Phosalone-induced inflammation and oxidative stress in the colon: evaluation and treatment

Ghasemi-Niri, Seyedeh Farnaz; Maqbool, Faheem; Baeeri, Maryam; Gholami, Mahdi; Abdollahi, Mohammad

doi:10.3748/wjg.v22.i21.4999

Cited by 18 publications

(10 citation statements)

References 44 publications

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“…In contrast, NF-κB was a potential target for the anti-inflammatory effect of ellagic acid incorporated into the normal diet (0.5 %) of mice in an ulcerative colitis experimental model [97]. Similar results for ellagic acid as an anti-inflammatory agent through modulation of the NF-κB activation pathway have been observed in several other studies [98][99][100][101][102].…”

Section: Anti-inflammatory Activity Of Ellagic Acidsupporting

confidence: 76%

A Pharmacological Update of Ellagic Acid

et al. 2018

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Ellagic acid is a common metabolite present in many medicinal plants and vegetables. It is present either in free form or as part of more complex molecules (ellagitannins), which can be metabolized to liberate ellagic acid and several of its metabolites, including urolithins. While ellagic acidʼs antioxidant properties are doubtless responsible for many of its pharmacological activities, other mechanisms have also been implicated in its various effects, including its ability to reduce the lipidemic profile and lipid metabolism, alter pro-inflammatory mediators (tumor necrosis factor-α, interleukin-1β, interleukin-6), and decrease the activity of nuclear factor-κB while increasing nuclear factor erythroid 2-related factor 2 expression. These events play an important role in ellagic acidʼs anti-atherogenic, anti-inflammatory, and neuroprotective effects. Several of these activities, together with the effect of ellagic acid on insulin, glycogen, phosphatases, aldose reductase, sorbitol accumulation, advanced glycation end-product formation, and resistin secretion, may explain its effects on metabolic syndrome and diabetes. In addition, results from recent research have increased the interest in ellagic acid, both as a potential protective agent of the liver and skin and as a potential anticancer agent, due to the specific mechanisms affecting cell proliferation, apoptosis, DNA damage, and angiogenesis and its aforementioned anti-inflammatory properties. Taken together, these effects make ellagic acid a highly interesting compound that may contribute to different aspects of health; however, more studies are needed, especially on the compoundʼs pharmacokinetic profile. In this review, we selected papers published from 2005 to the present.

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Section: Anti-inflammatory Activity Of Ellagic Acidsupporting

confidence: 76%

A Pharmacological Update of Ellagic Acid

et al. 2018

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“…(2013), who suggested that EA reduced NF-B, IL-6, and TNF levels compared to the control group in mice with ulcerative colitis [ 36 ]. EA inhibits inflammation through modulating the NF-B signaling pathway [ 37 ]. These findings are consistent with Cornélio Favarin et al .…”

Section: Discussionmentioning

confidence: 99%

Ellagic acid and cilostazol ameliorate amikacin-induced nephrotoxicity in rats by downregulating oxidative stress, inflammation, and apoptosis

et al. 2022

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Amikacin (AK) has the largest spectrum of aminoglycosides. However, its use is constrained because of nephrotoxicity and ototoxicity. Ellagic acid (EA) is a polyphenol present in plants. It has antioxidant, anticarcinogenic, and antimutagenic characteristics. Cilostazol (CTZ) is a phosphodiesterase Ш inhibitor, it is a potent vasodilator and antiplatelet drug. CTZ has an inhibitory effect on reactive oxygen species and superoxide generation in addition to hydroxyl radicals scavenging action. This study determines whether EA and cilostazol have a protective effect against AK-induced nephrotoxicity. Forty-nine rats were divided into seven equal groups: control normal; AK 400 mg/kg; EA 10 mg/kg; CTZ 10 mg/kg; AK 400 mg/kg plus EA 10 mg/kg; AK 400 mg/kg plus CTZ 10 mg/kg; AK 400 mg/kg plus EA 10 mg/kg and CTZ 10 mg/kg. For seven days, drugs were administered using gavage one hour before intramuscular injection of AK. Twenty-four hours after the last AK dosage, blood samples were collected to determine blood urea nitrogen and creatinine levels. Kidneys were removed for histopathological examination and measurement of: malondialdehyde (MDA), catalase (CAT), decreased glutathione (GSH), superoxide dismutase (SOD), interleukin 6 (IL6), tumor necrosis factor-alpha (TNFα), nuclear factor kappa B (NFκB), and Bcl-2 associated x protein (BAX). AK caused kidney damage, inflammatory mediator elevation, and oxidative stress and apoptotic markers. Rats receiving EA or CTZ indicated significant improvement in kidney function, decrease in oxidative stress and inflammation through NF-kB down-regulation and BAX expression. The combination of EA and CTZ showed a synergistic effect. In conclusion, EA and CTZ might play a beneficial role in preventing nephrotoxicity induced by AK partially by inhibition of tissue inflammation and apoptosis.

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“…Several pesticides exert cellular toxicity via the triggering of oxidative stress, such as organophosphorus insecticides (35), organochlorine insecticides (36), pyrethroid insecticides (37), and fungicides (38), but the mechanisms by which FEN induces oxidative hepatic damage are still poorly understood. Therefore, we first profiled hepatic gene expression in FEN-exposed rats.…”

Section: Discussionmentioning

confidence: 99%

Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway

et al. 2018

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Fenvalerate (FEN), a mainstream pyrethroid pesticide, was initially recommended as a low‐toxicity agent for controlling agricultural and domestic pests. Despite the widespread use of FEN worldwide, little data are available on FEN‐induced hepatic lesions and molecular mechanisms. In the present study, we first performed an occupational cross‐sectional study on FEN factory workers and found that the levels of serum alanine aminotransferase (ALT) and total antioxidant capacity increased, whereas malondialdehyde decreased in laborers in the working areas where the levels of airborne FEN were much higher compared with the office area. The results were then confirmed by animal experiments that abnormal hepatic histology, increased ALT level, and compromised hepatic oxidative capability were observed in rats exposed to a high concentration of FEN. Furthermore, the bioinformatics analysis of gene microarray in rat liver tissue showed that FEN significantly changed the expressions of genes related to the regulation of intracellular calcium ion homeostasis and the calcium signal pathway. Finally, the functional experiments in Buffalo rat liver (BRL) cells demonstrated that FEN first activated ERK MAPK, followed by IKK and NF‐κB, which triggered the transcription of genes responsible for accelerating an overload of intracellular calcium ions, prompted reactive oxygen species generation in the mitochondria, and finally, induced hepatic cellular apoptosis. The calcium signaling pathway and in particular, an overload of intracellular calcium play a critical role in this pathophysiological process via the ERK/IKK/NF‐κB pathway. Our study furthers the understanding of the mechanism of FEN‐induced hepatic injuries and may have implications in the prevention and control of liver diseases induced by environmental pesticides.—Qiu, L.‐L., Wang, C., Yao, S., Li, N., Hu, Y., Yu, Y., Xia, R., Zhu, J., Ji, M., Zhang, Z., Wang, S.‐L. Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway. FASEB J. 33, 2782–2795 (2019). http://www.fasebj.org

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Phosalone-induced inflammation and oxidative stress in the colon: evaluation and treatment

Abstract: This research highlights that EA is effective to alleviate the side effects of phosalone by reducing the level of oxidative stress and inflammatory proteins.

Cited by 18 publications

References 44 publications

A Pharmacological Update of Ellagic Acid

A Pharmacological Update of Ellagic Acid

Ellagic acid and cilostazol ameliorate amikacin-induced nephrotoxicity in rats by downregulating oxidative stress, inflammation, and apoptosis

Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway

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