Fabrication of multifunctional monometallic nanohybrids for reactive oxygen species-mediated cell apoptosis and enhanced fluorescence cell imaging

2018 ◽  
Vol 6 (8) ◽  
pp. 1187-1194 ◽  
Author(s):  
Shengqiang Hu ◽  
Baoyu Ye ◽  
Hailin Tang ◽  
Fan Wu ◽  
Xinyao Yi ◽  
...  

Multifunctional monometallic nanohybrids were fabricated for ROS-mediated cell apoptosis and enhanced fluorescence cell imaging.

2021 ◽  
Author(s):  
Senlin Wang ◽  
Hong-Shuai Wu ◽  
Kai Sun ◽  
Jinzhong Hu ◽  
Fanghui Chen ◽  
...  

Recently, the toxic hydroxyl radical (·OH) has received wide interest in inducing cell apoptosis by increasing the intracellular reactive oxygen species (ROS) levels. Herein, a cationic polymer (MV-PAH) was rationally...


2021 ◽  
Vol 20 (1) ◽  
pp. 76-83
Author(s):  
Chi-Sen Chang ◽  
Yuh-Chiang Shen ◽  
Chi-Wen Juan ◽  
Chia-Lin Chang ◽  
Po-Kai Lin

The neuroprotective mechanisms of Crataegus pinnatifida extracts and crataegolic acid were studied using paraquat induced cytotoxicity in PC12 cells. C. pinnatifida extracts were prepared using hexane, ethyl acetate, and 95% ethanol. Additionally, crataegolic acid (also known as maslinic acid) was found in C. pinnatifida extracts. Assessment methods included the examinations of cytotoxicity, intracellular reactive oxygen species and calcium changes, activity of caspase-3 and α-synuclein, apoptotic cell death, and the expression levels of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins to investigate the neuroprotective mechanisms of C. pinnatifida extracts and its active component, crataegolic acid. The three extracts and crataegolic acid exhibited potent neuroprotective actions against paraquat induced PC12 cell apoptosis at 5–20µg/mL and 80–100µM concentrations, respectively. The key protective mechanisms included decreasing cell apoptosis, upregulating Bcl-2 protein levels, and downregulating Bax protein levels. The 95% ethanol extract also decreased paraquat induced reactive oxygen species production, calcium overloading, and caspase-3 and α-synuclein activities. The beneficial effects of these extracts could be explained by the active component, crataegolic acid that also inhibited paraquat-induced apoptosis through the suppression of reactive oxygen species generation and the caspase-3 signaling pathway.


2018 ◽  
Vol 36 ◽  
pp. 48-56 ◽  
Author(s):  
Meiaoxue Han ◽  
Renjun Wang ◽  
Ning Ding ◽  
Xiuxia Liu ◽  
Ningning Zheng ◽  
...  

Metallomics ◽  
2014 ◽  
Vol 6 (8) ◽  
pp. 1502-1512 ◽  
Author(s):  
Kanwal Rehman ◽  
Yu Jie Fu ◽  
Yan Fang Zhang ◽  
Qian Qian Wang ◽  
Bin Wu ◽  
...  

Trivalent arsenic metabolites mediate HL-60 cell apoptosis via ROS.


Nanomaterials ◽  
2018 ◽  
Vol 8 (12) ◽  
pp. 1040 ◽  
Author(s):  
Ya Zhang ◽  
Xiangchun Zhang ◽  
Qing Yuan ◽  
Wenchao Niu ◽  
Chunyu Zhang ◽  
...  

Anticancer metallodrugs that aim to physiological characters unique to tumor microenvironment are expected to combat drug tolerance and side-effects. Recently, owing to the fact that reactive oxygen species’ is closely related to the development of tumors, people are committed to developing metallodrugs with the capacity of improving the level of reactive oxygen species level toinduce oxidative stress in cancer cells. Herein, we demonstrated that peptide templated gold clusters with atomic precision preferably catalyze the transformation of hydrogen peroxide into superoxide anion in oxidative pressure-type tumor cells. Firstly, we successfully constructed gold clusters by rationally designing peptide sequences which targets integrin ανβ3 overexpressed on glioblastoma cells. The superoxide anion, radical derived from hydrogen peroxide and catalyzed by gold clusters, was confirmed in vitro under pseudo-physiological conditions. Then, kinetic parameters were evaluated to verify the catalytic properties of gold clusters. Furthermore, these peptide decorated clusters can serve as special enzyme-like catalyst to convert endogenous hydrogen peroxide into superoxide anion, elevated intracellular reactive oxygen species levels, lower mitochondrial membrane potential, damage biomacromolecules, and trigger tumor cell apoptosis consequently.


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