The effect of different doses of flumazenil on acetaminophen toxicity in rats

Bozogluer, E; Madenoğlu, Halit; Aksu, Recep; Biçer, Cihangir; Yazıcı, Cevat; Boyacı, Adem

doi:10.4149/bll_2012_118

Cited by 2 publications

(1 citation statement)

References 16 publications

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“…Elevated serum levels of ALT and AST are indicative of the loss of functional integrity of hepatic cell membranes, and consequential release of the latter enzymes into the circulation after hepatocellular damage. These results come in line with previous studies (15,16), and (17).…”

Section: Discussionsupporting

confidence: 94%

Potential benefits of using hydrogen sulfide, vitamin E and necrostatin-1 to counteract acetaminophen‑induced hepatotoxicity in rats

Saleh¹,

Saad²,

Elbassuoni³

et al. 2021

BLL

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BACKGROUND: The use of acetaminophen (APAP) is increasing recently, especially with COVID-19 outbreaks. APAP is safe at therapeutic levels, however, an overdose can cause severe liver injury. This study aims to explore possible mechanisms involved in APAP-induced hepatotoxicity and compare different hepatoprotective agents, namely vitamin E, hydrogen sulfi de (H 2 S) and necrostatin-1 (NEC-1). METHODS: Adult male albino rats were divided into groups: Control group, APAP-induced hepatotoxicity group, Vitamin E-treated group, H 2 S-treated group and NEC-1-treated group. Serum levels for aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin-33 (IL-33), tumor necrosis factor alpha (TNF-α), reduced glutathione (GSH) and lipid profi le were measured. Histopathological examinations of liver tissue with H&E stain and immunohistochemistry for activated caspase-3 were also done. RESULTS: APAP-treated group showed elevated liver transaminases, hyperlipidemia, and defi cient liver anti-oxidative response together with disturbed hepatic architecture and increased immune-expression of activated caspase-3 in hepatic tissue. Pretreatment with vitamin E, H 2 S or NEC-1 reversed the affected parameters. Vitamin E and H 2 S showed greater improvement when compared to NEC-1. CONCLUSION: Vitamin E, H 2 S and NEC-1 showed protective effects against APAP-induced hepatotoxicity, thus they may be used as an adjuvant therapy when APAP is indicated for long periods as is the case in Fig. 2, Ref. 45).

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Section: Discussionsupporting

confidence: 94%

Potential benefits of using hydrogen sulfide, vitamin E and necrostatin-1 to counteract acetaminophen‑induced hepatotoxicity in rats

Saleh¹,

Saad²,

Elbassuoni³

et al. 2021

BLL

View full text Add to dashboard Cite

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Expression Levels of GABA-A Receptor Subunit Alpha 3, Gabra3 and Lipoprotein Lipase, Lpl Are Associated with the Susceptibility to Acetaminophen-Induced Hepatotoxicity

Kim

Yun

Shin

et al. 2016

Biomol Ther (Seoul)

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Drug-induced liver injury (DILI) is the serious and fatal drug-associated adverse effect, but its incidence is very low and individual variation in severity is substantial. Acetaminophen (APAP)-induced liver injury accounts for >50% of reported DILI cases but little is known for the cause of individual variations in the severity. Intrinsic genetic variation is considered a key element but the identity of the genes was not well-established. Here, pre-biopsy method and microarray technique was applied to uncover the key genes for APAP-induced liver injury in mice, and a cause and effect experiment employing quantitative real-time PCR was conducted to confirm the correlation between the uncovered genes and APAP-induced hepatotoxicity. We identified the innately and differentially expressed genes of mice susceptible to APAP-induced hepatotoxicity in the pre-biopsied liver tissue before APAP treatment through microarray analysis of the global gene expression profiles (Affymetrix GeneChip® Mouse Gene 1.0 ST for 28,853 genes). Expression of 16 genes including Gdap10, Lpl, Gabra3 and Ccrn4l were significantly different (t-test: FDR <10%) more than 1.5 fold in the susceptible animals than resistant. To confirm the association with the susceptibility to APAP-induced hepatotoxicity, another set of animals were measured for the expression level of selected 4 genes (higher two and lower two genes) in the liver pre-biopsy and their sensitivity to APAP-induced hepatotoxicity was evaluated by post hoc. Notably, the expressions of Gabra3 and Lpl were significantly correlated with the severity of liver injury (p<0.05) demonstrating that these genes may be linked to the susceptibility to APAP-induced hepatotoxicity.

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The effect of different doses of flumazenil on acetaminophen toxicity in rats

Cited by 2 publications

References 16 publications

Potential benefits of using hydrogen sulfide, vitamin E and necrostatin-1 to counteract acetaminophen‑induced hepatotoxicity in rats

Potential benefits of using hydrogen sulfide, vitamin E and necrostatin-1 to counteract acetaminophen‑induced hepatotoxicity in rats

Expression Levels of GABA-A Receptor Subunit Alpha 3, Gabra3 and Lipoprotein Lipase, Lpl Are Associated with the Susceptibility to Acetaminophen-Induced Hepatotoxicity

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