Ni(ii)/Cu(ii)/Zn(ii) 5,5-diethylbarbiturate complexes with 1,10-phenanthroline and 2,2′-dipyridylamine: synthesis, structures, DNA/BSA binding, nuclease activity, molecular docking, cellular uptake, cytotoxicity and the mode of cell death

Synthesis, structures, DNA/BSA binding affinity, antioxidant and cytotoxic activity, cell death and ROS generation of Ni(ii)/Cu(ii)/Zn(ii) 5,5-diethylbarbiturate complexes were reported.

Download Full-text

Poly-L-arginine: Enhancing Cytotoxicity and Cellular Uptake of Doxorubicin and Necrotic Cell Death

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520618666180412114750 ◽

2019 ◽

Vol 18 (10) ◽

pp. 1448-1456 ◽

Cited By ~ 3

Author(s):

Bahareh Movafegh ◽

Razieh Jalal ◽

Zobeideh Mohammadi ◽

Seyyede A. Aldaghi

Keyword(s):

Cell Death ◽

Cellular Uptake ◽

Combined Treatment ◽

Annexin V ◽

Cell Penetrating Peptides ◽

Short Exposure ◽

Dependent Manner ◽

Du145 Cells ◽

Induced Apoptosis ◽

Resistance To Doxorubicin

Objective: Cell resistance to doxorubicin and its toxicity to healthy tissue reduce its efficiency. The use of cell-penetrating peptides as drug delivery system along with doxorubicin is a strategy to reduce its side effects. In this study, the influence of poly-L-arginine on doxorubicin cytotoxicity, its cellular uptake and doxorubicin-induced apoptosis on human prostate cancer DU145 cells are assessed. Methods: The cytotoxicity of doxorubicin and poly-L-arginine, alone and in combination, in DU145 cells was evaluated at different exposure times using MTT assay. The influence of poly-L-arginine on doxorubicin delivery into cells was evaluated by fluorescence microscopy and ultraviolet spectroscopy. DAPI and ethidium bromide- acridine orange stainings, flow cytometry using annexin V/propidium iodide, western blot analysis with anti-p21 antibody and caspase-3 activity were used to examine the influence of poly-L-arginine on doxorubicininduced cell death. Results: Poly-L-arginine had no cytotoxicity at low concentrations and short exposure times. Poly-L-arginine increased the cytotoxic effect of doxorubicin in DU145 cells in a time-dependent manner. But no significant reduction was found in HFF cell viability. Poly-L-arginine seems to facilitate doxorubicin uptake and increase its intracellular concentration. 24h combined treatment of cells with doxorubicin (0.5 µM) and poly-L-arginine (1 µg ml-1) caused a small increase in doxorubicin-induced apoptosis and significantly elevated necrosis in DU145 cells as compared to each agent alone. Conclusion: Our results indicate that poly-L-arginine at lowest and highest concentrations act as proliferationinducing and antiproliferative agents, respectively. Between these concentrations, poly-L-arginine increases the cellular uptake of doxorubicin and its cytotoxicity through induction of necrosis.

Download Full-text

Lateral size of graphene oxide determines differential cellular uptake and cell death pathways in Kupffer cells, LSECs, and hepatocytes

Nano Today ◽

10.1016/j.nantod.2020.101061 ◽

2021 ◽

Vol 37 ◽

pp. 101061

Author(s):

Jiulong Li ◽

Xiang Wang ◽

Kuo-Ching Mei ◽

Chong Hyun Chang ◽

Jinhong Jiang ◽

...

Keyword(s):

Cell Death ◽

Graphene Oxide ◽

Cellular Uptake ◽

Kupffer Cells ◽

Lateral Size ◽

Cell Death Pathways

Download Full-text

Synthesis, characterization, antimicrobial, BSA binding, DFT calculation, molecular docking and cytotoxicity of Ni(II) complexes with Schiff base ligands

Journal of Molecular Liquids ◽

10.1016/j.molliq.2021.115457 ◽

2021 ◽

Vol 328 ◽

pp. 115457

Author(s):

J. Jeevitha Rani ◽

A. Mary Imelda Jayaseeli ◽

S. Rajagopal ◽

S. Seenithurai ◽

Jeng-Da Chai ◽

...

Keyword(s):

Schiff Base ◽

Molecular Docking ◽

Dft Calculation ◽

Schiff Base Ligands ◽

Bsa Binding

Download Full-text

Anticancer activity and cell death mechanism of Pt(II) complexes: their in vitro bio-transformation to Pt(II)-DNA adduct formation and BSA binding study by spectroscopic method

Spectrochimica Acta Part A Molecular and Biomolecular Spectroscopy ◽

10.1016/j.saa.2021.120096 ◽

2021 ◽

pp. 120096

Author(s):

Rituparna Bhaduri ◽

Subhajit Mukherjee ◽

Ishani Mitra ◽

Subarna Ghosh ◽

Urmi Chatterji ◽

...

Keyword(s):

Cell Death ◽

Anticancer Activity ◽

Spectroscopic Method ◽

Adduct Formation ◽

Dna Adduct ◽

Binding Study ◽

Cell Death Mechanism ◽

Bsa Binding

Download Full-text

MIF promotes neurodegeneration and cell death via its nuclease activity following traumatic brain injury

Cellular and Molecular Life Sciences ◽

10.1007/s00018-021-04037-9 ◽

2021 ◽

Author(s):

Zhi Ruan ◽

Qing Lu ◽

Jennifer E. Wang ◽

Mi Zhou ◽

Shuiqiao Liu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Cell Death ◽

Brain Injury ◽

Nuclease Activity

Download Full-text

Immunoregulatory mechanism studies of ginseng leaves on lung cancer based on network pharmacology and molecular docking

Scientific Reports ◽

10.1038/s41598-021-97115-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Zao-Hui Li ◽

Dan Yu ◽

Nan-Nan Huang ◽

Jun-Kai Wu ◽

Xiao-Wei Du ◽

...

Keyword(s):

Lung Cancer ◽

Molecular Docking ◽

Target Prediction ◽

Ginseng Root ◽

Network Pharmacology ◽

Chemical Components ◽

Signaling Proteins ◽

P53 Expression ◽

Docking Analysis ◽

Anticancer Properties

AbstractPanax ginseng is one of the oldest and most generally prescribed herbs in Eastern traditional medicine to treat diseases. Several studies had documented that ginseng leaves have anti-oxidative, anti-inflammatory, and anticancer properties similar to those of ginseng root. The aim of this research was to forecast of the molecular mechanism of ginseng leaves on lung cancer by molecular docking and network pharmacology so as to decipher ginseng leaves' entire mechanism. The compounds associated with ginseng leaves were searched by TCMSP. TCMSP and Swiss Target Prediction databases were used to sort out the potential targets of the main chemical components. Targets were collected from OMIM, PharmGKB, TTD, DrugBank and GeneCards which related to immunity and lung cancer. Ginseng leaves exert its lung cancer suppressive function by regulating the several signaling proteins, such as JUN, STAT3, AKT1, TNF, MAPK1, TP53. GO and KEGG analyses indicated that the immunoreaction against lung cancer by ginseng leaves might be related to response to lipopolysaccharide, response to oxidative stress, PI3K-Akt, MAPK and TNF pathway. Molecular docking analysis demonstrated that hydrogen bonding was interaction's core forms. The results of CCK8 test and qRT-PCR showed that ginseng leaves inhibit cell proliferation and regulates AKT1 and P53 expression in A549. The present study clarifies the mechanism of Ginseng leaves against lung cancer and provides evidence to support its clinical use.

Download Full-text