Ellagic acid impedes carbontetrachloride-induced liver damage in rats through suppression of NF-kB, Bcl-2 and regulating Nrf-2 and caspase pathway

Aslan, Abdullah Nabi; Gök, Özlem; Erman, Orhan; Kuloğlu, Tuncay

doi:10.1016/j.biopha.2018.06.020

Cited by 55 publications

(34 citation statements)

References 40 publications

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“…36 Studies have demonstrated NF-κB inhibition promotes HSC-T6 cell death via Bcl-2 suppression. 37,38 Our finding were consistent with those of Jeong and colleagues who showed that Agn inhibits NF-κB. 39 We further showed that Agn inhibits p65 and IκBα phosphorylation.…”

Section: Discussionsupporting

confidence: 89%

<p>Alginate Suppresses Liver Fibrosis Through the Inhibition of Nuclear Factor-κB Signaling</p>

Xia¹,

Ding²,

Zheng³

et al. 2020

DDDT

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Purpose: Liver fibrosis (or liver scarring) is a causative factor for hepatitis, cirrhosis and hepatocellular carcinoma (HCC). Alginate (Agn) isolated from brown algae is known to slow the proliferation of fibroblasts, through the mechanisms of these effects remain undefined. This study explored the benefits of Agn on hepatic health and its associated mechanism(s) of action in hepatic stellate cells (HSC-T6s). Materials and Methods: To assess the effects of Agn, HSC-T6s were treated with PDGF and cell proliferation, colony formation, cell migration, cell invasiveness and apoptosis were assessed. Rat models of liver fibrosis were produced through 12-week injections of intraperitoneal (IP) carbon tetrachloride (CCl 4 ). Rats were Agn-treated from weeks 8 to 12, and liver damage was assessed through Masson's and H Materials and Methods: & E staining. Gene expression profiles were assayed via RT-PCR, Western blot and commercial ELISA kits. Results: Agn reduced the proliferation of HSC-T6s and increased apoptotic rates through the downregulation of the Bcl-2:Bax ratio. Agn also inhibited the invasion and migration of HSC-T6s, prevented ECM deposition, and reduced the occurrence of liver fibrosis in rat models. Agn also prevented IκBα and p65 phosphorylation. Conclusion: Agn prevents liver fibrosis through its attenuation of HSC activation and division through the suppression of NF-κB in in vitro and animal models. This highlights how the clinical use of Agn can prevent hepatic fibrosis.

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Section: Discussionsupporting

confidence: 89%

<p>Alginate Suppresses Liver Fibrosis Through the Inhibition of Nuclear Factor-κB Signaling</p>

Xia¹,

Ding²,

Zheng³

et al. 2020

DDDT

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“…This increase could be attributed to the inductive role of CP on apoptosis in liver (40). On the other hand, EA at the concentration of both 50 mg/kg and 75 mg/kg were able to reduce caspase-3 reactivity significantly due to its antiapoptotic effects (41) in line with the previous studies (37,41,42). CP treatment causes significant elevations of liver enzymes such as ALT and AST in blood of rats (8).…”

Section: Discussionsupporting

confidence: 86%

Kemoterapi Kaynaklı Hepatotoksisiteye Karşı Ellajik Asitin Koruyucu Etkileri

Yalcin

Keleş

Kahraman

et al. 2020

Düzce Tıp Fakültesi Dergisi

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Aim: Cyclophosphamide (CP) is a commonly used chemotherapeutic agent despite its toxic adverse effects, including hepatotoxicity. Ellagic acid (EA) is an antioxidant agent and exhibits free radical scavenging activities. In this experimental study, the effects of EA on CP-induced liver injury were investigated. Material and Methods: Twenty-four Sprague-Dawley rats (180-220 gr) were separated into four equal groups. A single dose of 150 mg/kg CP was given intraperitoneally to generate hepatotoxicity. Different doses (50 and 75 mg/kg) of EA were administered orally 20 minutes before, 4 and 8 hours after CP administration. The histopathological evaluation of kidney tissues and immunohistochemical evaluation for caspase-3 were conducted as well as the serum biochemical analyses. Results: CP treated group exhibited a significant increase in serum hepatic enzymes, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), compared to the control group. Similarly, the total triglycerides (TG) and very-low-density lipoprotein cholesterol (VLDL-C) levels increased significantly. Additionally, the high-density lipoprotein cholesterol (HDL-C) levels decreased, which was not significant, compared to the control group. At both EA doses, VLDL-C, AST, ALT levels decreased significantly while HDL-C level revealed a significant increase. 75 mg/kg EA treatment caused a non-significant elevation in total cholesterol (TC) concentration. Microscopic analysis showed a significant congestion, edema, degeneration and necrosis in the livers of CP administered group. However, edema, degeneration, and necrosis were significantly reduced in animals treated with EA-75. In addition, caspase-3 expression significantly decreased in EA-75 group. Conclusion: These results indicate the protective effects of EA in CP-induced hepatotoxicity in rats.

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“…The cut tissue samples were centrifuged at 15,000 rpm for 45 min. The supernatant was collected and stored at −80°C until usage (Aslan et al, 2018).…”

Section: Methodsmentioning

confidence: 99%

“…Proteins. The increasing or decreasing of the expression of these proteins gives information about the development of the apoptotic process due to damage of the cells (Aslan, Gok, Erman, & Kuloglu, 2018).…”

Section: Introductionmentioning

confidence: 99%

The preventive effect of ellagic acid on brain damage in rats via regulating of Nrf‐2, NF‐kB and apoptotic pathway

et al. 2020

Self Cite

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The aim of this study was to investigate the neuroprotective role of ellagic acid (EA) on CCl4‐induced brain injury in rats. In this study, the rats were divided into four groups. Groups: (1) Control group; (2) EA group; (3) CCl4 group; (4) EA + CCl4 group. In brain tissue, tumor necrosis factor‐α (TNF‐α), nuclear factor kappa b (NF‐kB), cyclooxygenase‐2 (COX‐2), nuclear erythroid related factor 2 (Nrf‐2), cysteine‐aspartic acid protease (caspase‐3), VEGF (vascular endothelial growth factor) and B‐cell lymphoma‐2 (bcl‐2) protein expression levels were analyzed by western blotting. MDA (malondialdehyde), catalase enzyme activity (CAT) and glutathione (GSH) analysis were determined by spectrophotometer. In our findings, EA ameliorated Nrf‐2 and caspase‐3 protein expression levels, GSH and catalase activities, NF‐kB, TNF‐α, VEGF, Bcl‐2, COX‐2 protein expression levels and MDA levels in CCl4 intoxicated rats. These results suggest that EA demonstrated the neuroprotective effect on CCl4‐induced brain damage in rats. Practical applications Ellagic acid has different biological activities, these are; antioxidant, anti‐inflammatory, antidepressant, antifibrosis, anticancer, neuroprotective and hepatoprotective. For example it was reported that EA protects the cells against DNA injury induced by free radicals and it can prevent the traumatic brain injury. These results obtained from this study reveals that EA has a protective effect against rat brain damage and it may be used as an alternative drugs for the brain injury treatment in future.

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Ellagic acid impedes carbontetrachloride-induced liver damage in rats through suppression of NF-kB, Bcl-2 and regulating Nrf-2 and caspase pathway

Cited by 55 publications

References 40 publications

<p>Alginate Suppresses Liver Fibrosis Through the Inhibition of Nuclear Factor-κB Signaling</p>

<p>Alginate Suppresses Liver Fibrosis Through the Inhibition of Nuclear Factor-κB Signaling</p>

Kemoterapi Kaynaklı Hepatotoksisiteye Karşı Ellajik Asitin Koruyucu Etkileri

The preventive effect of ellagic acid on brain damage in rats via regulating of Nrf‐2, NF‐kB and apoptotic pathway

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