Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Carbontetrachloride (CCl 4 ) is closely related chemically to chloroform and likewise in hepatic poisons. This study was designed to evaluate the effects of carbon tetrachloride on liver of male rats and the reversing effects of L-carnitine and melatonin on established liver fibrosis. A total of 72 adult male albino rats were used in this study. The animals were divided into six groups. Group (1) animals of the first group were kept as control andtreated with paraffin oil twice weekly for eight weeks. Group (2) rats of the second group were injected with CCl4 intraperitoneally at 0.15 ml per rats (diluted 1:1 in liquid paraffin) twice weekly for eight weeks to produced liver fibrosis. Group (3) following establishment with CCl 4 which induced liver fibrosis, the rats were treated with L-carnitine at a dose level of 50 mg/kg for four weeks. Group (4) rats with liver fibrosis were injected intraperitoneally with melatonin at dose level of 10 mg/kg for four weeks. The fifth and sixth groups were given L-carnitine and/or melatonin at dose levels of 50 mg/kg and 10 mg/kg respectively for four weeks.Histological changes in the liver of rats treated with CCl 4 including liver fibrosis, architecture distortion and appearance of many pseudolobule. The fibrous tissues run in septa between the nodules. The liver damage varied from one area to another and varied from moderate fibrosis to cirrhosis.Quantitative measurement of the severity of liver fibrosis (area damage) was achieved by using computerized image analysis (Leica image) showed that highly significant increase in area of fibrosis was recorded in the case of rats treated with CCl 4 only.Quantitative DNA image analysis showed that 3% of aneuploid cells could be noticed in liver of rats treated with CCl 4 only. Histochemical results of rats treated with CCl 4 showed highly significant increase in grey level of mucopolysaccharides and protein levels. No histological and histochemical changes could be noticed in the liver of rats treated with either Lcarnitine or melatonin only. Both L-carnitine and melatonin were found to reverse CCl 4 induced liver damage.
Carbontetrachloride (CCl 4 ) is closely related chemically to chloroform and likewise in hepatic poisons. This study was designed to evaluate the effects of carbon tetrachloride on liver of male rats and the reversing effects of L-carnitine and melatonin on established liver fibrosis. A total of 72 adult male albino rats were used in this study. The animals were divided into six groups. Group (1) animals of the first group were kept as control andtreated with paraffin oil twice weekly for eight weeks. Group (2) rats of the second group were injected with CCl4 intraperitoneally at 0.15 ml per rats (diluted 1:1 in liquid paraffin) twice weekly for eight weeks to produced liver fibrosis. Group (3) following establishment with CCl 4 which induced liver fibrosis, the rats were treated with L-carnitine at a dose level of 50 mg/kg for four weeks. Group (4) rats with liver fibrosis were injected intraperitoneally with melatonin at dose level of 10 mg/kg for four weeks. The fifth and sixth groups were given L-carnitine and/or melatonin at dose levels of 50 mg/kg and 10 mg/kg respectively for four weeks.Histological changes in the liver of rats treated with CCl 4 including liver fibrosis, architecture distortion and appearance of many pseudolobule. The fibrous tissues run in septa between the nodules. The liver damage varied from one area to another and varied from moderate fibrosis to cirrhosis.Quantitative measurement of the severity of liver fibrosis (area damage) was achieved by using computerized image analysis (Leica image) showed that highly significant increase in area of fibrosis was recorded in the case of rats treated with CCl 4 only.Quantitative DNA image analysis showed that 3% of aneuploid cells could be noticed in liver of rats treated with CCl 4 only. Histochemical results of rats treated with CCl 4 showed highly significant increase in grey level of mucopolysaccharides and protein levels. No histological and histochemical changes could be noticed in the liver of rats treated with either Lcarnitine or melatonin only. Both L-carnitine and melatonin were found to reverse CCl 4 induced liver damage.
BackgroundAcute myocardial infarction (AMI) is a critical cardiovascular disease (CVD). Laminin (LN) is involved in the process of myocardial fibrosis and ventricular remodeling observed in AMI; however, there are currently no studies on the correlation between LN and AMI prognosis.PurposeTo explore the predictive value of serum LN levels for major adverse cardiovascular events (MACE) in patients, 6 months after an acute myocardial infarction.MethodsA total of 202 AMI patients who were hospitalized in the Department of Cardiology of the Second Affiliated Hospital of Nantong University between December 2019 and December 2020 were included. The observation endpoint was the occurrence of MACE. Univariate and multivariate logistic analyses were used to evaluate the relationships between the variables and endpoint. The predictive value of LN for MACE in AMI patients was assessed using receiver operating characteristic (ROC) analysis.ResultsA total of 47 patients developed MACE. Univariate logistic analysis showed that smoking, emergency percutaneous coronary intervention (EPCI), age, cardiac troponin I (c-TNI) levels, N-terminal prohormone brain natriuretic peptide (NT-proBNP) levels, and LN levels were associated with the occurrence of MACE (p < 0.05). Multivariate logistic analysis showed that LN was an independent predictor of MACE (odds ratio [OR] = 1.021, 95%CI: 1.014–1.032, p < 0.001). According to the ROC curve, LN can be used as an effective predictor of MACE (AUC = 0.856, 95%CI: 0.794–0.918, p < 0.001). According to the cutoff value, LN>58.80 ng/ml (sensitivity = 83.00%, specificity = 76.80%) or LN>74.15 ng/ml (sensitivity = 76.6%, specificity = 83.2%) indicate a poor prognosis for AMI. Different cut-off values are selected according to the need for higher sensitivity or specificity in clinical applications.ConclusionsLN may be a predictor of MACE following AMI in patients and could be utilized as a novel substitute marker for the prevention and treatment of AMI.
Laminin is a glycoprotein which has an important role in the mechanism of fibrogenesis and is, thus, related to hepatic fibrosis in addition to presenting increased levels in several types of neoplasias. However, its determination is not routinely considered in the study of hepatic fibrosis. In this review, the authors critically comment on the role of this glycoprotein compared to other markers of fibrosis through non-invasive procedures (Fibroscan). They also consider its clinical investigational potential and believe that the continuation of these investigations might contribute to a better understanding of the fibrogenic mechanism, which could in turn either lead to the identification of patients at risk of developing fibrosis non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) or at least be used as an indicator for hepatic biopsy in such patients. Finally, the authors believe that serum laminin determination might contribute to the diagnosis of epithelial tumor metastasis and peritoneal carcinomatosis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.