Naringin regulates glutamate-nitric oxide cGMP pathway in ammonium chloride induced neurotoxicity

Arumugam, R.; Vijayakumar, Natesan; Mani, Renuka

doi:10.1016/j.biopha.2016.10.080

Cited by 28 publications

(21 citation statements)

References 53 publications

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“…Previous research from our lab showed significant increase in lipid peroxidation in the liver, brain, and kidney of NH 4 Cl-induced hyperammonemic rats [10, 11]. Other studies have reported increased lipid peroxidation in animal models of hyperammonemia [16, 65, 66]. Moreover, NH 4 Cl-induced hyperammonemic rats showed a marked increase in NO levels in the liver, kidney, and cerebrum.…”

Section: Discussionmentioning

confidence: 66%

“…Excess ammonia also increases the activity of Na + /K + -ATPase in the brain [25]; however, the underlying mechanism remains unclear. Increased activity of the brain Na + /K + -ATPase in hyperammonemia has been demonstrated in multiple previous studies [16, 26]. …”

Section: Introductionmentioning

confidence: 77%

“…The increased NO production in the brain is a direct result of the upregulated nNOS in hyperammonemic rats. Accordingly, Ramakrishnan et al [16] have reported increased expression of nNOS in the brain of NH 4 Cl-induced rats. Hyperammonemia is known to activate nNOS and increase NO production in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, ammonia-induced oxidative stress occurs due to increased production of reactive oxygen species (ROS) and subsequent damage of proteins, lipids, and DNA [15]. Previous studies have demonstrated increased ROS production and oxidative stress in hyperammonemia [10, 11, 16]. Hence, counteracting oxidative/nitrosative stress may represent a protective strategy against hyperammonemia-induced brain injury.…”

Section: Introductionmentioning

confidence: 99%

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Commiphora molmol Modulates Glutamate‐Nitric Oxide‐cGMP and Nrf2/ARE/HO‐1 Pathways and Attenuates Oxidative Stress and Hematological Alterations in Hyperammonemic Rats

Mahmoud

Alqahtani

Othman

et al. 2017

Oxidative Medicine and Cellular Longevity

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Hyperammonemia is a serious complication of liver disease and may lead to encephalopathy and death. This study investigated the effects of Commiphora molmol resin on oxidative stress, inflammation, and hematological alterations in ammonium chloride- (NH4Cl-) induced hyperammonemic rats, with an emphasis on the glutamate-NO-cGMP and Nrf2/ARE/HO-1 signaling pathways. Rats received NH4Cl and C. molmol for 8 weeks. NH4Cl-induced rats showed significant increase in blood ammonia, liver function markers, and tumor necrosis factor-alpha (TNF-α). Concurrent supplementation of C. molmol significantly decreased circulating ammonia, liver function markers, and TNF-α in hyperammonemic rats. C. molmol suppressed lipid peroxidation and nitric oxide and enhanced the antioxidant defenses in the liver, kidney, and cerebrum of hyperammonemic rats. C. molmol significantly upregulated Nrf2 and HO-1 and decreased glutamine and nitric oxide synthase, soluble guanylate cyclase, and Na+/K+-ATPase expression in the cerebrum of NH4Cl-induced hyperammonemic rats. Hyperammonemia was also associated with hematological and coagulation system alterations. These alterations were reversed by C. molmol. Our findings demonstrated that C. molmol attenuates ammonia-induced liver injury, oxidative stress, inflammation, and hematological alterations. This study points to the modulatory effect of C. molmol on glutamate-NO-cGMP and Nrf2/ARE/HO-1 pathways in hyperammonemia. Therefore, C. molmol might be a promising protective agent against hyperammonemia.

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Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Commiphora molmol Modulates Glutamate‐Nitric Oxide‐cGMP and Nrf2/ARE/HO‐1 Pathways and Attenuates Oxidative Stress and Hematological Alterations in Hyperammonemic Rats

Mahmoud

Alqahtani

Othman

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…This compound shows a wide variety of pharmacological effects such as antioxidant, blood lipid-lowering and anticarcinogenic activity. Moreover, several studies have highlighted its potential to suppress the production of proinflammatory cytokines and attenuate the A C C E P T E D M A N U S C R I P T inflammatory response [7,8,9,10,11,12] and it has been proposed in combination with corticoids to treat skin diseases such as dermatitis [13].…”

Section: Introductionmentioning

confidence: 99%

A novel ultradeformable liposomes of Naringin for anti-inflammatory therapy

Pleguezuelos-Villa

Mir-Palomo

Dı́ez-Sales

et al. 2018

Colloids and Surfaces B: Biointerfaces

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The article has 4636 words including ackwonledgment and references. The abstract has 127 words. There are 5 figures and 2 tables. Highlights Nanovesicles were small in size and monodispersed independently of the NA concentration. No citotoxity effects were observed in 3T3 fibroblasts treated with ultradeformable liposomes. Ultradeformable liposomes have the ability to reduce skin inflammation. Graphical abstract AbstractUltradeformable liposomes were formulated using naringin (NA), a flavanone glycoside, at different concentrations (3, 6 and 9 mg/mL). Nanovesicles were small size (~100 nm), regardless of the NA concentration used, and monodisperse (PI < 0.30). All formulations showed a high entrapment efficiency (~88%) and a highly negative zeta potential (around -30 mV). The selected formulations were highly biocompatible as confirmed by in vitro studies using 3T3 fibroblasts.In vitro assay showed that the amounts (%) of NA accumulated in the epidermis (~ 10%) could explain the anti-inflammatory properties of ultradeformable liposomes. In vivo studies confirmed the higher effectiveness of ultradeformable liposomes respect to betamethasone cream and NA dispersion in reducing skin inflammation in mice. Overall, it can conclude that NA ultradeformable liposomes can be considered as a promising formulation for the treatment of skin inflammatory diseases.

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Naringin corrects renal failure related to Lesch‐Nyhan disease in a rat model via NOS–cAMP–PKA and BDNF/TrkB pathways

Akintunde,

Falomo,

Akinbohun

et al. 2023

J Biochem & Molecular Tox

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This study explored the effect of naringin (NAR) on HGPRT1 deficiency and hyperuricemia through NOS–cAMP–PKA and BDNF/TrkB signaling pathways induced by caffeine (CAF) and KBrO3 in a rat model. Sixty‐three adult male albino rats were randomly assigned into nine (n = 7) groups. Group I: control animals, Group II was treated with 100 mg/kg KBrO3, Group III was treated with 250 mg/kg CAF, Group IV was treated with 100 mg/kg KBrO3 + 250 mg/kg CAF, Group V was administered with 100 mg/kg KBrO3 + 100 mg/kg haloperidol, Group VI was administered with 100 mg/kg KBrO3 + 50 mg/kg NAR, Group VII was administered with 500 mg/kg CAF + 50 mg/kg NAR, and Group VIII was administered with 100 mg/kg KBrO3 + 250 mg/kg CAF + 50 mg/kg NAR. Finally, group IX was treated with 50 mg/kg NAR. The exposure of rats to KBrO3 and CAF for 21 days induced renal dysfunction linked with Lesch‐Nyhan disease. NAR obliterated renal dysfunction linked with Lesch‐Nyhan disease by decreasing uric acid, renal malondialdehyde level, inhibiting the activities of arginase, and phosphodiesterase‐51 (PDE‐51) with corresponding upregulation of brain derived‐neurotrophic factor and its receptor (BDNF‐TrkB), Bcl11b, HGPRT1, and DARPP‐32. Additionally, renal failure related to Lesch‐Nyhan disease was remarkably corrected by NAR as shown by the reduced activities of AChE and enzymes of ATP hydrolysis (ATPase, AMPase, and ADA) with affiliated increase in the NO level. This study therefore validates NAR as nontoxic and effective chemotherapy against kidney‐related Lesch‐Nyhan disease by mitigating effects of toxic food additives and enzymes of ATP‐hydrolysis via NOS–cAMP–PKA and BDNF/TrkB signaling pathways.

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Naringin regulates glutamate-nitric oxide cGMP pathway in ammonium chloride induced neurotoxicity

Cited by 28 publications

References 53 publications

Commiphora molmol Modulates Glutamate‐Nitric Oxide‐cGMP and Nrf2/ARE/HO‐1 Pathways and Attenuates Oxidative Stress and Hematological Alterations in Hyperammonemic Rats

Commiphora molmol Modulates Glutamate‐Nitric Oxide‐cGMP and Nrf2/ARE/HO‐1 Pathways and Attenuates Oxidative Stress and Hematological Alterations in Hyperammonemic Rats

A novel ultradeformable liposomes of Naringin for anti-inflammatory therapy

Naringin corrects renal failure related to Lesch‐Nyhan disease in a rat model via NOS–cAMP–PKA and BDNF/TrkB pathways

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