scholarly journals Tilapia viscera hydrolysate extract alleviates oxidative stress and renal damage in deoxycorticosterone acetate-salt-induced hypertension rats

2020 ◽  
Vol 13 (11) ◽  
pp. 2477-2483
Author(s):  
Putut Har Riyadi ◽  
Mochammad Fitri Atho'illah ◽  
Wendy Alexander Tanod ◽  
Irma Sarita Rahmawati

Background and Aim: Hypertension is closely related to oxidative stress conditions, which increases malondialdehyde (MDA) expression and renal damage. Tilapia viscera hydrolysate extract (TVHE) contains compounds and peptides that act as antioxidants. This study aimed to investigate TVHE therapy effect on MDA levels and renal histological conditions in deoxycorticosterone acetate (DOCA)-salt-induced hypertension rats. Materials and Methods: Tilapia viscera were defatted and hydrolyzed using Alcalase enzyme to obtain TVHE. TVHE antioxidant activity was measured using the 1,1-diphenyl-2-picrylhydrazyl method. Fifteen Wistar male rats were divided into five groups: Normal control (without induced DOCA-salt), DOCA-salt, DOCA-salt+Captopril 5 mg/kg body weight (BW), DOCA-salt+TVHE 150 mg/kg BW, and DOCA-salt+TVHE 300 mg/kg BW. MDA level and renal histology were observed in each group. Results: TVHE half maximal inhibitory concentration values ranged from 3.87±0.35 μg/mL to 42.03±3.55 μg/mL, which were identified as in the very strong Blois category. TVHE and captopril therapy reduced MDA expression significantly (p<0.05) compared to DOCA-salt only. TVHE and captopril therapy also improved glomerular damage in DOCA-salt-induced hypertension rats. Conclusion: TVHE has antioxidant ability, decreased MDA level, and decreased glomerular damage in DOCA-salt-induced hypertension rats.

2016 ◽  
Vol 7 (8) ◽  
pp. 3444-3457 ◽  
Author(s):  
Te-Hua Liu ◽  
Tsung-Yu Tsai

Oxidative stress is the major cause of neuronal cell degeneration observed in neurodegenerative diseases including vascular dementia (VaD), and hypertension has been found to increase the probability of VaD.


Hypertension ◽  
2015 ◽  
Vol 65 (2) ◽  
pp. 352-361 ◽  
Author(s):  
Wencheng Li ◽  
Michelle N. Sullivan ◽  
Sheng Zhang ◽  
Caleb J. Worker ◽  
Zhenggang Xiong ◽  
...  

Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Estrellita Uijl ◽  
David Severs ◽  
A.H. Jan Danser ◽  
Robert Zietse ◽  
Ewout J Hoorn

2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.


2007 ◽  
Vol 34 (4) ◽  
pp. 280-285 ◽  
Author(s):  
Hideaki Kawanishi ◽  
Youichi Hasegawa ◽  
Daisuke Nakano ◽  
Mamoru Ohkita ◽  
Masanori Takaoka ◽  
...  

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