Effects of peripherally and centrally applied ghrelin on the oxidative stress induced by renin angiotensin system in a rat model of renovascular hypertension

Boshra, Vivian; Abbas, Amr M.

doi:10.1515/jbcpp-2016-0145

Cited by 10 publications

(7 citation statements)

References 48 publications

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“…Besides, studies have shown that hypertension can aggravate cerebrovascular oxidative stress caused by mild craniocerebral injury through the protective effect of the mitochondrial-targeted antioxidant peptide SS-31 [299]. Renovascular hypertension also significantly increases brain AT1R and oxidative stress in the brain and plasma [300].…”

Section: Hypertensionmentioning

confidence: 99%

Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases

Song

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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The blood-brain barrier (BBB), as a crucial gate of brain-blood molecular exchange, is involved in the pathogenesis of multiple neurological diseases. Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the scavenger system. Since oxidative stress plays a significant role in the production and maintenance of the BBB, the cerebrovascular system is especially vulnerable to it. The pathways that initiate BBB dysfunction include, but are not limited to, mitochondrial dysfunction, excitotoxicity, iron metabolism, cytokines, pyroptosis, and necroptosis, all converging on the generation of ROS. Interestingly, ROS also provide common triggers that directly regulate BBB damage, parameters including tight junction (TJ) modifications, transporters, matrix metalloproteinase (MMP) activation, inflammatory responses, and autophagy. We will discuss the role of oxidative stress-mediated BBB disruption in neurological diseases, such as hemorrhagic stroke, ischemic stroke (IS), Alzheimer’s disease (AD), Parkinson’s disease (PD), traumatic brain injury (TBI), amyotrophic lateral sclerosis (ALS), and cerebral small vessel disease (CSVD). This review will also discuss the latest clinical evidence of potential biomarkers and antioxidant drugs towards oxidative stress in neurological diseases. A deeper understanding of how oxidative stress damages BBB may open up more therapeutic options for the treatment of neurological diseases.

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Section: Hypertensionmentioning

confidence: 99%

Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases

Song

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…The antioxidative stress effect of ghrelin was due to its reverse action on plasma renin activity (PRA) and angiotensin II receptor type 1 (AT1R). Ghrelin actions were elucidated through decreasing PRA levels and down-regulating angiotensin II receptor type 1 [87].…”

Section: Antioxidant and Protective Effect Related To Renal Systemmentioning

confidence: 99%

“…Moreover, other studies report ghrelin kidney protective effects through its antioxidant properties. These results demonstrated that treatment with exogenous ghrelin alleviated oxidative damage via decreased lipid peroxidation [87] and subsequently elevated the activity of antioxidant enzymes, such as GPx, CAT, SOD, and GSH content on rat kidney [89][90][91].…”

Section: Antioxidant and Protective Effect Related To Renal Systemmentioning

confidence: 99%

Potentiality of ghrelin as antioxidant and protective agent

2021

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Background: Oxidative stress is the result of cellular troubles related to aerobic metabolism. Furthermore, this stress is always associated with biological responses evoked by physical, chemical, environmental, and psychological factors. Several studies have developed many approaches of antioxidant defense to diminish the severity of many diseases. Ghrelin was originally identified from the rat stomach, and it is a potent growth hormone-releasing peptide that has pleiotropic functions. Methods: A systematic review was conducted within PubMed, ScienceDirect, MEDLINE, and Scopus databases using keywords such as ghrelin, antioxidant, oxidative stress, and systemic oxidative stress sensor. Results: In the last decade, many studies show that ghrelin exhibits protection effects against oxidative stress derived probably from its antioxidant effects. Pieces of evidence demonstrate that systemic oxidative stress increase ghrelin levels in the plasma. The expression of ghrelin and its receptor in ghrelin peripheral tissues and extensively in the central nervous system suggests that this endogenous peptide plays an important role as a systemic oxidative stress sensor Conclusion: The current evidence confirms that ghrelin and its derived peptides (Desacyl-ghrelin, obestatin) act as a protective antioxidant agent. Therefore, stressor modality, duration, and intensity are the parameters of oxidative stress that must be taken into consideration to determine the role of ghrelin, Desacyl-ghrelin, and obestatin in the regulation of cell death pathways.

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“…Therefore, NSAIDs lower blood pressure and inhibit the renin-angiotensin system. [9][10] The inhibition of cyclooxygenase COX activity of isoform COX-2 inhibitors have designed to overcome pain and inflammation with less toxic effects. 11 Clinical studies about the COX-2 inhibitor reported the less prevalence of gastrointestinal complications noticed with nonspecific-NSAIDs.…”

Section: Introductionmentioning

confidence: 99%

Effect of Celecoxib and Diclofenac on Blood Pressure, Renal Function and Vasoactive Prostanoids in Young Early Subjects

Arjumand¹,

Slam²,

Perveen³

et al. 2022

PJMHS

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Objective: Determination of celecoxib and diclofenac effects in early young subjects. Study design: Randomized study designed Methodology: All the participants received celecoxib 225 mg two times/day and diclofenac 80mg two times/day. First 21 days all participants received celecoxib treatment, before the start of the following medicine diclofenac 3.5 weeks gap was given. The blood pressure (BP) of patients was measured using the ambulatory blood pressure monitoring device (space labs model 90217A). Results: Group one consisted of young participants had a mean ± SD age 29 ± 3.4 while group 2 elderly had a mean ± SD age 55 ± 5.5. The mean body mass index was (group 1) 21.7 ± 1.8 kg/m2 and for group 2 = 27.3 ± 1.0 kg/m2. Group one had 5 (38.46%) females and 8 (61.53%) males while group 2 had 4 (30.76%) females and 9 (69.23%) males. The celecoxib medication baseline BP shows that there was no significant difference found in systolic blood pressure. Similar results for diastolic (mm Hg) for day and night time. Mean arterial pressure was higher in the elderly group -2 than in young group 1, Plasma renin activity was less in group 2 on day one compared to group 1. Plasma renin activity and concentration were decreased after 7 days of celecoxib and diclofenac treatment. A non-significant result was obtained. Group 1 Aldosterone serum (ng/l) for celecoxib received patients 11 ± 2.2 (ng/l) value for day one, day 7 = 13.2 ± 3.2, day 14 = 14.2 ± 3.4. Similarly in the case of diclofenac, the Aldosterone serum (ng/l) value for day one = 11.3 ± 21, day 7= 12.2 ± 2.3, and day 14 = 12.3 ± 2.1. A decrease in values was observed in both groups for aldosterone serum. For group-2 celecoxib, day one=15 ± 2.2, day 7= 14 ± 2.4*. day14= 14 ± 1.4. For diclofenac day one 15 ± 2.2, 7day= 15 ± 1.5, and 14 days = 14 ± 5.1. The comparison of both groups shows that the sodium and potassium decrease in both treatments in both groups. Conclusion: Overall, we got a non-significant response of both drugs on renal function and blood pressure. Keywords: blood pressure, renin angiotensin aldosterone system, non-steroidal anti-inflammatory drugs (NSAIDs)

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Effects of peripherally and centrally applied ghrelin on the oxidative stress induced by renin angiotensin system in a rat model of renovascular hypertension

Abstract: The hypotensive effect of ghrelin is mediated through the amelioration of oxidative stress, which is induced by RAS centrally and peripherally.

Cited by 10 publications

References 48 publications

Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases

Oxidative Stress-Mediated Blood-Brain Barrier (BBB) Disruption in Neurological Diseases

Potentiality of ghrelin as antioxidant and protective agent

Effect of Celecoxib and Diclofenac on Blood Pressure, Renal Function and Vasoactive Prostanoids in Young Early Subjects

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