Kampo formula “Hochu-ekki-to” suppressed carbon tetrachloride-induced hepatotoxicity in mice

Yoshioka, Hiroki; Fukaya, Shiori; Onosaka, Satomi; Nonogaki, Tsunemasa; Nagatsu, Akito

doi:10.1007/s12199-016-0571-x

Cited by 7 publications

(5 citation statements)

References 30 publications

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“…Our previous investigation found that Sasa veitchii leaf extract (SE) prevented carbon tetrachloride (CCl 4 )-induced hepatotoxicity in mice [ 12 ], suggesting that SE might maintain liver homeostasis. Although CCl 4 is commonly used in animal models to study chemical toxin-induced liver injury [ 13 , 14 ], exposure to CCl 4 does not reflect a real-life scenario. The most common etiologies of liver damage in real life are acute viral hepatitis A and B, drug-related liver injury, and the alcohol-acetaminophen syndrome (AAS).…”

Section: Introductionmentioning

confidence: 99%

Sasa veitchii extracts suppress acetaminophen-induced hepatotoxicity in mice

Yoshioka

Usuda

Fujii

et al. 2017

Environ Health Prev Med

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Background: The aim of this study was to investigate the therapeutic effects of a Sasa veitchii leaf extract (SE) on acetaminophen (APAP)-induced hepatotoxicity. Methods: Seven-week-old male ddY mice were orally administered SE or saline (0.2 mL) once a day for a week. Twenty-four hours after the last pretreatment, the mice were intraperitoneally injected with 550 mg/kg APAP or saline under fasting conditions. The mice from each group were euthanized and bled for plasma analysis 2, 6, 24, and 72 h after the injection.

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Section: Introductionmentioning

confidence: 99%

Sasa veitchii extracts suppress acetaminophen-induced hepatotoxicity in mice

Yoshioka

Usuda

Fujii

et al. 2017

Environ Health Prev Med

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“…Few of the authors have also used it as an acetaminophen overdose antidote examined on the mice. The induction of hepatotoxicity was made through acetaminophen single dose (750 mg / kg) (15) . Numerous treatments such as normal saline, zinc sulphate 15 or 30 mg/kg, 150 mg/kg / V-acetyl cysteine, zinc sulphate, 15 mg / kg zinc sulphate + 150 mg / kg A/-acetyl cysteine) were also administrated at the interval of one hour after the administration of overdose of acetaminophen (16) .…”

Section: Discussionmentioning

confidence: 99%

An Observationa Study on the Role of Zinc Sulphate in Paracetamol Toxicity

Afzal,

Tariq,

Ahmad

et al. 2023

PJMHS

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Aim: The aim of this study was to determine the role of Zinc Sulphate as an agent of hepatoprotective in the acetaminophen-induced changes of histopathological nature in the model of animals. Methodology: The design of this study was observational study design. This study was conducted at Allied Hospital Faisalabad and the duration of this study was from April 2022 to July 2022. Our research sample was 90 albino rats with the range of weight from 18 – 32 grams and we made three groups each group consisting of thirty albino rats. Control group was A group and normal saline level was maintained in this group as 0.9%; acetaminophen was given (250 mg / kg) in B group through a single dose; Zinc Sulphate (1 – 5 mg / kg) was given to C group for a duration of 1 – 7 days before the acetaminophen (250 mg / kg) Sigle dose. After the six hours’ duration was conducted biochemical studies after giving acetaminophen to albino rats. At last step of the treatment weight of all animals was checked at than sacrificed. Histopathological and gross examination was carried out for liver and statistical evaluation of the data was carried out through Chi-Square test. Results: Demonstration of the zinc’s protective effect was made through serum concentration reduction level of the enzymes of liver such as aspartate aminotransferase, lactate dehydrogenase, alanine aminotransferase and serum sorbitol dehydrogenase, including the histopathological centrilobular congestion changes, necrosis and hepatocellular degeneration. We observed through the histopathological evaluation that typical changes in pathological environment of centri-zonal necrosis, leukocyte infiltration, steatosis, edema in animals and portal tiraditos those were treated only with acetaminophen. Animal pretreatment through zinc sulphate lead the whole procedure to dependent on the dose for the avoidance of various changes. Practical Implication: In the practical implication of this study the determination of the Zinc Sulphate role as an agent of hepatoprotective in the acetaminophen-induced changes of histopathological nature in the model of animals. Conclusion: It is concluded that Zinc is responsible for the production of hepato-protective effect with the prevention of ultrastructural hepatic tissue injuries and also causes free amino acid metabolism disturbance which is a result of the acetaminophen toxic dose. Keywords: Acetaminophen, Zinc, Liver Toxicity And Hepato-Protective Effect.

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“…Plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured using the Transaminase CII Test (Fujifilm Wako Pure Chemical) according to the manufacturer's instructions and our pre-vious studies [22][23][24]. Calibration curves were prepared using standard solutions for relative quantification.…”

Section: Plasma Biochemical Analysismentioning

confidence: 99%

Copper-induced diurnal hepatic toxicity is associated with <i>Cry2</i> and <i>Per1</i> in mice

Tominaga,

Yoshioka,

Yokota

et al. 2023

Environ Health Prev Med

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Background: This study aimed to investigate diurnal variations in copper-induced hepatic toxicity and the molecular mechanisms underlying this chronotoxicity. Methods: Male C57BL/6J mice were intraperitoneally injected with copper chloride (CuCl 2 ) at zeitgeber time 2 (ZT2) or 14 (ZT14), twice per week for 5 or 8 weeks. Seventy-two hours after the final CuCl 2 injection, the mice were euthanized, and plasma samples were collected. The livers and kidneys were collected and weighed. In vitro experiments were performed to assess cell viability and fluctuations in clock gene expression levels in Hepa1-6 cells after CuCl 2 treatment. We examined copper homeostasis-and apoptosisrelated genes under clock genes overexpression. Results: Repeated CuCl 2 administration for 8 weeks resulted in more severe toxicity at ZT14 compared to ZT2. CuCl 2 administration at ZT14 elevated plasma aspartate aminotransferase, hepatic tumor necrosis factor-¡, and interleukin-6 for 5 weeks, whereas the toxic effects of CuCl 2 administration at ZT2 were weaker. Moreover, CuCl 2 treatment inhibited Hepa1-6 cell viability in a dose-dependent manner. We observed increased expression of three clock genes (Ciart, Cry2, and Per1) after CuCl 2 treatment. Among them, overexpression of Cry2 and Per1 accelerated CuCl 2 -induced inhibition of Hepa1-6 cell viability. Moreover, we found that the overexpression of Cry2 and Per1 regulates cleaved caspase-3 by modulating the copper transporter genes ATP7B and CTR1. Conclusion: These results suggest that CuCl 2 -induced diurnal toxicity is associated with Cry2 and Per1 expression through the regulation of copper transporter genes in mice.

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Kampo formula “Hochu-ekki-to” suppressed carbon tetrachloride-induced hepatotoxicity in mice

Cited by 7 publications

References 30 publications

Sasa veitchii extracts suppress acetaminophen-induced hepatotoxicity in mice

Sasa veitchii extracts suppress acetaminophen-induced hepatotoxicity in mice

An Observationa Study on the Role of Zinc Sulphate in Paracetamol Toxicity

Copper-induced diurnal hepatic toxicity is associated with <i>Cry2</i> and <i>Per1</i> in mice

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