Protective effect of Panax ginseng against N-acetyl-p-aminophenol-induced hepatotoxicity in rats

Uzkeser, Mustafa

doi:10.5897/ajpp12.658

Cited by 19 publications

(13 citation statements)

References 54 publications

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“…SV for 21 days and paracetamol in the last 4 days resulted in a significant increase in serum AST, ALT, ALP, and total bilirubin levels and significant decrease in serum albumin and total protein levels associated with significant increase in liver MDA, TNF‐α, Caspase‐3 and significant decreased liver SOD, GPx, and GSH. These results are in agreement with Knight et al., Uzkeser et al., Hassanin et al., Alantary et al., and Enogieru et al . who found that paracetamol resulted in elevation of liver enzymes and increased MDA level, lipid peroxidation, and elevation of TNF‐α.…”

Section: Discussionsupporting

confidence: 92%

Modulatory effects of some natural products on hepatotoxicity induced by combination of sodium valproate and paracetamol in rats

Zaky¹,

Gad

Nemr

et al. 2018

J Biochem & Molecular Tox

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Possible hepatoprotective effect of Curcuma longa and/or Nigella sativa against hepatotoxicity induced by coadministration of sodium valproate (SV) and paracetamol was studied. Rats were divided into 10 groups, control groups 1, 2, 3, and 4 received vehicles, C. longa (200 mg/kg, p.o.), N. sativa (250 mg/kg, p.o.), or both herbs for 21 days, respectively. Toxicity groups 5, 6, and 7 received SV (300 mg/kg, i.p.), paracetamol (1000 mg/kg, p.o.) for the last 4 days or both for 21 days, respectively. Protection groups 8, 9, and 10 received C. longa, N. sativa, or both, respectively, 1 h before the administration of both the drugs for 21 days. SV and/or paracetamol significantly increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, relative liver/body weight ratio, malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and caspase-3 (Casp-3) while significantly decreased albumin, total protein, glutathione (GSH) reduced, GSH peroxidase, and superoxide dismutase (SOD). Preadministration of C. longa and/or N. sativa caused protective effect against the hepatotoxicity induced by both drugs.

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Section: Discussionsupporting

confidence: 92%

Modulatory effects of some natural products on hepatotoxicity induced by combination of sodium valproate and paracetamol in rats

Zaky¹,

Gad

Nemr

et al. 2018

J Biochem & Molecular Tox

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“…Until now, although the exact mechanisms underlying APAP-induced hepatotoxicity remain unclear, growing evidence indicates that multiple mediators of inflammation and oxidative stress contribute to the pathology process of APAP-induced acute liver damage [6]. These inflammatory mediators include tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-10 (IL-10), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) [7].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rk1 ameliorates paracetamol-induced hepatotoxicity in mice through inhibition of inflammation, oxidative stress, nitrative stress and apoptosis

et al. 2019

Journal of Ginseng Research

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BackgroundFrequent overdose of paracetamol (APAP) has become the major cause of acute liver injury. The present study was designed to evaluate the potential protective effects of ginsenoside Rk1 on APAP-induced hepatotoxicity and investigate the underlying mechanisms for the first time.MethodsMice were treated with Rk1 (10 mg/kg or 20 mg/kg) by oral gavage once per d for 7 d. On the 7th d, all mice treated with 250 mg/kg APAP exhibited severe liver injury after 24 h, and hepatotoxicity was assessed.ResultsOur results showed that pretreatment with Rk1 significantly decreased the levels of serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor, and interleukin-1β compared with the APAP group. Meanwhile, hepatic antioxidants, including superoxide dismutase and glutathione, were elevated compared with the APAP group. In contrast, a significant decrease in levels of the lipid peroxidation product malondialdehyde was observed in the ginsenoside Rk1-treated group compared with the APAP group. These effects were associated with a significant increase of cytochrome P450 E1 and 4-hydroxynonenal levels in liver tissues. Moreover, ginsenoside Rk1 supplementation suppressed activation of apoptotic pathways by increasing Bcl-2 and decreasing Bax protein expression levels, which was shown using western blotting analysis. Histopathological observation also revealed that ginsenoside Rk1 pretreatment significantly reversed APAP-induced necrosis and inflammatory infiltration in liver tissues. Biological indicators of nitrative stress, such as 3-nitrotyrosine, were also inhibited after pretreatment with Rk1 compared with the APAP group.ConclusionThe results clearly suggest that the underlying molecular mechanisms in the hepatoprotection of ginsenoside Rk1 in APAP-induced hepatotoxicity may be due to its antioxidation, antiapoptosis, anti-inflammation, and antinitrative effects.

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“…Pretreatment with nobiletin decreased the levels of proinflammatory cytokines, such as TNF‐α, IL‐1β, and IL‐6, compared with the APAP group. TNF‐α is one of the major proinflammatory cytokines that mediate acute phase responses causing various liver and kidney toxicities, such as APAP . Among the types of inflammatory damage affecting visceral organs, IL‐1β is one of the earliest proinflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Nobiletin attenuates acetaminophen‐induced hepatorenal toxicity in rats

Güvenç

Cellat

Gökçek

et al. 2019

J Biochem & Molecular Tox

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The study aimed to examine the effects of nobiletin on the toxicity model induced with acetaminophen (APAP). For this purpose, 24 adult male rats were equally divided into four groups. The groups were the control group (group 1); dimethyl sulfoxide only, the APAP group (group 2) received a single dose of APAP 1000 mg/kg on the 10th day of experiment; the Nobiletin group (group 3), nobiletin (10 mg/kg) for 10 days; and the APAP + Nobiletin group (group 4), nobiletin (10 mg/kg) for 10 days with a single dose of APAP (1000 mg/kg) administered on the 10th day and the experiment ended after 48 hours. At the end of the study, a significant increase in malondialdehyde, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels and a significant decrease in glutathione levels, glutathione peroxidase activities and nuclear factor erythroid-derived 2-like 2 (Nrf-2) and heme oxygenase-1 (HO-1) expressions were observed with APAP application in liver and kidney tissues. Serum aspartate transaminase (AST), alanine transaminase (ALT), urea, and creatinine levels were also significantly increased in the APAP group. However, nobiletin treatment in group 4 reversed oxidative stress and inflammatory and histopathological signs caused by APAP. It is concluded that nobiletin may be a beneficial substance that confers hepatorenal protection to APAP-induced toxicity via antioxidant and anti-inflammatory mechanisms. K E Y W O R D Sacetaminophen, nobiletin, Nrf-2/HO-1, oxidative stress

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Protective effect of Panax ginseng against N-acetyl-p-aminophenol-induced hepatotoxicity in rats

Cited by 19 publications

References 54 publications

Modulatory effects of some natural products on hepatotoxicity induced by combination of sodium valproate and paracetamol in rats

Modulatory effects of some natural products on hepatotoxicity induced by combination of sodium valproate and paracetamol in rats

Ginsenoside Rk1 ameliorates paracetamol-induced hepatotoxicity in mice through inhibition of inflammation, oxidative stress, nitrative stress and apoptosis

Nobiletin attenuates acetaminophen‐induced hepatorenal toxicity in rats

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