Ginkgo biloba attenuated hepatotoxicity induced by combined exposure to cadmium and fluoride via modulating the redox imbalance, Bax/Bcl-2 and NF-kB signaling pathways in male rats

Arab-Nozari, Milad; Ahangar, Nematollah; Mohammadi, Ebrahim; Lorigooini, Zahra; Shokrzadeh, Mohammad; Amiri, Fereshteh Talebpour; Shaki, Fatemeh

doi:10.1007/s11033-020-05755-2

Cited by 12 publications

(7 citation statements)

References 42 publications

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“…By activating in response to pro-inflammatory stimuli such as oxidative stress and cytokines, NF-kB triggers the expression of pro-inflammatory genes and the creation of pro-inflammatory cytokines, resulting in inflammation and fibrosis of the liver . NF-kB is a transcription factor that can regulate both pro- and anti-apoptotic genes, thereby controlling liver apoptosis as well . Europinidin can diminish the appearance of pro-inflammatory genes and the generation of pro-inflammatory cytokines by declining NF-kB initiation.…”

Section: Discussionmentioning

confidence: 99%

Effect of Europinidin against Alcohol-Induced Liver Damage in Rats by Inhibiting the TNF-α/TGF-β/IFN-γ/NF-kB/Caspase-3 Signaling Pathway

et al. 2023

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Background: The effect of europinidin on alcoholic liver damage in rats was examined in this research. Methods: A total of 24 Wistar rats were grouped in the same way into four groups: normal control (normal), ethanol control (EtOH), europinidin low dose (10 mg/kg), and europinidin higher dose (20 mg/kg). The test group rats were orally treated with europinidin-10 and europinidin-20 for 4 weeks, whereas 5 mL/kg distilled water was administered to control rats. In addition, 1 h after the last dose of the above-mentioned oral treatment, 5 mL/kg (i.p.) EtOH was injected to induce liver injury. After 5 h of EtOH treatment, samples of blood were withdrawn for biochemical estimations. Results: Administration of europinidin at both doses restored all of the estimated serum, i.e., liver function tests (ALT, AST, ALP), biochemical test (Creatinine, albumin, BUN, direct bilirubin, and LDH), lipid assessment (TC and TG), endogenous antioxidants (GSH-Px, SOD, and CAT), malondialdehyde (MDA), nitric oxide (NO), cytokines (TGF-β, TNF-α, IL-1β, IL-6, IFN-γ, and IL-12), caspase-3, and nuclear factor kappa B (NF-κB) associated with the EtOH group. Conclusion: The results of the investigation showed that europinidin had favorable effects in rats given EtOH and may have hepatoprotective potential property.

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Section: Discussionmentioning

confidence: 99%

Effect of Europinidin against Alcohol-Induced Liver Damage in Rats by Inhibiting the TNF-α/TGF-β/IFN-γ/NF-kB/Caspase-3 Signaling Pathway

et al. 2023

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“…Moreover, damaged mitochondria induced a slight increase in NF-κB activation, evidenced by the increased translocation to the nucleus of p65, which was boosted in response to the exposure to the inflammatory cytokine TNFα, as well as to the combination of PQ and TNFα. Other studies have obtained similar results, reporting enhanced activation of NF-κB under conditions of mitochondrial impairment [ 15 , 56 , 57 ], but it would be interesting to consider other inflammatory cascades that are further related to mitochondrial damage, such as RIPK, MAPK, ERK, JNK, or JAK-STAT signaling, which could affect this pathway. It is worth noting that IL-8 stimulates the expression of key mediators of angiogenesis, such as VEGF and the autocrine activation of VEGFR2 in endothelial cells by activating NF-κB [ 58 ].…”

Section: Discussionmentioning

confidence: 69%

Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent

et al. 2022

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Recent studies have related mitochondrial impairment with peritoneal membrane damage during peritoneal dialysis (PD) therapy. Here, we assessed the involvement of mitochondrial dysfunction in the inflammatory response in human mesothelial cells, a hallmark in the pathogenesis of PD-related peritoneal membrane damage. Our ex vivo studies showed that IL-1β causes a drop in the mitochondrial membrane potential in cells from peritoneal effluent. Moreover, when mitochondrial damage was induced by inhibitors of mitochondrial function, a low-grade inflammatory response was generated. Interestingly, mitochondrial damage sensitized mesothelial cells, causing a significant increase in the inflammatory response induced by cytokines, in which ROS generation and NF-κB activation appear to be involved, since inflammation was counteracted by both mitoTEMPO (mitochondrial ROS scavenger) and BAY-117085 (NF-κB inhibitor). Furthermore, the natural anti-inflammatory antioxidant resveratrol significantly attenuated the inflammatory response, by reversing the decline in mitochondrial membrane potential and decreasing the expression of IL-8, COX-2 and PGE2 caused by IL-1β. These findings suggest that IL-1β regulates mitochondrial function in mesothelial cells and that mitochondrial dysfunction could induce an inflammatory scenario that sensitizes these cells, causing significant amplification of the inflammatory response induced by cytokines. Resveratrol may represent a promising strategy in controlling the mesothelial inflammatory response to PD.

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“…Cadmium can cause glomerular dysfunction and nephropathy, leading to proteinuria, glycosuria, enzyme urea, and phosphaturia [23]. Cadmium toxicity occurs through indirect induction of ROS production in mitochondria and affects the expression of mitochondrial genes and impaired cellular respiratory activity [9,24,25].…”

Section: Discussionmentioning

confidence: 99%

“…Then, the tube was centrifuged to separate. The fluorescence intensity of rhodamine was monitored using Shimadzu RF-5000U fluorescence spectrophotometer at the excitation and emission wavelengths of 490 and 535 nm [9].…”

Section: Assessment Of the Mitochondrial Membrane Potentialmentioning

confidence: 99%

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L-arginine Ameliorated Mitochondrial Oxidative Damage Induced by Sub-chronic Exposure to Cadmium in Mice Kidney

Shaki¹,

Teymoori²,

Motafeghi³

et al. 2021

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Background:Cadmium is a heavy metal that can cause various injuries in the body, including nephrotoxicity. L-Arginine is a metal chelator that can prevent oxidative damage caused by oxygen free radicals. Objectives:This study aimed to investigate the effect of L-arginine in inhibiting mitochondrial toxicity induced by subchronic cadmium exposure in the kidney of male mice. Methods: A total of 42 male mice were randomly divided into six groups (n=6): control (normal saline), cadmium (2 mg/kg), cadmium (2 mg/kg) plus three doses of L-arginine (50, 100, and 200 mg/kg) and finally cadmium (2 mg/kg) plus vitamin C (500 mg/kg). After 42 days, the animals were anesthetized with ketamine/xylazine. Their kidney tissues were removed, and mitochondrial fractions were isolated. Oxidative stress factors and mitochondrial damage parameters (MTT, swelling, and mitochondrial membrane potential) were measured in renal isolated mitochondria. Also, evaluation of Blood Urea Nitrogen (BUN) and Creatinine (Cr) tests were done. Results: Significant rise in BUN and Cr were observed in cadmium-treated mice (P<0.05). Cadmium enhanced oxidative stress in the kidney via increasing lipid peroxidation and oxidation of protein and glutathione. It caused significant mitochondrial dysfunction, mitochondrial membrane potential collapse, and swelling in isolated mitochondria (P<0.05). L-Arginine significantly ameliorated cadmium-induced oxidative stress and mitochondrial damage (P<0.05). Furthermore, a significant reduction in serum BUN and Cr were observed in L-arginine received group (P<0.05). Conclusion: The results showed that L-arginine has significant protective effects against cadmium-induced renal toxicity in male mice.

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Ginkgo biloba attenuated hepatotoxicity induced by combined exposure to cadmium and fluoride via modulating the redox imbalance, Bax/Bcl-2 and NF-kB signaling pathways in male rats

Cited by 12 publications

References 42 publications

Effect of Europinidin against Alcohol-Induced Liver Damage in Rats by Inhibiting the TNF-α/TGF-β/IFN-γ/NF-kB/Caspase-3 Signaling Pathway

Effect of Europinidin against Alcohol-Induced Liver Damage in Rats by Inhibiting the TNF-α/TGF-β/IFN-γ/NF-kB/Caspase-3 Signaling Pathway

Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent

L-arginine Ameliorated Mitochondrial Oxidative Damage Induced by Sub-chronic Exposure to Cadmium in Mice Kidney

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