A Fermented Substance from<i>Aspergillus phoenicis</i>Reduces Liver Fibrosis Induced by Carbon Tetrachloride in Rats

Fang, Hsun-Lang; Lai, Jinn-Jsyy; Lin, Wen; Lin, Wen‐Chuan

doi:10.1271/bbb.60604

Cited by 12 publications

(10 citation statements)

References 28 publications

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“…One part is soaked with 10% neutral formalin for preparation of the pathological slices. After weighing, a second part is completely dried at 100°C for examination of collagen contents [ 13 ]. The remaining parts are stored in 4 packs at −80°C for further use.…”

Section: Methodsmentioning

confidence: 99%

Fermented Citrus Lemon Reduces Liver Injury Induced by Carbon Tetrachloride in Rats

Chen

Chou

Hsu

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Fermented lemon juice displays a variety of important biological activities, including anti-inflammatory and antioxidant capabilities. The aim of the present study is to investigate hepatic-protective effects of no-sugar-added fermented lemon juice (FLJ) for liver inflammation caused by carbon tetrachloride (CCl4) in rats. Rats are divided into six groups: H2O, CCl4 + H2O, CCl4 + silymarin, and CCl4 plus three different FLJ doses by oral administration, respectively. The results show that the contents of plasma ALT and AST, hepatic lipid peroxidation, splenomegaly, and liver water are reduced significantly in rats under FLJ treatment, and pathological examination of liver fibrosis is improved. The reduced hepatic injury by increasing liver soluble protein and glutathione and albumin is observed in FLJ treated groups, and FLJ has comparable efficacies to medicine silymarin in liver therapies. The no-sugar-added FLJ differs from traditional fermentation by adding lots of sugar and prevents any hidden sugar intake while taking it as a complimentary treatment for liver inflammation. The green color and the taste of sourness are both associated with treating and healing the liver based on the five-element theory in traditional Chinese medicine, and the green and sour FLJ may be applied to the ancient theory in preventing hepatic injury accordingly.

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Section: Methodsmentioning

confidence: 99%

Fermented Citrus Lemon Reduces Liver Injury Induced by Carbon Tetrachloride in Rats

Chen

Chou

Hsu

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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“…Cirrhosis was induced when rats were 4 months old by intragastric administration of carbon tetrachloride (CCl 4 ; 0.2 ml (100 g body weight) –1 , twice a week; diluted 1:4 in olive oil) along with phenobarbital in the drinking water (0.35 g l −1 ), for 9 weeks, as previously described (Xu et al 2000; Fang et al 2007).…”

Section: Methodsmentioning

confidence: 99%

Cirrhosis decreases vasoconstrictor response to electrical field stimulation in rat mesenteric artery: role of calcitonin gene-related peptide

Blanco-Rivero

Márquez-Rodas

Sastre

et al. 2011

Experimental Physiology

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Our study determines alterations in the vasoconstrictor response elicited by electric field stimulation (EFS) in mesenteric arteries from cirrhotic rats treated with CCl 4 , and how calcitonin gene-related peptide (CGRP) participates in this response. Vasoconstriction induced by EFS was analysed in the absence and presence of the CGRP receptor antagonist CGRP(8-37) in arterial segments from control and cirrhotic rats. The vasodilator response to exogenous CGRP was tested in both groups of rats, and the interference of the guanylate cyclase inhibitor ODQ or the K ATP channel blocker glibenclamide was analysed only in segments from cirrhotic rats. The vasodilator response to the K ATP channel opener pinacidil and to 8-bromo-cyclic GMP was tested. The K ATP currents were recorded using the patch-clamp technique. Expression of receptor activity-modifying protein 1 (RAMP1), calcitonin receptor-like receptor, Kir 6.1 and sulfonylurea receptor 2B (SUR2B) was also analysed. Release of CGRP and cGMP was measured. The EFS-elicited vasoconstriction was less in segments from cirrhotic rats. The presence of CGRP(8-37) increased the EFS-induced response only in segments from cirrhotic rats. The CGRP-induced vasodilatation was greater in segments from cirrhotic rats, and was inhibited by ODQ or glibenclamide. Both pinacidil and 8-bromo-cyclic GMP induced a stronger vasodilator response in segments from cirrhotic rats. Pinacidil induced greater K ATP currents in cirrhotic myocytes. Expression of RAMP1, calcitonin receptor-like receptor, Kir 6.1 and SUR2B was not modified by liver cirrhosis. Liver cirrhosis increased CGRP release, but did not modify cGMP formation. The decreased vasoconstrictor response to EFS in cirrhosis is mediated by increased vasodilator response to CGRP, as well as increased K ATP channel gating. This effect of CGRP may play a role in the splanchnic vasodilatation present in liver cirrhosis.

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“…The sections were stained with hematoxylin and eosin (H&E) and masson trichrome (MT) according to standard protocols. The presence of fibrous extensions in liver sections were graded as described [22,23]: 0, normal liver; 1, accumulation of collagen fibrils around the central veins, but no visible extension of fibrous tissue from the central venous area; 2, fibrous septae extending from the central veins but no bridging to portal tracts or between adjacent Fig. 1 Illustration outlining the experimental groups for assessment of liver injury and cell transplantation in vivo for liver fibrosis.…”

Section: Histopathology Of the Livermentioning

confidence: 99%

Differentiation of Bone Marrow-derived Mesenchymal Stem Cells into Hepatocyte-like Cells on Nanofibers and Their Transplantation into a Carbon Tetrachloride-Induced Liver Fibrosis Model

Piryaei

Valojerdi

Shahsavani

et al. 2010

Stem Cell Rev and Rep

110

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There are limited data available on the effect of a physicochemical microenvironment on mesenchymal stem cell (MSC) differentiation and repopulation of the liver. Therefore, in this study nanofibers have been used to better differentiate and maintain the function and engraftment of differentiating MSCs both in vitro and in vivo. Mouse MSCs were differentiated into early (day 18) and late (day 36) hepatocyte-like cells (HLCs) in the presence or absence of ultraweb nanofibers (nano(+) and nano(-)) and their transplantation for recovery in mice with CCl(4) induced hepatic fibrosis was investigated. In the nano(+) group, hepatocyte markers-ALB and HNF4α- were elevated in a time-dependent manner; however, those were similar levels or slightly decreased in the nano(-) group from day 18 to 36. Ultrastructural studies of the differentiated cells revealed some similarities to hepatocytes. Urea production, secretion of albumin and α-fetoprotein, and metabolic activity of the CYP450 enzymes were significantly increased within in vitro differentiated HLCs on nanofibers at day 36. MSCs, early and late HLCs in both nano(-) and nano(+) culture conditions that were transplanted by an intravenous route caused a decrease in liver fibrosis when engrafted in the recipient liver and were able to differentiate into functional hepatocytes (ALB(+)), except for late HLCs in the nano(-) group. Late HLCs transplanted in the nano(+) group were more effective in rescuing liver failure, enhancing serum ALB, homing transplanted cells and undergoing functional engraftment than the other groups. These results showed that topographic properties of nanofibers enhance differentiation of HLCs from MSCs and maintain their function in long-term culture, which has implications for cell therapies.

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A Fermented Substance fromAspergillus phoenicisReduces Liver Fibrosis Induced by Carbon Tetrachloride in Rats

Cited by 12 publications

References 28 publications

Fermented Citrus Lemon Reduces Liver Injury Induced by Carbon Tetrachloride in Rats

Fermented Citrus Lemon Reduces Liver Injury Induced by Carbon Tetrachloride in Rats

Cirrhosis decreases vasoconstrictor response to electrical field stimulation in rat mesenteric artery: role of calcitonin gene-related peptide

Differentiation of Bone Marrow-derived Mesenchymal Stem Cells into Hepatocyte-like Cells on Nanofibers and Their Transplantation into a Carbon Tetrachloride-Induced Liver Fibrosis Model

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