Effect of <scp>R</scp>osiglitazone, a <scp>PPAR</scp>‐γ Ligand on <scp>H</scp>aloperidol‐<scp>I</scp>nduced <scp>C</scp>atalepsy

Gupta, Gaurav; Singh, Ramandeep; David, Sheba R; Verma, Rohit Kumar

doi:10.1111/cns.12137

Cited by 32 publications

(16 citation statements)

References 5 publications

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“…DPP-4 inhibitors increase the glucagon-like peptide 1 hormone (GLP-1) secretion, which successively stimulates the secretion of insulin and suppresses glucagon secretion. Emerging proof has proposed the neuroprotective effects of Sita (Al-Awar et al, 2018;Gupta, Singh, David, & Verma, 2013;Samuel et al, 2019). Number of reported literatures have demonstrated that Sita can increases the GLP-1 level in the brain along with improve the cognitive behaviors in rat model of AD (Civantos et al, 2017).…”

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confidence: 99%

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Tian

et al. 2019

Drug Development Research

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The objective of this study was to evaluate the neuroprotective effect of sitagliptin (Sita), quercetin (QCR) and its combination in β‐amyloid (Aβ) induced Alzheimer's disease (AD). Male Sprague–Dawley rats, weighing between 220 and 280 g were used for experiment. Rats were divided into 5 groups (n = 10) and the groups were as follows: (a) Sham control; (b) Aβ injected; (c) Aβ injected + Sita 100; (d) Aβ injected + QCR 100; and (e) Aβ injected + Sita 100 + QCR 100. Cognitive performance was observed by the Morris water maze (MWM), biochemical markers, for example, MDA, SOD, CAT, GSH, Aβ1‐42 level, Nrf2/HO‐1 expression and histopathological study of rat brain were estimated. Pretreatment with Sita, QCR and their combination showed a significant increase in escape latency in particular MWM cognitive model. Further co‐administration of sita and QCR significantly reduced Aβ1‐42 level when compared with individual treatment. Biochemical markers, for example, increased SOD, CAT and GSH, decreased MDA were seen, and histopathological studies revealed the reversal of neuronal damage in the treatment group. Additionally, Nrf2/HO‐1 pathway in rat's brain was significantly increased by Sita, QCR and their combination. Pretreatment with QCR potentiates the action of Sita in Aβ induced AD in rats. The improved cognitive memory could be because of the synergistic effect of the drugs by decreasing Aβ1‐42 level, antioxidant activity and increased expression of Nrf2/HO‐1 in rat brain.

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mentioning

confidence: 99%

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Tian

et al. 2019

Drug Development Research

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“…However, increased GRK2 activity has proven to be maladaptive in HF and its inhibition has emerged as a therapeutic target. The role of β2-AR-Gi signaling in CHF is complicated (Gupta, Singh, David, & Verma, 2013;Chellappan et al, 2016). It has also been reported that β2-ARs are cardio protective through the β2-AR-Gi-Gβγ-PI3K-PKB signaling pathway (Chesley et al, 2000).…”

Section: Involvement Of G-protein-coupled Receptor Kinase (Grk) Sigmentioning

confidence: 99%

Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

Altamish

Samuel

Dahiya

et al. 2019

Drug Development Research

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The well‐known condition of heart failure is a clinical syndrome that results when the myocardium's ability to pump enough blood to meet the body's metabolic needs is impaired. Most of the cardiac activity is maintained by adrenoceptors, are categorized into two main α and β and three distinct subtypes of β receptor: β1‐, β2‐, and β3‐adrenoceptors. The β adrenoreceptor is the main regulatory macro proteins, predominantly available on heart and responsible for down regulatory cardiac signaling. Moreover, the pathological involvement of Angiotensin‐converting enzyme 1 (ACE1)/angiotensin II (Ang II)/angiotensin II type 1 (AT1) axis and beneficial ACE2/Ang (1‐7)/Mas receptor axis also shows protective role via Gi βγ, during heart failure these receptors get desensitized or internalized due to increase in the activity of G‐protein‐coupled receptor kinase 2 (GRK2) and GRK5, responsible for phosphorylation of G‐protein‐mediated down regulatory signaling. Here, we investigate the various clinical and preclinical data that exhibit the molecular mechanism of upset level of GRK change the cardiac activity during failing heart.

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“…The MC1R agonists α‐MSH and ACTH stimulate the formation of eumelanin While the synthesis of pheomelanin is performed by the stimulating protein agonist (ASP) . However, it was thought that α‐melanocyte stimulating hormone (α‐MSH) was the primary ligand for this receptor and was found in the pituitary and proopiomelanocortin (POMC) gene product.…”

Section: Insight Of Molecular Mechanism Involve In Melanin Productionmentioning

confidence: 99%

“…The MC1R agonists α-MSH and ACTH stimulate the formation of eumelanin [44][45][46] While the synthesis of pheomelanin is performed by the stimulating protein agonist (ASP). 27,47 However, it was thought that α-melanocyte stimulating hormone (α-MSH) was the primary li- [48][49][50][51][52] A recent genetic study explores ALDH3A2, which codes for an aldehyde dehydrogenase isozyme involved in lipid metabolism.…”

Section: In S I G Ht Of Molecul Ar Mechanis M Involve In Mel Anin Pmentioning

confidence: 99%

Sjogren‐Larsson syndrome associated hypermelanosis

Hou

Zhu

et al. 2019

J of Cosmetic Dermatology

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Background/Objectives Sjogren – Larsson syndrome (SLS) is a rare autosomal recessive disease of the mutation ALDH3A2 that identifies a part of fatty acids for fatty aldehyde dehydrogenase: NAD‐oxidoreductase enzyme complex. This study aimed to access variant ALDH3A2 gene coded for FALDH and products regulating pathogenic melanogenesis owing to increased oxidative stress and reactive oxygen species resulting in DNA harm in SLS. By turning them into fatty acids, FALDH avoids the accumulation of toxic fatty aldehydes. The mutation results in the accumulation of aldehyde‐modified lipids or fatty alcohols that may interfere with skin and brain function. Methods In Nov 2018, we performed a literature search in PubMed for clinical studies, clinical trials, case reports, controlled trials, randomized controlled trials, and systemic reviews. The search terms we used were “SJOGREN‐LARSSON SYNDROME” AND “HYPERMELANNOSIS” OR “FALDH” (from 1985). The search resulted in 1,289 articles, out of these 95 articles met our inclusion exclusion criteria. Our inclusion criteria included relevant original articles relevant, critical systemic reviews, and crucial referenced articles, ex‐clusion criteria included duplicates and articles not published in English language. Results Toxicity of long‐chain aldehydes to FALDH‐deficient cells owing to accumulation under the profound epidermis layer improves oxidative stress in the cell resulting in keratinocyte hyperproliferation. Conclusion While it continues to be determined whether accumulated fatty alcohol and fatty aldehydes obtained from ether glycerolipids and sphingolipids improve the susceptibility of melanocytes and their element accountable for skin hyperpigmentation to biological colour.

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Effect of Rosiglitazone, a PPAR‐γ Ligand on Haloperidol‐Induced Catalepsy

Cited by 32 publications

References 5 publications

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

Sjogren‐Larsson syndrome associated hypermelanosis

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