scholarly journals CCl4 INDUCED LIVER INJURY;

2018 ◽  
Vol 24 (05) ◽  
pp. 739-744
Author(s):  
Sana Naz ◽  
Faisal Irshad ◽  
Hina Mawani
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Liver Enzymes ◽  
Isotonic Saline ◽  
Saline Group ◽  
Hepatocellular Injury ◽  
Albino Rat ◽  
Medical College ◽  
Group 2 ◽  
Animal House

Objectives: Evaluate the mitigating effect of aqueous extract of Ginkgobiloba (GkbE) on liver enzymes and histology in carbon tetrachloride (CCl4) induced liverinjury in albino rat. Study design: Experimental study. Setting and Duration: Animal house,Bhitai Dental and Medical College Mirpurkhas and Agriculture University Tando Jam fromAnimal house from May 2015 - August 2016. Subjects and Methods: Sixty rats were equallydivided into 3 groups Group 1- Controls (0.9% isotonic saline), Group 2- (CCl4 CCl4 1.0mg/kg intraperitoneal) and Group 3- (CCl4+ GkbE). Blood samples were collected at end ofexperiment from tail veins. Liver was obtained after rat sacrifice by cervical dislocation. Tissuewas fixed in formaldehyde and embedded in paraffin. Microscopy of 3μ tissue sections wasperformed after H & E staining. Statistix 10.0 (USA) software was used for data analysisat 95% confidence interval. Results: Four weeks GkbE administration in CCl4 rat showedsignificant amelioration of liver enzymes and improved liver histology (p=0.0001). In GkbEtreated rats, the histological changes of degeneration, fatty change, inflammatory cellinfiltration, sinusoid congestion and necrosis was minimal (p=0.0001). GkbE was provedof mitigating the hepatocellular injury inflicted by carbon tetrachloride. Conclusion: GkbEmitigates the carbon tetrachloride induced liver injury in rat model. GkbE may be used in drugand chemical induced liver injury.

Hydralazine-induced liver injury: a review and discussion

2021 ◽  
Vol 14 (8) ◽  
pp. e243278 ◽  
Author(s):  
Meeta Bhardwaj ◽  
Nakul Jay Bhardwaj ◽  
Kendra Cueto ◽  
T Colin Killeen
Keyword(s):  
Side Effects ◽  
Liver Injury ◽  
Antihypertensive Agent ◽  
Adverse Reactions ◽  
Liver Enzymes ◽  
Injury Pattern ◽  
Hypertension Management ◽  
Close Monitoring ◽  
Hepatocellular Injury ◽  
Specific Symptoms

Hydralazine is a commonly prescribed antihypertensive agent. Some of its labelled adverse reactions include lupus-like syndrome, tachycardia, headache and fever. Despite its well-known side effects, little is known about hydralazine’s hepatotoxic effects. We report the case of a 54-year-old female patient who was started on hydralazine for hypertension management but later presented with hydralazine-induced liver injury. Her initial presentation consisted of non-specific symptoms and a hepatocellular injury pattern. Liver biopsy revealed hepatic steatosis. Three weeks after discontinuation of hydralazine, the patient’s liver enzymes normalised, and her symptoms resolved. Few studies have examined the incidence and mechanism by which hydralazine induces a liver injury pattern. With this case, we review the literature, the pathogenesis involved and the eventual management of hydralazine-induced liver injury. We propose close monitoring of liver enzymes for patients on hydralazine throughout their treatment course.

scholarly journals Enoxaparin-Induced Liver Injury

2020 ◽  
Vol 14 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Shehriyar Mehershahi ◽  
Nikhitha Mantri ◽  
Aneesh Kumar ◽  
Shaikh Danial ◽  
Patel Harish
Keyword(s):  
Molecular Weight ◽  
Pulmonary Embolism ◽  
Liver Injury ◽  
Low Molecular Weight Heparin ◽  
Liver Enzymes ◽  
Low Molecular Weight ◽  
Dramatic Improvement ◽  
Hepatocellular Injury

Enoxaparin, a form of low-molecular-weight heparin, can cause a rare, underreported, and often reversible form of hepatocellular injury. This report describes a case of enoxaparin-induced hepatotoxicity in a 61-year-old male diagnosed with pulmonary embolism. Elevations of liver enzymes were noted within 1 week of starting the drug, followed by a dramatic improvement upon its discontinuation, with subsequent normalization in the following days.

Hepatoprotective effect of methanolic extracts of Phyllanthus virgatus against carbon tetrachloride-induced liver injury in rats

2016 ◽  
Vol 2 (1) ◽  
pp. 1-7
Author(s):  
Chattu Maheswara Rao
Keyword(s):  
Carbon Tetrachloride ◽  
Serum Level ◽  
Total Protein ◽  
Liver Enzymes ◽  
Methanolic Extract ◽  
Hepatocellular Injury ◽  
Significant Extent ◽  
Methanolic Extracts ◽  
Hepatic Cells ◽  
Glutamate Pyruvate

In this study, the methanolic extract of Phyllanthus virgatus was evaluated against carbon tetrachloride (CCl4) induced hepatotoxicity in rats. The results of this study indicated that Phyllanthus virgatus exhibited moderate protective effect at a dose of 100-200 mg/kg by lowering serum level of liver enzymes such as alanine amino transferees (ALT), glutamate pyruvate transaminases (SGPT), aspartate aminotransferase (AST), glutamate oxaloacetate transaminases (SGOT), and total protein to a significant extent. Further, no significant effects were seen on blood serum level at a dose of 100-200 mg/kg body weight. The highest activity was observed at a dose of 200 mg/kg with a reduction of serum concentration of ALT, AST, total bilirubin and total protein. The methanolic extract of P. virgatus showed significant decrease in the levels of liver enzymes, indicating the protection of hepatic cells thereby protecting against CCl4 induced hepatocellular injury.

scholarly journals Inflammatory stress and idiosyncratic drugs hepatotoxicity in rabbit

2013 ◽  
Vol 12 (2) ◽  
pp. 7
Author(s):  
H. T. Mohamed
Keyword(s):  
Liver Enzymes ◽  
Saline Group ◽  
Rabbit Serum ◽  
Inflammatory Reactions ◽  
Inflammatory Stress ◽  
Group 4 ◽  
Hepatotoxic Effect ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Idiosyncratic drug hepatotoxicity is none or time-related, unpredictable, occur infrequently and can be fatal. It was proposed that inflammatory or oxidative stress occurs randomly in patients even after asymptomatic incidence can precipitate drug hepatotoxicity. To measure the hepatotoxicity of diclofenac in rabbit serum following the incidence of inflammatory stress by lipopolysaccharide (LPS) and correlate this to various stress parameters as Malondialdehyde (MDA). 24 rabbits were divided into four groups (6 each) according to the type of treatment. Group 1: control (received normal saline). Group 2 received diclofenac sod. (5mg/kg, orally 3times daily for three days). Group 3: received lipopolysaccharide (150μg/kg, i.v, 24 hours before killing. Group 4: received diclofenac sod. + Lipopolysaccharide (5mg/kg orally + 150μg/kg, i.v 24 hours before killing). Then for each animal were measure, liver M D A, liver enzymes. LPS potentiated the hepatotoxic effect of diclofenac sod. The effect is mediated by oxidative and inflammatory reactions as demonstrated by increase in a liver tissue M D A.

scholarly journals Important Role of P-Selectin for Leukocyte Recruitment, Hepatocellular Injury, and Apoptosis in Endotoxemic Mice

2004 ◽  
Vol 11 (1) ◽  
pp. 56-62 ◽  
Author(s):  
Daniel Klintman ◽  
Xiang Li ◽  
Henrik Thorlacius
Keyword(s):  
Liver Injury ◽  
Liver Enzymes ◽  
Leukocyte Recruitment ◽  
Leukocyte Rolling ◽  
Hepatocellular Injury ◽  
Principal Role ◽  
Step Procedure ◽  
Pathophysiological Role ◽  
The Individual

ABSTRACT Leukocyte recruitment in the liver includes a two-step procedure in which selectin-dependent leukocyte rolling is a prerequisite for subsequent CD18-dependent leukocyte firm adhesion in postsinusoidal venules. However, the roles of the individual selectins in leukocyte rolling and adhesion, hepatocellular injury, and apoptosis remain elusive. Therefore, we examined the pathophysiological role of P-, E-, and L-selectin in male C57BL/6 mice challenged with lipopolysaccharide (LPS) and d-galactosamine (Gal) by use of intravital microscopy of the liver microcirculation. In control animals, administration of LPS-Gal provoked reproducible hepatic damage, including marked increases of leukocyte recruitment, liver enzymes, and hepatocyte apoptosis and reduced sinusoidal perfusion. Interestingly, pretreatment with an anti-P-selectin antibody (RB40.34) markedly reduced leukocyte rolling and firm adhesion by 65 and 71%, respectively. Moreover, interference with P-selectin function significantly improved sinusoidal perfusion and reduced the increase in liver enzymes by 49 to 84% in endotoxemic mice. Moreover, the activity of caspase-3 and the number of apoptotic hepatocytes were significantly reduced by 55 and 54%, respectively, in RB40.34-treated animals. In contrast, administration of an anti-E-selectin antibody (10E9.6) and an anti-L-selectin antibody (Mel-14) did not protect against endotoxin-induced leukocyte responses or hepatic injury. In conclusion, our novel findings document a principal role of P-selectin in mediating leukocyte rolling, a precondition to the subsequent firm adhesion of leukocytes in liver injury. Furthermore, our novel data demonstrate that inhibition of P-selectin function reduces hepatocellular injury and apoptosis, suggesting a causal relationship between leukocyte recruitment on one hand and hepatocellular injury and apoptosis on the other hand. Based on these findings, it is suggested that P-selectin may be an important therapeutic target in endotoxin-induced liver injury.

scholarly journals CURCUMA LONGA

2018 ◽  
Vol 25 (07) ◽  
Author(s):  
Sana Naz ◽  
Faisal Irshad ◽  
Hina Mawani
Keyword(s):  
Carbon Tetrachloride ◽  
Histopathological Examination ◽  
Curcuma Longa ◽  
Statistical Significance ◽  
Male Rats ◽  
P Value ◽  
Medical College ◽  
Group A ◽  
Group B ◽  
Animal House

Objectives: To analyze the hepatoprotective effects of Curcuma longa (CL)against carbon tetrachloride (CCl4) induced chemical injury in experimental rats. Study Design:Experimental study. Setting: Indus Medical College in collaboration with Animal house of SindhAgriculture University Tando Jam. Period: March 2016 to August 2016. Methodology: Sixtyadult male rats were selected according to inclusion and exclusion criteria. Rats were dividedrandomly into 3 groups – as group A. controls, group B – received CCl4 and group C- receivedCCl4 + CL orally. Blood samples were taken after 4 weeks of therapy by cardiac puncture.5μ thick liver tissue sections were stained for light microscopy examination. Analysis of datawas performed on Statistix 9.0 (USA) at statistical significance of p-value ≤ 0.5. Results: Livercell biochemical markers of injury and histopathological examination show the Curcuma longais effective against carbon tetrachloride induced liver injury (P <0.05). Liver histology wasimproved by the curcuma longa therapy. Conclusion: Liver aminotransferase and histologywere improved significantly by the curcuma longa therapy in carbon tetrachloride induced liverinjury.

Aloe-Emodin Quinone Pretreatment Reduces Acute Liver Injury Induced by Carbon Tetrachloride

2000 ◽  
Vol 87 (5) ◽  
pp. 229-233 ◽  
Author(s):  
Beatrice Arosio ◽  
Nicoletta Gagliano ◽  
Lorena Maria Pia Fusaro ◽  
Luciano Parmeggiani ◽  
Jacopo Tagliabue ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Aloe Emodin

Evaluating the Proposed Mechanism by Which Atorvastatin Can Protect Renal Tissue against Contrast Media: An Animal study

2019 ◽  
pp. 75-84
Keyword(s):  
Contrast Media ◽  
Kidney Injury ◽  
Saline Group ◽  
Pleiotropic Effect ◽  
Renal Tissue ◽  
Male Rats ◽  
Dependent Manner ◽  
Group 2 ◽  
Dose Dependent ◽  
Media Group

Contrast- induced nephropathy (CIN) is an elevation of serum creatinine of ≥ 0.5 mg/dL from baseline after two to three days of exposure to contrast substance if there is no other cause for acute kidney injury. Atorvastatin may protect normal kidney physiology from contrast- induced kidney injury by effects unrelated to hypolipidemia termed pleiotropic effect by decline of endothelin production, angiotensin system down regulation, and under expression of endothelial adhesion molecules. This study was conducted to assess the strategy by which atorvastatin can achieve protective effect for kidneys after exposure to contrast media in an animal model. A 40 male rats were distributed randomly into 4 groups; ten rats for each: group (1): given normal saline; group (2): CIN group given iopromide as contrast media; group (3): given atorvastatin (20mg/kg) and iopromide; and group (4): given atorvastatin (40mg/kg) and iopromide. Blood collected by cardiac puncture for detection of serum glutathione, malondialdehyde, matrix metalloproteinase-9, and interleukin-18. The results have shown a significant increase in inflammatory and oxidative stress markers in contrast media group, and significant reduction in these markers in atorvastatin treated groups, in a dose-dependent manner. As conclusion, atorvastatin mechanism for protection against CIN in a dose-dependent manner can mediate by anti-inflammatory and antioxidant effects.

Sign in / Sign up

Export Citation Format

Share Document