Liver resistance to CCl4-induced injury after stimulation of macrophages with various preparations

Kutina, S. N.; Zubakhin, A. A.

doi:10.1007/bf02434865

Cited by 4 publications

(4 citation statements)

References 10 publications

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“…Activated resident Kupffer cells and the neutrophils recruited at the site of parenchymal liver injury are considered as the primary culprits in damaging surrounding healthy cells as the result of nonspecific action (Laskin and Pendino, 1995; Luster et al, 2001). However, recent evidence suggests that the contribution of the inflammatory cells does not or is not sufficient to mediate progression of injury (Ju et al, 2002; Kutina and Zubakhin, 2000; Lawson et al, 2002). The second leading theory regarding progression of injury is production of free radicals and oxidative stress, and subsequent lipid peroxidation that propagates injury (Kellogg and Fridovich, 1975; Mylonas and Kouretas, 1999).…”

Section: Introductionmentioning

confidence: 99%

Tissue Repair: An Important Determinant of Final Outcome of Toxicant-Induced Injury

2005

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Tissue repair is a dynamic compensatory cell proliferation and tissue regeneration response stimulated in order to overcome acute toxicity and recover organ/tissue structure and function. Extensive evidence in rodent models using structurally and mechanistically diverse hepatotoxicants such as acetaminophen (APAP), carbon tetrachloride (CCl4), chloroform (CHCl3), thioacetamide (TA), trichloroethylene (TCE), and allyl alcohol (AA) have demonstrated that tissue repair plays a critical role in determining the final outcome of toxicity, i.e., recovery from injury and survival or progression of injury leading to liver failure and death. Tissue repair is a complex process governed by intricate cellular signaling involving a number of chemokines, cytokines, growth factors, and nuclear receptors leading to promitogenic gene expression and cell division. Tissue repair also encompasses regeneration of hepatic extracellular matrix and angiogenesis, the processes necessary to completely restore the structure and function of the liver tissue lost to toxicant-induced initiation followed by progression of injury. New insights have emerged over the last quarter century indicating that tissue repair follows a dose response. Tissue repair increases with dose until a threshold dose, beyond which it is delayed and impaired due to inhibition of cellular signaling resulting in runaway secondary events causing tissue destruction, organ failure, and death. Prompt and adequately stimulated tissue repair response to toxic injury is critical for recovery from toxic injury. Tissue repair is modulated by a variety of factors including species, strain, age, nutrition, and disease condition causing marked changes in susceptibility and toxic outcome. This review focuses on the properties of tissue repair, different factors affecting tissue repair, and the mechanisms that govern tissue repair and progression of injury. It also highlights the significance of tissue repair as a target for drug development strategies and an important consideration in the assessment of risk from exposure to toxicants.

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Section: Introductionmentioning

confidence: 99%

Tissue Repair: An Important Determinant of Final Outcome of Toxicant-Induced Injury

2005

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“…Hypolipemic and associated anti-atherosclerosis effects of β-glucan have been previously investigated ( 16 , 17 ), with evidence demonstrating the favorable effects of β-glucan on the hepatopathies ( 18 , 19 ). However, the direct effects of β-glucan on hyperlipemic liver damage, and the effects on hypolipemia and associated anti-atherosclerosis using the β-glucan originating from Aureobasidium , have not yet been determined.…”

Section: Discussionmentioning

confidence: 99%

“…Previous clinical and animal studies have used concentrated β-glucan preparations from oats and barley and have demonstrated strong hypolipemic and associated anti-atherosclerosis effects on hypercholesterolemic hamsters ( 16 , 17 ). Although certain studies have demonstrated evidence of the direct effects of β-glucan on hepatopathies ( 18 , 19 ), the direct effects of β-glucan on hyperlipemic liver damage are seldom. In addition, the effects of the β-glucan originating from Aureobasidium on hypolipemia and associated anti-atherosclerosis have not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

Effect of polycan, a β-glucan originating from Aureobasidium, on a high-fat diet-induced hyperlipemic hamster model

Lim

Choi

et al. 2015

Experimental and Therapeutic Medicine

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The aim of the present study was to analyze the effect of polycan, a β-glucan originating from Aureobasidium, on high-fat diet (HFD)-induced hyperlipemia and hepatic damage. A total of 30 hamsters were divided into 6 groups based on their body weight following acclimatization: control, sham, simvastatin (SIMVA) and 3 Polycan groups. In the polycan groups, Polycan, at three concentrations (31.25, 62.5 and 125 mg/kg), was administered orally once a day for 56 days, in addition to the HFD. On the day of sacrifice, changes in the body weight, food consumption, liver weight and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride and total cholesterol (T-CHOL) were observed, as well as changes to the liver and aorta (thoracic and abdominal) histopathology and histomorphometry. The results from the polycan groups were compared with a SIMVA 10 mg/kg oral treatment group, in addition to the sham and vehicle control groups. After the HFD-induced hyperlipidemic hamsters were administered Polycan, there was no significant change in their body weight and food consumption when compared with the hamsters in the vehicle control group. However, the serum levels of AST, ALT, triglyceride, T-CHOL and LDL were significantly reduced in a dose-dependent manner when compared with the vehicle control group (P<0.05). Furthermore, the levels of liver steatosis and arteriosclerosis in the abdominal and thoracic aorta were significantly decreased in a dose-dependent manner (P<0.01). In the SIMVA-treated group, body weight (P<0.05), the serum level of lipids (triglyceride, T-CHOL and LDL; P<0.01) and the level of arteriosclerosis (P<0.01) were significantly reduced when compared with the vehicle control group. However, liver weight and the serum levels of AST, ALT, and liver steatosis increased when compared with the vehicle control group. Based on these results, it was concluded that polycan exerts a favorable effect in decreasing HFD-induced hyperlipemia and associated atherosclerosis, with relatively good protective effects on liver damage.

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“…However, in addition to bacteriolytic activity, lysozyme affects many biochemical and physiological processes in the body. So, it increases the chemotaxis of leukocytes [1], stimulates the lymphocytic system of specific immunity [5], and has hepatoprotective and mucosoprotective effects [6,7].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide increases lysozyme adhesion to chitin

Levitsky

Mudrik

Khromagina

et al. 2019

J Educ Health Sport

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Background. To study the effect of lipopolysaccharide on the adsorption of lysozyme on chitin. Methods. Egg white lysozyme, lipopolysaccharide and chitin were used. The lyophilized cells of M. lyzodeikticus were used as a lysozyme substrate. Lysozyme activity was determined by the bacteriolytic method using different concentrations (8-512 μg/ml). Lysozyme adsorption on chitin was determined by the loss of lysozyme from solution after shaking with chitin. The effect of lipopolysaccharide (0.6-40 μg/ml) on lysozyme adsorption was evaluated by the loss of lysozyme from the solution after shaking with 50 mg of chitin. Results. In determining the activity of lysozyme by the bacteriolytic method, the linear nature of the dependence of activity on the concentration of the enzyme is observed only at low concentrations (8-100 μg / ml). Lipopolysaccharide does not affect the bacteriolytic 241 activity of lysozyme, however, dose-dependently increases the adsorption of lysozyme on chitin. Conclusion. Lipopolysaccharide increases the adsorption of lysozyme on chitin.

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Liver resistance to CCl4-induced injury after stimulation of macrophages with various preparations

Cited by 4 publications

References 10 publications

Tissue Repair: An Important Determinant of Final Outcome of Toxicant-Induced Injury

Tissue Repair: An Important Determinant of Final Outcome of Toxicant-Induced Injury

Effect of polycan, a β-glucan originating from Aureobasidium, on a high-fat diet-induced hyperlipemic hamster model

Lipopolysaccharide increases lysozyme adhesion to chitin

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