Experimental Obstructive Jaundice Research Articles

The effect of Ankaferd blood stopper on liver damage in experimental obstructive jaundice

Background/aimsTo evaluate the potential protective effects of Ankaferd blood stopper (ABS) in an experimental obstructive jaundice (OJ) model.Materials and methodsThe study included 26 female rats, which were divided into 3 groups. The sham group, consisting of 10 rats, (group 1) only received solely laparotomy. In the control group, consisting of 8 rats, (group 2), ligation was applied to the biliary tract and no treatment was implemented. In the treatment group, consisting of 8 rats, (group 3), following ligation of biliary tract, 0.5 mL/day ABS was given for 10 days. Liver tissue and blood samples were taken for histopathological and biochemical examination.ResultsCompared to group 2, group 3 had higher aspartate aminotransferase (AST), total oxidant status (TOS) malondialdehyde (MDA), fluorescent oxidant products (FOP), and lower expression of albumin and total antioxidant status (TAS) (P < 0.05). In histopathological analysis, the mean scores of all histopathological parameters (fibrosis, portal inflammation, confluent necrosis, interphase activity, bile duct proliferation) have statistical significance between group 2 and group 3 (P < 005).ConclusionsABS has promising results in the treatment of experimental OJ because of its antioxidant and antiinflammatory properties. It may be used in clinical practice after more extensive studies about the effects of ABS on OJ.

The effect of Farnesoid X receptor agonist tropifexor on liver damage in rats with experimental obstructive jaundice.

ABSTRACTPurpose:To investigate experimentally the effects of Tropifexor, a farnesoid X receptor agonist, on liver injury in rats with obstructive jaundice.Methods:Forty healthy Wistar albino female rats were divided randomly in selected groups. These groups were the sham group, control group, vehicle solution group, Ursodeoxycholic acid group and Tropifexor group. Experimental obstructive jaundice was created in all groups, except the sham one. In the blood samples obtained, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), total bilirubin and direct bilirubin levels were established and recorded. Additionally, liver malondialdehyde, myeloperoxidase and catalase enzyme activity in the tissue samples were studied. Histopathological analysis was also performed.Results:No statistical difference was found between the control group and the Tropifexor group when AST, ALT and ALP values were compared. However, it was found that the Tropifexor group had statistically significant decreases in the values of GGT, total bilirubin and direct bilirubin (p < 0.05). Additionally, Tropifexor decreased the median values of malondialdehyde and myeloperoxidase, but this difference was not statistically significant compared to the control group. Finally, the Tropifexor group was statistically significant in recurring histopathological liver damage indicators (p < 0.05).Conclusions:Tropifexor reduced liver damage due to obstructive jaundice.

Altered Expression of Differential Genes in Thoracic Spinal Cord Involved in Experimental Cholestatic Itch Mouse Model.

The spinal origin of cholestatic itch in experimental obstructive jaundice mouse model remains poorly understood. In this study, the jaundice model was established by bile duct ligation (BDL) in mice, and differential gene expression patterns were analyzed in the lower thoracic spinal cord involved in cholestatic pruritus after BDL operation using high-throughput RNA sequencing. At 21st day after BDL, the expression levels of ENSRNOG00000060523, ENSRNOG00000058405 and ENSRNOG00000055193 mRNA were significantly up-regulated, and those of ENSRNOG00000042197, ENSRNOG00000008478, ENSRNOGOOOOOO19607, ENSRNOG00000020647, ENSRNOG00000046289, Gemin8, Serpina3n and Trim63 mRNA were significantly down-regulated in BDL group. The RNAseq data of selected mRNAs were validated by RT-qPCR. The expression levels of ENSRNOG00000042197, ENSRNOG00000008478, ENSRNOGOOOOOO 19607, ENSRNOG00000020647, ENSRNOG00000046289 and Serpina3n mRNA were significantly down-regulated in BDL group. This study suggested that cholestatic pruritus in experimental obstructive jaundice mouse model is related with in the changes of gene expression profiles in spinal cord.

Sa1433 - Expressions of Intestinal Tlr2 and Tlr4 in the Process of Experimental Obstructive Jaundice and their Effects

Sa1433 - Expressions of Intestinal Tlr2 and Tlr4 in the Process of Experimental Obstructive Jaundice and their Effects

The Effect of Calcium Dobesilate on Liver Damage in Experimental Obstructive Jaundice

ABSTRACTPurpose/Aim of the study: Inflammation and oxidative stress are two significant factors affecting the degree of liver damage in obstructive jaundice. The aim of this study was to evaluate the effect of calcium dobesilate (CaDob), an effective antioxidant and anti-inflammatory drug, on damage to liver caused by experimental obstructive jaundice. Materials and Methods: 30 rats in total were randomly placed into three groups, each group consisting of 10 rats. The sham group (Group 1) only received solely laparotomy. In the control group (Group 2), ligation was applied to the biliary tract and no treatment was implemented. In the CaDob group (Group 3), following ligation of the biliary tract, 100 mg/kg/day CaDob was implemented via an orogastric tube for a 10–day period. Liver tissue and blood samples were taken for histopathological and biochemical examination. Results: The CaDob group had significantly lower test values for serum liver functions when compared to the control group. Statistically lower levels of tissue malondialdehyde (MDA) and fluorescent oxidation products (FOP) were detected in the CaDob group, and the CaDob group had significantly higher levels of sulfydryl (SH) than the control group. Histopathological scores in the CaDob group were found out to be statistically less than the scores the control group received (p < 0.05). Conclusions: CaDob treatment repaired the histpatological changes induced by bile duct ligation. The hepatoprotective effects of CaDob can be associated with its antioxidant properties of the drug.

Altered expression of differential gene and lncRNA in the lower thoracic spinal cord on different time courses of experimental obstructive jaundice model accompanied with altered peripheral nociception in rats.

The spinal origin of jaundice-induced altered peripheral nociceptive response poorly understood. In the current study, we aimed to first validate rats with bile duct ligation (BDL) as a jaundice model accompanied by altered peripheral nociceptive response, and then to analyze differential gene and lncRNA expression patterns in the lower thoracic spinal cord on different time courses after BDL operation by using high-throughput RNA sequencing. The differentially expressed genes (DEGs) identified using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, followed by clustering analysis, Gene Ontology analysis and pathway analysis. As a result, a total of 2033 lncRNAs were differentially expressed 28d after BDL, in which 1545 probe sets were up-regulated and 488 probe sets were down-regulated, whereas a total of 2800 mRNAs were differentially expressed, in which 1548 probe sets were up-regulated and 1252 probe sets were down-regulated. The RNAseq data of select mRNAs and lncRNAs was validated by RT-qPCR. 28d after BDL, the expressions of lncRNA NONRATT002335 and NONRATT018085 were significantly up-regulated whereas the expression of lncRNA NONRATT025415, NONRATT025388 and NONRATT025409 was significantly down-regulated. 14d after BDL, the expressions of lncRNA NONRATT002335 and NONRATT018085 were significantly up-regulated; the expression of lncRNA NONRATT025415, NONRATT025388 and NONRATT025409 was significantly down-regulated. In conclusion, the present study showed that jaundice accompanied with decreased peripheral nociception involved in the changes of gene and lncRNA expression profiles in spinal cord. These findings extend current understanding of spinal mechanism for obstructive jaundice accompanied by decreased peripheral nociception.

The correlation between individual biochemical parameters of functional state of the liver in expe¬rimental obstructive jaundice and course administration of L-lysine escinate and glutargine.

The aim of this study was to determine the correlations between markers of oxidant-antioxidant stress in the blood of experimental animals, as well as the content of bilirubin and activity of enzymes in experimental obstructive jaundice. Studies were conducted on 84 adult male Wistar rats (180-230 g). Animals were divided into 4 groups: intact (n = 12), control (n = 24), L-lysine escinate (0,5 mg/kg, n = 24) and glutargin (40 mg/kg, n = 24). The isolation and ligation of the common bile duct below confluence was carried out under general anesthesia. The test preparations were administered 1 time per day, intraperitoneally. Evaluation of the treatment efficacy was carried out on 4th and 10th day of the study. The content of malonic dialdehyde (MDA), aldehyde- (APH) and ketone-phenylhydrazones (CPH), bilirubin and the activity of superoxide dismutase (SOD), catalase, aspartate aminotransferase (ALT) and alanine aminotransferase (AST) in the blood were determined using conventional techniques. The correlation links between common markers (bilirubin, AST, ALT) and indicators characterizing oxidant-antioxidant stress (MDA, APH, CPH, SOD, catalase) were determined in the study. High rate of correlation between them was established. The results allow to evaluate indirectly the intensity of oxidative metabolism processes in the liver, which can be used in clinical practice to assess the severity degree of the patients with progressive obstructive jaundice.

Морфологічні основи розвитку хронічного інтерстиційного сіалоаденіту при патології гепатобіліарної системи

Reactive changes of different nature in salivary glands is accompanied by many diseases of internal organs. Due to the complex neurohormonal regulation, bile secretion system is functionally interconnected with all organs and systems of the digestive tract. The article presents data of structural changes of acinar tissue and bloodstream of parotid salivary gland in experimental obstructive jaundice. It was established that the degree of morphological changes in the parotid gland, angioarchitectonics state and nature of degenerative and destructive processes is directly dependent on the duration of obstructive cholestasis.

Ginsenoside Rg1 prevents cerebral and cerebellar injury induced by obstructive jaundice in rats via inducing expression of TIPE-2

The aim of the study was to analyze the effect of Ginsenoside Rg1 (Rg1) on cerebral and cerebellar injury in experimental obstructive jaundice (OJ). OJ was done by ligature and section of extrahepatic biliary duct. Rg1 was injected intraperitoneally (10mgkg−1d−1 or 20mgkg−1d−1). Comparison of serum total bile salts (TBA), total bilirubin (TBil), direct bilirubin (DBil), TNF-α, IL-6 and IL-1β among groups. Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined, also apoptosis and mRNA and protein levels of TIPE2 (TNF-α-inducible protein 8-like 2) were tested in cerebrum and cerebellum. Our results showed that Rg1 reduced MDA and apoptosis in cerebrum and cerebellum induced by OJ, also GSH and antioxidant enzyme activity were raised obviously in rats treated with Rg1. Moreover, decreased mRNA and protein levels of TIPE2 in OJ rats and Rg1 could improve the decreased mRNA and protein levels of TIPE2 in OJ rats. In conclusion, Rg1 decreased oxidative stress and apoptosis, also recovered the antioxidant status and mRNA and protein levels of TIPE2 in the cerebrum and cerebellum of OJ rats.

L-carnitine reduces acute lung injury in experimental biliary obstruction.

Objectives:To investigate the protective effects of L-carnitine (LC) on lungs in an experimental obstructive jaundice (OJ) model.Methods:This was conducted for 2 months between May 2011 and July 2011 at Suleyman Demirel University School of Medicine Experimental and Clinical Research Center, Isparta, Turkey. Thirty-eight Wistar-Albino rats with an average weight of 250-300 g were divided into 3 groups of control, OJ, and OJ + L-carnitine treatment (LCT). L-carnitine was injected intravenously into the tail vein at a dose of 50 mg/kg/day for 10 days to the LCT group. Animals were sacrificed 10 days later. Enzyme levels were measured in the lung tissue; malondialdehyde, myeloperoxidase (MPO), glutathione peroxidase (GSH-Px), catalase, and superoxide dismutase. Tumor necrosis factor-alfa, interleukin 6 (IL-6), IL-8, and C-reactive protein levels were studied in plasma samples. Histopathological changes in the lungs were examined.Results:There was a decreased in GSH-Px, MPO, and IL-8 levels (p<0.05) in the LCT group. The histopathological examination showed that neutrophil leukocyte infiltration and edema formation decreased and destruction of lung parenchyma disappeared following the treatment with LC (p<0.05).Conclusion:L-carnitine has a protective effect against lung damage due to experimental obstructive jaundice, possibly by altering anticytokine and antioxidant activity, and by decreasing the neutrophil migration.

The Effect of Montelukast on Liver Damage in an Experimental Obstructive Jaundice Model

Background: Montelukast is a cysteinyl-leukotriene type 1 (CysLT₁) selective receptor antagonist. In recent years, investigations have shown that montelukast possesses secondary anti-inflammatory activities and also antioxidant effects. For this reason, we aimed to determine the possible effects of montelukast on liver damage in experimental obstructive jaundice. Methods: 30 Wistar-Albino male rats were randomized and divided into three groups of 10 animals each: group I, sham-operated; group II, ligation and division of the common bile duct (BDL) followed by daily intraperitoneal injection of 1 ml of saline; group III, BDL followed by daily intraperitoneal injection of 10 mg/kg montelukast dissolved in saline. The animals were killed on postoperative day 7 by high-dose diethyl ether inhalation. Blood and liver samples were taken for examination. Results: In this study, liver malondialdehyde (MDA) (p = 0.001), myeloperoxidase (p = 0.003), and total sulfhydryl (SH) (p = 0.009) were found to be significantly different between the BDL + montelukast and the BDL groups. Plasma total SH (p = 0.002) and MDA (p = 0.027) values were also statistically different between these groups. Statistical analyses of histological activity index scores showed that the histopathological damage in the BDL + montelukast group was significantly less than the damage in the control group (p < 0.05 for all pathological parameters). Conclusion: According to the results of this study, montelukast showed a significant hepatoprotective effect in this experimental obstructive jaundice model, which might be due to its antioxidant and anti-inflammatory activities.

Glutathione Supplementation Attenuates Oxidative Stress and Improves Vascular Hyporesponsiveness in Experimental Obstructive Jaundice.

We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(−) from the reaction of excessive NO with O2 ∙- and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.

Resveratrol attenuates both small bowel and liver changes in obstructive jaundice.

It is well known that mucosal changes and alterations in liver function occur in the experimental obstructive jaundice model. We aimed to evaluate the effect of resveratrol on obstructive jaundice-induced changes in the small bowel mucosa and liver using ischaemia-modified albumin as a marker of oxidative damage. Animal experimentation. The study used a rodent experimental model of obstructive jaundice, including a sham group (1), a control group (2), and a study group (3). Wistar albino rats were used. Jaundice was produced by ligation of the bile duct in Groups 2 and 3. In Group 3, resveratrol was administered intraperitoneally for 14 days. In terms of the structure and the size of the mucosal villi, significant thickening and blunting were detected in Group 2 compared with Group 1. These changes were significantly less noticeable in Group 3 compared with Group 2. Levels of ischaemia-modified albumin were significantly higher in Group 2 compared with those in Group 1, and they were significantly decreased in Group 3 compared with Group 2. Resveratrol administration to obstructive jaundiced rats reduced the organic effects of obstructive jaundice on small bowel mucosa and liver oxidative stress. We believe that this reduction might attenuate bacterial translocation and systemic effects of secreted cytokines.

Vitamin A supplementation alleviates extrahepatic cholestasis liver injury through Nrf2 activation.

Aim. To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats. Methods. Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays. Results. Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1. Conclusion. Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

Protective effects of ginseng total saponins against hepatic ischemia/reperfusion injury in experimental obstructive jaundice rats

Context: Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is one of the most extensively used herbs for stroke and chronic debilitating conditions in East Asian countries. Ginsenosides (GS) are the main bioactive compounds for ginseng's efficacy, but the mechanisms have not been fully clarified.Objective: To investigate hepatoprotective effects of GS against ischemia/reperfusion (IR) injury in the experimental obstructive jaundice rats.Materials and methods: GS was fed to cholestatic rats with IR injury daily for 6 d at a dose of 1.10 g/kg. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by colorimetric method. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling method. Protein expression of Bax and Bcl-2 was detected by immunohistochemistry.Results and discussion: After intervention of GS to cholestatic rats with IR injury, the levels of activating blood flow were significantly improved, and the levels of serum ALT were decreased 1.7-times, AST decreased 1.3-times, but SOD activities were increased 1.1-times compared with those of the model rats. It could also reverse histopathological changes and inhibit IR-induced apoptosis of hepatic tissues via decrease of Bax/Bcl-2 ratio (from 2.87 ± 0.57 to 1.65 ± 0.29). Oral administration of GS in a dosage of 26.4 g/kg did not lead to toxic effects in rats.Conclusion: GS attenuated the IR injury in the presence of cholestasis and could be considered for the clinical treatment of cholestasis.

The protective effect of Nigella sativa oil in the brain of the biliary obstructed rats

ABSTRACT: Oxidative stress is one of the important mechanisms of jaundice induced encephalopathy. The aim of this study was to examine the possible protective effect of Nigella sativa (NS) seed oil against the oxidative stress of brain tissue induced by experimental obstructive jaundice in rats. BiliarY obstruction was performed in male Wistar albino rats by bile duct ligation and scission (BDL). Intragastric NS oil (1 mg/kg p.o.) or saline was administered for 28 days. At the end of the experiment, in the half of the rats the blood brain barrier (BBB) permeability was evaluated by Evans blue (EB) extravasation. Other rats were decapitated and brain tissue samples were obtained for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) and Na+,K+-ATPase activities. ChronIC biliary obstruction caused a significant increase in the BBB permeability which was verified by EB extravasation while this effect was attenuated by NS oil treatment. On the other hand, BDL-induced decrease in brain GSH level and Na+,K+-ATPase activity were elevated back to control level in NS oil-treated BDL group. Increase in tissue MDA level, and MPO activity due to BDL were also attenuated by NS oil treatment. Our results suggest that NS oil treatment protects the brain from oxidative damage following bile duct ligation in rats. This effect possibly involves the inhibition of neutrophil infiltration and lipid peroxidation and the restoration of antioxidant status in the tissue. Accordingly, supplementing cirrhotic patients with adjuvant therapy of NS oil may have some benefit against hepatic encephalopathy. KEYWORDS: Nigella, black cumin, bile duct, brain, edema

The Protective Effect of Ellagic Acid on Lung Damage Caused by Experimental Obstructive Jaundice Model

Aim : This study aimed to investigate protective effects of ellagic acid on lungs in an experimental obstructive jaundice model.Methods : Four groups were established, each consisting of ten randomly selected rats: Group 1: sham, Group 2: ellagic acid, Group 3: obstructive jaundice, and Group 4: obstructive jaundice + ellagic acid. Ellagic acid was administered orally at a dose of 60 mg/kg/day to group 2 and 4. The animals were sacrificed eight days later. The total oxidative status and the total antioxidant capacity in their lung tissue were determined, and malondialdehyde levels in their blood were measured. Histopathological changes in the lungs were examined.Results : In the obstructive jaundice group treated with ellagic acid, there was a decrease in malondialdehyde levels and a reduction in the total oxidative status and the oxidative stress index, whereas the total antioxidant capacity increased (p < 0.001). The histopathological examination showed that neutrophil leukocyte infiltration and edema formation decreased and destruction of lung parenchyma disappeared following the treatment with the ellagic acid (p < 0.05). Conclusion : This study shows that ellagic acid has a protective effect against oxidative damage in lung tissue in obstructive jaundice.

Effect of Ginger Extract on Liver Damage in Experimental Obstructive Jaundice Produced by Main Bile Duct Ligation

Background : Obstructive jaundice is one of the most important surgical causes of childhood jaundices. The aim of this study is to investigate effects of ginger (Gingiber officinalis) extracts on liver damage in experimental obstructive jaundice produced by main bile duct ligation.Materials and Methods : Forty two Wistar-albino rats were randomly allocated into 7 groups (n = 6). Nothing was performed in the control (C) group. Only laparatomy was performed in the sham (Sh) group. The ginger 1 and 2 (Gi and G2) groups received only 100 and 200 mg/kg/day doses of ginger extract for 1 week orally. In study group, common bile duct ligation was done. In treatment 1 and 2 (T and T2) groups common bile duct ligation was followed by administration of 100 and 200 mg/kg/day doses of ginger extract for 1 week orally from the third post operative day, respectively. Blood samples and liver were harvested in order to evaluate the serum aspartate aminotransferase (AST), alanine amino transferase (ALT), gama glutamyltransferase (GGT), total bilirubin (bil), superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and liver tissue SOD, GSH, MDA levels and liver apoptosis. Results were analyzed by Mann-Whitney U test statistically.Results : Ginger administration did not result in any differences of serum or tissue levels of the studied parameters and liver apoptosis between the groups statistically (except AST levels in group T2). Tissue GSH and serum SOD levels were only mildly increased in groups receiving ginger alone.Conclusions : There is no evidence for protective, inhibitive and decreasing effects of ginger extract on liver injury in experimental obstructive jaundice with these findings.

Superiority of Ceftriaxon to Cefazolin in a Rat Model of Obstructive Jaundice: An Experimental Study

ABSTRACTObjective: The objective of this study was to evaluate the serum and bile concentrations of cefazolin and ceftriaxone at the third and sixth hours in an experimental obstructive jaundice model and to identify the rate of excretion of these antibiotics into the bile. Material and methods: Thirty-two Wistar albino rats were used in this study. The bile and serum levels of cefazolin were measured at the third hour in the A1 group and at the sixth hour in the A2 group, with cefazolin administered as 5 mg/rat; while the bile and serum levels of ceftriaxone were studied at the third hour in the B1 group and at the sixth hour in the B2 group, with ceftriaxone administered as 5 mg/rat. Results: After 3 hr of cefazolin administration, the serum concentration in the A1 group reached a mean of 1.8 μg/ml, while the bile concentration was 90% of the serum concentration, with a mean of 1.6 μg/ml; whereas in the B1 group, the third-hour serum concentration of ceftriaxone was 18.6 μg/ml, while the bile concentration was found to be as high as 330% of this level, i.e., 56 μg/ml. The serum value of cefazolin decreased to 1.4 μg/ml in the A2 group and ceftriaxone decreased to 3.7 μg/ml in the B2 group at the sixth hour. Conclusions: Although the excretory level of cefazolin and ceftriaxone into the bile reaches therapeutic doses, the duration for which these levels are above those required for bactericidal activity is short. Ceftriaxone is better concentrated in the serum and bile than cefazolin.

Effect of beta-glucan in preventing bacterial translocation in a model of experimental obstructive jaundice

Effect of beta-glucan in preventing bacterial translocation in a model of experimental obstructive jaundice