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Relevant bibliographies by topics / CCl4-induced hepatic injury

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Journal articles

Academic literature on the topic 'CCl4-induced hepatic injury'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "CCl4-induced hepatic injury"

1

Cui, Ming-Xia, Jun-Feng Jiang, Guang-Ning Min, Wei Han, and Yong-Jie Wu. "Ciliary neurotrophic factor analogue aggravates CCl4-induced acute hepatic injury in rats." Canadian Journal of Physiology and Pharmacology 95, no. 5 (2017): 620–23. http://dx.doi.org/10.1139/cjpp-2016-0564.

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Ciliary neurotrophic factor (CNTF) and CNTF analogs were reported to have hepatoprotective effect and ameliorate hepatic steatosis in db/db or high-fat-diet-fed mice. Because hepatic steatosis and injury are also commonly induced by hepatotoxin, the aim of the present study is to clarify whether CNTF could alleviate hepatic steatosis and injury induced by carbon tetrachloride (CCl4). Unexpectedly, when combined with CCl4, CNTF aggravated hepatic steatosis and liver injury. The mechanism is associated with effects of CNTF that inhibited lipoprotein secretion and drastically impaired the ability

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2

Nakade, Yukiomi, Masashi Yoneda, Kimihide Nakamura, Isao Makino, and Akira Terano. "Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 6 (2002): R1782—R1788. http://dx.doi.org/10.1152/ajpregu.00514.2001.

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Central neuropeptides play important roles in many physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Central injection of corticotropin-releasing factor (CRF) aggravates carbon tetrachloride (CCl4)-induced acute liver injury through the sympathetic nervous pathway in rats. However, still nothing is known about a role of endogenous neuropeptides in the brain in hepatic pathophysiological regulations.

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3

Xiong, Rui, Shuzhong Shan, Xiaoming Wang, et al. "Aloperine attenuates carbon tetrachloride-induced mouse hepatic injury via Nrf2/HO-1 pathway." Tropical Journal of Pharmaceutical Research 19, no. 5 (2020): 983–88. http://dx.doi.org/10.4314/tjpr.v19i5.11.

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Purpose: To investigate whether aloperine pretreatment ameliorates acute liver injury in carbon tetrachloride (CCl4)-treated mice.Methods: Mice were injected with CCl4 and orally administered aloperine. Blood samples and liver tissues were used for histopathological and biochemical analyses, respectively. Protein expression levels were determined by western blotting.Results: Histopathological analysis indicate that aloperine pretreatment significantly alleviated CCl4- induced mouse hepatic injury. CCl4 treatment induced the upregulation of aspartate aminotransferase (AST), alkaline phosphatase

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4

Yokohama, Shiro, Masashi Yoneda, Kimihide Nakamura, and Isao Makino. "Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (1999): G622—G628. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g622.

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Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of

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5

Dorsaf, Hallegue, Moujahed Sabrine, Ben Lamine Houda, Ben Rhouma Khémais, Sakly Mohsen, and Tebourbi Olfa. "Pecan pericarp extract protects against carbon tetrachloride-induced liver injury through oxidative mechanism in rats." Toxicology Research 9, no. 5 (2020): 652–60. http://dx.doi.org/10.1093/toxres/tfaa071.

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Abstract The purpose of this study was to quantify the proanthocyanidin content of pecan (Carya illinoinensis) pericarp extract (PPE) and to assess its useful impacts against carbon tetrachloride (CCl4)-induced hepatotoxicity. Rats were randomly divided into four groups: Group 1: received intraperitoneal injection of saline solution, Group 2: was injected with PPE (25 mg/kg body weight) for 10 consecutive days, Group 3: received CCl4 (0.5 ml/kg, subcutaneous injection), Group 4: was coadministred with PPE + CCl4. The CCl4 was administered every 3 days during 10 days. Results revealed the prese

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6

Hsieh, Po-Chow, Yu-Ling Ho, Guan-Jhong Huang, et al. "Hepatoprotective Effect of the Aqueous Extract of Flemingia macrophylla on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats Through Anti-Oxidative Activities." American Journal of Chinese Medicine 39, no. 02 (2011): 349–65. http://dx.doi.org/10.1142/s0192415x11008877.

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This study investigated the protective effect of the aqueous extract of Flemingia macrophylla (AFM) against hepatic injury induced by CCl4. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected as biomarkers in the blood to indicate hepatic injury. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and reduced glutathione (GSH) contents were evaluated for oxidative stress in hepatic injury. Moreover, histopathological observation was assayed for the degree of hepatic injury. After oral administration of

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7

Mori, Mutsuki, Takeshi Izawa, Yohei Inai, et al. "Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats." Nutrients 12, no. 9 (2020): 2784. http://dx.doi.org/10.3390/nu12092784.

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Hepatic iron overload is well known as an important risk factor for progression of liver diseases; however, it is unknown whether it can alter the susceptibility to drug-induced hepatotoxicity. Here we investigate the pathological roles of iron overload in two single-dose models of chemically-induced liver injury. Rats were fed a high-iron (Fe) or standard diet (Cont) for four weeks and were then administered with allyl alcohol (AA) or carbon tetrachloride (CCl4). Twenty-four hours after administration mild mononuclear cell infiltration was seen in the periportal/portal area (Zone 1) in Cont-A

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8

Berlanga, J., M. E. Caballero, D. Ramirez, et al. "Rapid Communication: Epidermal Growth Factor Protects against Carbon Tetrachloride-Induced Hepatic Injury." Clinical Science 94, no. 3 (1998): 219–23. http://dx.doi.org/10.1042/cs0940219.

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1. Epidermal growth factor (EGF) is known to protect the gastrointestinal tract against various noxious agents. Its potential value in preventing/treating hepatic injury is, however, largely unexplored. We therefore examined whether EGF could influence CCl4-induced hepatic injury. 2. Female Sprague—Dawley rats (8 per group) received saline or recombinant EGF (500 or 750 μg/kg, intraperitoneal) 30 min before CCU (20% v/v, in olive oil, intraperitoneal). Eighteen hours later, animals were killed, serum was collected for assay of biochemical markers of hepatic injury and livers were removed for h

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9

Lai, Tung-Yuan, Yueh-Wern Wu, Jaung-Geng Lin та Wen-Chuan Lin. "Effect of Pretreatment of Rats with an Urinary Preparation on Liver Injuries Induced by Carbon Tetrachloride and α-Naphthylisothiocyanate". American Journal of Chinese Medicine 26, № 03n04 (1998): 343–51. http://dx.doi.org/10.1142/s0192415x98000385.

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The effect of oral administration of a preparation of human urine (PHU) on the progression of acute liver injury was examined in rats intoxicated with carbon tetrachloride (CCl4) and α-naphthylisothiocyanate (ANIT). PHU protected the liver from CCl4-induced injury as judged by morphological and biochemical observations. In contrast, PHU aggravated ANIT-induced injury as judged also by morphological and biochemical observation. PHU prevented the increase in hepatic glutathione (GSH) and lipid peroxidation induced by CCl4. But PHU enhanced the increase in hepatic GSH caused by ANIT. These result

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10

Jeong, Tae Bin, Doyoung Kwon, Seung Won Son, et al. "Weaning Mice and Adult Mice Exhibit Differential Carbon Tetrachloride-Induced Acute Hepatotoxicity." Antioxidants 9, no. 3 (2020): 201. http://dx.doi.org/10.3390/antiox9030201.

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Age is a risk factor for drug-induced liver injury (DILI). However, there is a limited understanding of pediatric DILI. Here, 2-week-old weaning and 8-week-old adult male ICR mice were intraperitoneally injected with CCl4 (0.1 mmol/kg equal to 15.4 mg/kg) to comparatively evaluate the time-dependent liver damage and cellular events. CCl4 significantly enhanced the serum alanine aminotransferase/aspartate aminotransferase levels and hepatic centrilobular necrosis in the weaning mice, whereas it induced mild liver injury in the adult mice. CCl4-treated weaning mice exhibited higher hepatic level

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