Combinational treatment of 5‐fluorouracil and casticin induces apoptosis in mouse leukemia WEHI ‐3 cells in vitro

2020 ◽  
Vol 35 (9) ◽  
pp. 911-921
Author(s):  
Zheng‐Yu Cheng ◽  
Fu‐Shin Chueh ◽  
Shu‐Fen Peng ◽  
Chia‐Hsin Lin ◽  
Chao‐Lin Kuo ◽  
...  
Keyword(s):  
Mouse Leukemia ◽  
Combinational Treatment

scholarly journals Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

2015 ◽  
Vol 35 (9) ◽  
pp. 1435-1444 ◽  
Author(s):  
Tingting Dong ◽  
Qi Zhang ◽  
Michael R Hamblin ◽  
Mei X Wu
Keyword(s):  
Learning And Memory ◽  
Memory Function ◽  
Light Illumination ◽  
Low Level ◽  
Metabolic Substrates ◽  
Secondary Damage ◽  
Injured Brain ◽  
Combinational Treatment

Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue–like injured brain.

Mechanistic aspects of the cytocidal action of ulithiacyclamide on mouse leukemia L1210 cells in vitro

1989 ◽  
Vol 38 (24) ◽  
pp. 4497-4500 ◽  
Author(s):  
Kohda Kohfuku ◽  
Ohta Yuko ◽  
Yokoyama Yumi ◽  
Kawazoe Yutaka ◽  
Kato Taketoshi ◽  
...  
Keyword(s):  
Mouse Leukemia ◽  
L1210 Cells

scholarly journals Assesment of Anticarcinogenic Activities of the Soft Coral Sarcophyton Glaucum Extract on Mouse Leukemia In Vivo and In vitro

2017 ◽  
Vol 29 (2) ◽  
Author(s):  
Najah Al-baqami ◽  
Osama Abuzinadah ◽  
M ELassouli ◽  
Mohammed Almatry ◽  
Yasir Anwar ◽  
...  
Keyword(s):  
Soft Coral ◽  
Mouse Leukemia ◽  
Sarcophyton Glaucum

Cytotoxicity of bacteriohopane-32-ol against mouse leukemia L1210 and P388 cells in vitro

1991 ◽  
Vol 58 (3) ◽  
pp. 309-313 ◽  
Author(s):  
Akira Nagumo ◽  
Kazuya Takanashi ◽  
Hiroshi Hojo ◽  
Yasuo Suzuki
Keyword(s):  
Mouse Leukemia

scholarly journals Antiviral Candidates for Treating Hepatitis E Virus Infection

2019 ◽  
Vol 63 (6) ◽  
Author(s):  
Natalie E. Netzler ◽  
Daniel Enosi Tuipulotu ◽  
Subhash G. Vasudevan ◽  
Jason M. Mackenzie ◽  
Peter A. White
Keyword(s):  
Hepatitis E Virus ◽  
Drug Repurposing ◽  
Hepatitis E ◽  
Genotype 1 ◽  
Rna Quantification ◽  
Half Maximal Effective Concentration ◽  
Combinational Treatment ◽  
Further Development ◽  
Rna Levels

ABSTRACT Globally, hepatitis E virus (HEV) causes significant morbidity and mortality each year. Despite this burden, there are no specific antivirals available to treat HEV patients, and the only licensed vaccine is not available outside China. Ribavirin and alpha interferon are used to treat chronic HEV infections; however, severe side effects and treatment failure are commonly reported. Therefore, this study aimed to identify potential antivirals for further development to combat HEV infection. We selected 16 compounds from the nucleoside and nonnucleoside antiviral classes that range in developmental status from late preclinical to FDA approved and evaluated them as potential antivirals for HEV infection, using genotype 1 replicon luminescence studies and replicon RNA quantification. Two potent inhibitors of HEV replication included NITD008 (half-maximal effective concentration [EC50], 0.03 μM; half-maximal cytotoxic concentration [CC50], >100 μM) and GPC-N114 (EC50, 1.07 μM, CC50, >100 μM), and both drugs reduced replicon RNA levels in cell culture (>50% reduction with either 10 μM GPC-N114 or 2.50 μM NITD008). Furthermore, GPC-N114 and NITD008 were synergistic in combinational treatment (combination index, 0.4) against HEV replication, allowing for dose reduction indices of 20.42 and 8.82 at 50% inhibition, respectively. Sofosbuvir has previously exhibited mixed results against HEV as an antiviral, both in vitro and in a few clinical applications; however, in this study it was effective against the HEV genotype 1 replicon (EC50, 1.97 μM; CC50, >100 μM) and reduced replicon RNA levels (47.2% reduction at 10 μM). Together these studies indicate drug repurposing may be a promising pathway for development of antivirals against HEV infection.

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