Effects of equol on deoxycorticosterone acetate salt-induced hypertension and associated vascular dementia in rats

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.

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

Veterinary World ◽

10.14202/vetworld.2020.2477-2483 ◽

2020 ◽

Vol 13 (11) ◽

pp. 2477-2483

Author(s):

Putut Har Riyadi ◽

Mochammad Fitri Atho'illah ◽

Wendy Alexander Tanod ◽

Irma Sarita Rahmawati

Keyword(s):

Oxidative Stress ◽

Renal Damage ◽

Inhibitory Concentration ◽

Male Rats ◽

Deoxycorticosterone Acetate ◽

Acetate Salt ◽

Therapy Effect ◽

Renal Histology ◽

Induced Hypertension ◽

Glomerular Damage

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.

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Intracerebroventricular Infusion of the (Pro)renin Receptor Antagonist PRO20 Attenuates Deoxycorticosterone Acetate-Salt–Induced Hypertension

Hypertension ◽

10.1161/hypertensionaha.114.04458 ◽

2015 ◽

Vol 65 (2) ◽

pp. 352-361 ◽

Cited By ~ 52

Author(s):

Wencheng Li ◽

Michelle N. Sullivan ◽

Sheng Zhang ◽

Caleb J. Worker ◽

Zhenggang Xiong ◽

...

Keyword(s):

Receptor Antagonist ◽

Deoxycorticosterone Acetate ◽

Intracerebroventricular Infusion ◽

Acetate Salt ◽

Induced Hypertension

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Abstract P156: Toll-Like Receptor 2 Deficiency Exacerbates Deoxycorticosterone Acetate-Salt-Induced Hypertension

Hypertension ◽

10.1161/hyp.72.suppl_1.p156 ◽

2018 ◽

Vol 72 (Suppl_1) ◽

Author(s):

Estrellita Uijl ◽

David Severs ◽

A.H. Jan Danser ◽

Robert Zietse ◽

Ewout J Hoorn

Keyword(s):

Toll Like Receptor ◽

Deoxycorticosterone Acetate ◽

Acetate Salt ◽

Induced Hypertension ◽

Toll Like Receptor 2

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Neuroprotective Effect of Antioxidants in the Brain

International Journal of Molecular Sciences ◽

10.3390/ijms21197152 ◽

2020 ◽

Vol 21 (19) ◽

pp. 7152 ◽

Cited By ~ 1

Author(s):

Kyung Hee Lee ◽

Myeounghoon Cha ◽

Bae Hwan Lee

Keyword(s):

Oxidative Stress ◽

Neurodegenerative Diseases ◽

Intracellular Signaling ◽

Neuronal Damage ◽

Neuroprotective Effect ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

High Energy ◽

Antioxidant Compounds ◽

The Brain

The brain is vulnerable to excessive oxidative insults because of its abundant lipid content, high energy requirements, and weak antioxidant capacity. Reactive oxygen species (ROS) increase susceptibility to neuronal damage and functional deficits, via oxidative changes in the brain in neurodegenerative diseases. Overabundance and abnormal levels of ROS and/or overload of metals are regulated by cellular defense mechanisms, intracellular signaling, and physiological functions of antioxidants in the brain. Single and/or complex antioxidant compounds targeting oxidative stress, redox metals, and neuronal cell death have been evaluated in multiple preclinical and clinical trials as a complementary therapeutic strategy for combating oxidative stress associated with neurodegenerative diseases. Herein, we present a general analysis and overview of various antioxidants and suggest potential courses of antioxidant treatments for the neuroprotection of the brain from oxidative injury. This review focuses on enzymatic and non-enzymatic antioxidant mechanisms in the brain and examines the relative advantages and methodological concerns when assessing antioxidant compounds for the treatment of neurodegenerative disorders.

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