scholarly journals Protective Effect of Luteolin on an Oxidative-Stress Model Induced by Microinjection of Sodium Nitroprusside in Mice

2013 ◽  
Vol 122 (2) ◽  
pp. 109-117 ◽  
Author(s):  
Qand Agha Nazari ◽  
Toshiaki Kume ◽  
Yuki Takada-Takatori ◽  
Yasuhiko Izumi ◽  
Akinori Akaike
2014 ◽  
Vol 5 (5) ◽  
pp. 984-989 ◽  
Author(s):  
Qand Agha Nazari ◽  
Yuki Takada-Takatori ◽  
Tadashi Hashimoto ◽  
Atsushi Imaizumi ◽  
Yasuhiko Izumi ◽  
...  

The protective effects of conventional curcumin or highly bioavailable curcumin, Theracurmin®, against oxidative stress is investigated using our in vivo oxidative stress model.


2016 ◽  
Vol 34 (4) ◽  
pp. 777-786 ◽  
Author(s):  
K.S. SILVA ◽  
L.J. K. URBAN ◽  
A. BALBINOT ◽  
F.S. GNOCATO ◽  
N.D. KRUSE ◽  
...  

ABSTRACT The nitric oxide acts on the antioxidant system of plants and can discontinue the damage of herbicides elicitors of oxidative stress that cause the disruption of membranes and leakage of cellular contents. In order to evaluate the protective effect of nitric oxide in electrolytes leakage, leaf segments of the Puita INTA CL rice cultivar were incubated with 0, 5, 50, 500 and 5,000 μM clomazone (360 g a.i. L-1), oxadiazon (250 g a.i. L-1), oxyfluorfen (240 g a.i. L-1) and the formulated mixture of paraquat (200 g a.i. L-1) + diuron (100 g a.i. L-1) to obtain the maximum potential conductivity of 50% (MPC50). Subsequently, leaf segments were pre-treated with 0, 200 and 2,000 μM of sodium nitroprusside (SNP) for four hours and further incubated for 48 hours with 0, 0.5, 1, 2 and 4 times the concentration of the herbicide that caused the CMP50, and the protective effect was reassessed in the presence of nitric oxide scavenger, cPTIO. The MPC50 was caused by exposure to 188.9, 273.4, 410.2 + 205.1 and 917.0 μM of Oxadiazon, Oxyfluorfen, Paraquat + Diuron and Clomazone. Pretreatment with 200 μM of SNP reduced electrolyte leakage in leaf segments exposed to 2 and 4 times the MPC50 to oxadiazon and paraquat + diuron, while 2,000 μM reduced the damage caused by oxyfluorfen, at the same concentrations. Also, 200 and 2,000 μM of SNP were efficient for clomazone, and the protection was confirmed by cPTIO in all cases.


2012 ◽  
Vol 120 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Qand Agha Nazari ◽  
Keita Mizuno ◽  
Toshiaki Kume ◽  
Yuki Takada-Takatori ◽  
Yasuhiko Izumi ◽  
...  

2018 ◽  
Vol 24 (1) ◽  
pp. 53-59
Author(s):  
Jong Min Kim ◽  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Seong-kyeong Bae ◽  
Ga-Hee Jeong ◽  
...  

Author(s):  
Pu-xi XIONG ◽  
Lin HAN ◽  
Xiao-hong LIU ◽  
De-jun GONG ◽  
Wei-jun PAN ◽  
...  

2012 ◽  
Vol 32 (1) ◽  
pp. 88-91
Author(s):  
Zhi-yong WANG ◽  
Ling-zhen TANG ◽  
Tian-wen GAO

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.


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