Vinpocetine and Ischemic Stroke

Al-Kuraishy, Hayder M; Al-Gareeb, Ali I

doi:10.5772/intechopen.90551

Cited by 5 publications

(7 citation statements)

References 71 publications

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“…Our findings demonstrated that gentamicin-treated mice had a significant rise in MDA and a significant drop in GSH levels. El Gamal et al 38 and Al-Kuraishy et al 39 showed large increases in renal MDA and significant decreases in renal GSH in gentamicin-treated rats, which is consistent with our results. We discovered that giving celecoxib before or after gentamicin caused MDA and GSH levels in kidney tissues to be corrected to near-control values, which matched the findings of previous studies by Suddek et al 21 and Ahmed et al 1 .…”

Section: Discussionsupporting

confidence: 92%

Celecoxib has Preventive and Therapeutic Benefits against Nephrotoxicity Caused by Gentamicin in Mice

et al. 2022

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It’s crucial to comprehend the impact of oxidative stress and pro-inflammatory cytokines in the gentamicin-induced kidney injury mechanism. Celecoxib was administered orally either before or after intraperitoneal therapy with gentamicin in mice. The serum levels of creatinine (SCr), blood urea nitrogen (BUN), IL-6, and TNF-α were measured by ELISA test, as well as the levels of the kidney tissue malondialdehyde (MDA), and glutathione (GSH) were also estimated spectrophotometrically. The renal expression of nuclear factor-κB (NF-κB), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and cyclooxygenase 2 (COX-2) mRNAs were evaluated by qPCR. Histopathological evaluation and Immunohistochemical examination of kidney NF-κB, IL-6, and COX-2 were also, performed. Celecoxib successfully prevented gentamicin-induced kidney damage as indicated by reducing blood BUN, SCr, and tissue MDA levels and increasing renal tissue GSH levels as well as lowering the blood IL-6 and TNF-α in comparison to mice received gentamicin. Furthermore, celecoxib has inhibited COX-2, NF-κB, IL-6, and TNF-α expression in the renal tissue. It is noteworthy that celecoxib therapy after gentamicin administration brought about substantially the same results as celecoxib treatment before gentamicin injection in mice. Our results showed the role of celecoxib as a therapeutic tool for gentamicin-induced nephrotoxicity as well as raised its beneficial prophylactic role in this medical challenge by attenuating oxidative stress and inflammation.

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Section: Discussionsupporting

confidence: 92%

Celecoxib has Preventive and Therapeutic Benefits against Nephrotoxicity Caused by Gentamicin in Mice

et al. 2022

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“…ASP in circulation increases substantially with overweight and obesity and declines with weight loss. ASP levels are correlated with cardiometabolic risk markers in obese people (Al-Kuraishy & Al-Gareeb, 2017;Mishra et al, 2019;Onat et al, 2017). ASP and its component proteins (C3, factor B and adipsin) have been demonstrated to be meaningfully increased in type 2 diabetes as well as in some research on type I diabetes (Cianflone et al, 2003).…”

Section: Asp and Cardiometabolic Risk Factorsmentioning

confidence: 99%

Acylation stimulating protein/C3adesArg in the metabolic states: role of adipocyte dysfunction in obesity complications

Rezvani,

Shadmand Foumani Moghadam,

Cianflone

2024

The Journal of Physiology

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Adipose tissue, as an endocrine organ, secretes several adipocyte‐derived hormones named ‘adipokines’ that are implicated in regulating energy haemostasis. Substantial evidence shows that white adipose tissue‐derived adipokines mediate the link between obesity‐related exogenous factors (like diet and lifestyle) and various biological events (such as pre‐ and postmenopausal status) that have obesity consequences (cardiometabolic disorders). One of the critical aetiological factors for obesity‐related diseases is the dysfunction of adipokine pathways. Acylation‐stimulating protein (ASP) is an adipokine that stimulates triglyceride synthesis and storage in adipose tissue by enhancing glucose and fatty acid uptake. ASP acts via its receptor C5L2. The primary objective of this review is to address the existing gap in the literature regarding ASP by investigating its diverse responses and receptor interactions across multiple determinants of obesity. These determinants include diet composition, metabolic disorders, organ involvement, sex and sex hormone levels. Furthermore, this article explores the broader paradigm shift from solely focusing on adipose tissue mass, which contributes to obesity, to considering the broader implications of adipose tissue function. Additionally, we raise a critical question concerning the clinical relevance of the insights gained from this review, both in terms of potential therapeutic interventions targeting ASP and in the context of preventing obesity‐related conditions, highlighting the potential of the ASP–C5L2 interaction as a pharmacological target. In conclusion, these findings validate that obesity is a low‐grade inflammatory status with multiorgan involvement and sex differences, demonstrating dynamic interactions between immune and metabolic response determinants. image

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“…[59][60][61] Nrf2 controls various genes involved in iron and heme metabolism, such as heme oxygenase one and the genes encoding the iron storage protein ferritin, to reduce the harmful effects of free iron. [62] Nrf2 is a critical factor in cellular components, which helps in cellular repair and OS control [63][64][65][66] (Figure 3). metabolites.…”

Section: Nrf2 and Cellular Metabolomicsmentioning

confidence: 99%

The possible role of nuclear factor erythroid‐2‐related factor 2 activators in the management of Covid‐19

Al‐kuraishy,

Al‐Gareeb,

Eldahshan

et al. 2023

J Biochem & Molecular Tox

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COVID‐19 is caused by a novel SARS‐CoV‐2 leading to pulmonary and extra‐pulmonary manifestations due to oxidative stress (OS) development and hyperinflammation. COVID‐19 is primarily asymptomatic though it may cause acute lung injury (ALI), acute respiratory distress syndrome (ARDS), systemic inflammation, and thrombotic events in severe cases. SARS‐CoV‐2‐induced OS triggers the activation of different signaling pathways, which counterbalances this complication. One of these pathways is nuclear factor erythroid 2‐related factor 2 (Nrf2), which induces a series of cellular interactions to mitigate SARS‐CoV‐2‐mediated viral toxicity and OS‐induced cellular injury. Nrf2 pathway inhibits the expression of pro‐inflammatory cytokines and the development of cytokine storm in COVID‐19. Therefore, Nrf2 activators may play an essential role in reducing SARS‐CoV‐2 infection‐induced inflammation by suppressing NLRP3 inflammasome in COVID‐19. Furthermore, Nrf2 activators can attenuate endothelial dysfunction (ED), renin‐angiotensin system (RAS) dysregulation, immune thrombosis, and coagulopathy. Thus this mini‐review tries to clarify the possible role of the Nrf2 activators in the management of COVID‐19. Nrf2 activators could be an effective therapeutic strategy in the management of Covid‐19. Preclinical and clinical studies are recommended in this regard.

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Vinpocetine and Ischemic Stroke

Cited by 5 publications

References 71 publications

Celecoxib has Preventive and Therapeutic Benefits against Nephrotoxicity Caused by Gentamicin in Mice

Celecoxib has Preventive and Therapeutic Benefits against Nephrotoxicity Caused by Gentamicin in Mice

Acylation stimulating protein/C3adesArg in the metabolic states: role of adipocyte dysfunction in obesity complications

The possible role of nuclear factor erythroid‐2‐related factor 2 activators in the management of Covid‐19

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