-income households participated in the study. Participants had stronger skills in Spanish (first language [L1]) and were in the initial stages of learning English (second language [L2]). The children's lexical, semantic, and grammar abilities were assessed using normative and researcher-developed tools in English and Spanish. Hierarchical linear regressions of cross-sectional data were conducted using measures of sentence repetition tasks, language-specific vocabulary, and conceptual bilingual lexical and semantic abilities in Spanish and English. Results Results indicate that language-specific vocabulary abilities support the development of grammar in L1 and L2 in this population. L1 vocabulary also contributes to L2 grammar above and beyond the contribution of L2 vocabulary skills. However, the cross-linguistic association between vocabulary in L2 and grammar skills in the stronger or more proficient language (L1) is not observed. In addition, conceptual vocabulary significantly supported grammar in L2, whereas bilingual semantic skills supported L1 grammar. Conclusions Our findings reveal that the same language-specific vocabulary abilities drive grammar development in L1 and L2 in DLLs with SLI. In the early stages of L2 acquisition, vocabulary skills in L1 also seem to contribute to grammar skills in L2 in this population. Thus, it is critical to support vocabulary development in both L1 and L2 in DLLs with SLI, particularly in the beginning stages of L2 acquisition. Clinical and educational implications are discussed.

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