Liver Aspartate Aminotransferase Research Articles

Can dietary ethanolic extract of propolis alter growth performance, digestive enzyme activity, antioxidant, and immune indices in juvenile beluga sturgeon (Huso huso)?

The present study investigated the effects of dietary ethanolic extract of propolis on growth performance, digestive enzyme activity, liver antioxidant capacity, and skin mucus immunity in beluga sturgeon. For this purpose, a total of 120 juvenile fish (595.55 ± 31.61 g) were distributed in 12 tanks and fed with ethanolic extract of propolis at 0, 1, 2, and 3% for 60 days. The current study results showed that growth indices and the survival rate did not change in the juvenile fish fed with this extract compared to the control group. However, the protease activity, pepsin, and chymotrypsin were significantly higher in beluga sturgeon fed with the treated diet than the control fish (P < 0.05). The results also showed a higher white blood cell count in fish provided with 2 and 3% extract than in the control group (P < 0.05). The level of the alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase activities in the fish liver remained unaffected in all groups (P˃0.05). Meanwhile, the activities of antioxidant-related enzymes were significantly higher (P < 0.05) in the liver of beluga sturgeon fed with dietary ethanolic extract of propolis, especially at 3%, than the control fish. In 2 and 3% treated groups, the skin mucus of beluga sturgeon showed an enhanced lysozyme activity and total immunoglobulin level (P < 0.05) compared to the control group. In parallel, the in vitro assay revealed an elevated serum antibacterial activity against Aeromonas hydrophila in the fish fed with 2 and 3% extract compared with the control group (P < 0.05). It can be concluded that the supplementation of ethanolic extract of propolis, especially at 3%, could improve some digestive enzyme activities, liver antioxidant capacity, and skin mucus immunity of juvenile beluga sturgeon.

EVALUATION OF HEPATOPROTECTIVE ACTIVITY OF DRACAENA TERNIFLORA ROXB. AGAINST ETHANOL INDUCED HEPATIC INJURY IN WISTAR ALBINO RATS

Objectives: The objectives of the study were to investigate hepatoprotective activity of ethanolic root extract of Dracaena terniflora Roxb. (DTR-E) in alcohol-induced hepatotoxicity in rats. Methods: Hepatotoxicity was induced in albino Wistar rats by oral administration of 40% ethanol (2 mL/100 g body weight). DTR-E root extract was administered at a dose level of 100 mg/kg and 200 mg/kg orally for 21 days. On the 22nd day blood was taken by puncturing retro orbital plexus and used for the estimation of biochemical parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, creatinine, urea, triglycerides, total cholesterol, albumin, and total protein. Animals were sacrificed by cervical dislocation and liver was dissected out and histopathological analysis of liver and kidney was carried out. Results: Obtained results revealed that administration of ethanol caused a significant increase in liver weight, plasma ALT, AST, ALP, bilirubin creatinine, urea, triglycerides,and total cholesterol compared to the control group, while total protein and albumin concentration are significantly declined which were effectively prevented by the DTR-E extract. The histopathological observations supported the biochemical evidence of hepatoprotection. Conclusions: The findings suggest that DTR-E root extract protects the liver cell from ethanol induced liver damages due to its antioxidative effect on hepatocytes. The results of the present investigation indicated that roots of D. terniflora Roxb. possesses significant hepatoprotective activity.

Protective Effects of Non-Encapsulated and Microencapsulated Lactobacillus Delbrueckii Subsp. Bulgaricus in Rainbow Trout (Oncorhynchus Mykiss) Exposed to Lead (Pb) Via Diet

Abstract The present study was designed to investigate the effects of dietary non-encapsulated and microencapsulated Lactobacillus delbrueckii subsp. bulgaricus on growth performance, intestinal enzymatic activities, antioxidant capacity and hepato-biochemical parameters of rainbow trout before or after exposure to lead via diet. Fingerling fish (16 ± 4 g) were divided into four groups: negative control (NC), positive control (PC), probiotic (PR) and encapsulated probiotic (EN-PR). During the pre-exposure period (days 0–45), fish in the NC and PC groups received the basal diet, whereas fish in the PR and EN-PR groups were fed with basal diet containing 108 CFU g−1 feed of non-encapsulated and microencapsulated probiotic, respectively. During the exposure period (days 46–66), the fish in the probiotic and PC groups were co-treated with 500 μg g−1 feed of lead nitrate. Blood, liver and gut samples were taken at days 0, 45, 52, 59 and 66. The results revealed that growth performance and intestinal enzymatic activities were significantly (P&lt;0.05) improved in the probiotic groups compared to the NC group (day 45). Dietary exposure to lead resulted in the highest levels of liver aspartate aminotransferase (AST), liver alkaline phosphatase (ALP) and serum malondialdehyde (MDA), and the lowest activities of serum superoxide dismutase (SOD) and catalase (CAT) in the PC group (day 66). The levels of liver ALP were significantly (P&lt;0.05) lower in the probiotic groups compared to the NC and PC groups prior to and after exposure to dietary lead. Serum levels of total protein, albumin, SOD, CAT and glutathione (GSH) were significantly increased in fish fed with both non-encapsulated and microencapsulated probiotics (P&lt;0.05). However, microencapsulated probiotic showed the greatest potential for alleviation of the disturbed activities of intestinal and hepatic enzymes, and improvement of serum biochemical and antioxidant parameters. Our findings suggest that L. delbrueckii subsp. bulgaricus, particularly in the microencapsulated form, can be used as a potential probiotic to protect rainbow trout from dietborne lead toxicity.

Differential iNKT and T Cells Activation in Non-Alcoholic Fatty Liver Disease and Drug-Induced Liver Injury.

Background: Non-alcoholic fatty liver disease (NAFLD) and idiosyncratic drug-induced liver injury (DILI) could share molecular mechanisms involving the immune system. We aimed to identify activation immunological biomarkers in invariant natural killer T (iNKT) and CD4/CD8+ T cells in NAFLD and DILI. Methods: We analyzed the activation profile (CD69, CD25, and HLA-DR) and natural killer group 2 member D (NKG2D) on iNKT cells, and CD4/CD8 T cells in peripheral blood mononuclear cells from NAFLD, with or without significant liver fibrosis, and DILI patients. Results: There was an increase in iNKT cells in NAFLD patients compared to DILI or control subjects. Regarding the cellular activation profile, NAFLD with significant liver fibrosis (F ≥ 2) displayed higher levels of CD69+iNKT cells compared to NAFLD with none or mild liver fibrosis (F ≤ 1) and control patients. CD69+iNKT positively correlated with insulin resistance, aspartate aminotransferase (AST) level, liver fibrosis-4 index (FIB4) and AST to Platelet Ratio Index (APRI). DILI patients showed an increase in CD69+ and HLA-DR+ in both CD4+ and CD8+ T cells, detecting the most relevant difference in the case of CD69+CD8+ T cells. Conclusions: CD69+iNKT may be a biomarker to assess liver fibrosis progression in NAFLD. CD69+CD8+ T cells were identified as a potential distinctive biomarker for distinguishing DILI from NAFLD.

Hepatoprotective Effect of Cereal Vinegar Sediment in Acute Liver Injury Mice and Its Influence on Gut Microbiota.

Cereal vinegar sediment (CVS) is a natural precipitate formed during the aging process of traditional grain vinegar. It has been used as Chinese traditional medicine, while its composition and function are reported minimally. In this study, we measured CVS in terms of saccharide, protein, fat and water content, and polyphenol and flavonoid content. Furthermore, we determined the amino acids, organic acids, and other soluble metabolites in CVS using reverse-phase high-performance liquid chromatography (RP-HPLC), HPLC, and liquid chromatography with tandem mass spectrometry (LC-MS/MS) platforms. The hepatoprotective effect of CVS was evaluated in acute CCl4-induced liver injury mice. Administration of CVS for 7 days prior to the CCl4 treatment can significantly decrease liver alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and reactive oxygen species (ROS) levels, compared with those in the hepatic injury model group. The gut microbiota was changed by CCl4 administration and was partly shifted by the pretreatment of CVS, particularly the Muribaculaceae family, which was increased in CVS-treated groups compared with that in the CCl4 administration group. Moreover, the abundances of Alistipes genus and Muribaculaceae family were correlated with the liver ALT, AST, and malondialdehyde (MDA) levels. Our results illustrated the composition of CVS and its hepatoprotective effect in mice, suggested that CVS could be developed as functional food to prevent acute liver injury.

Effects of Three-Layer Encapsulated Tea Tree Oil on Growth Performance, Antioxidant Capacity, and Intestinal Microbiota of Weaned Pigs.

Tea tree oil (TTO) exerts key roles in improving growth performance of pigs. However, knowledge is limited regarding comparative effects of Encp TTO and Un-encp TTO supplementation on growth performance of pigs. A study determined the effects of TTO or its capsulation on growth performance, antioxidant capacity, and intestinal microbiome of weaned pigs. A total of 144 healthy pigs (8.5 ± 0.24 kg) were subjected to four treatments for a 28-d trial with six replicates per treatment and six pigs per pen: negative control, NC; positive control, PC (antibiotic supplemented); Un-encp TTO (supplemented with unencapsulated TTO); Encp TTO (supplemented with encapsulated TTO). NC, TTO, and PC treatments were compared with regard to improved average daily gain (ADG), average daily feed intake (ADFI), feed conversion rate, nutrient digestibility, and intestinal morphology (p < 0.05) and decreased diarrhea rate. TTO- and PC-treated pigs had higher levels of serum superoxide dismutase, glutathione peroxidase, and immunoglobulin G; lower levels of liver aspartate aminotransferase and alanine aminotransferase; and improved concentrations of interleukin 10 (IL-10), tumor necrosis factor α, and IL-1β (p < 0.05). TTO- and PC-treated pigs had higher abundance of beneficial bacterial species Subdoligranulum and lower abundance of diarrhea associated species Escherichia–Shigella in cecal and colonic digesta (p < 0.05). Encapsulation of TTO preserved more activities of TTO than its unencapsulated counterpart by showing higher ADG, ADFI, and feed conversion rate during day 1 (d1) to d14 (p < 0.05) and tended to lower diarrhea rate (p = 0.083) and improve villous height/crypt depth (VH/CD) ratio (p = 0.089) in jejunum. Encapsulation of TTO also improved antioxidant indexes and decreased liver injury and inflammation accordingly (p < 0.05). Encapsulated TTO-treated pigs had higher abundance of beneficial Clostridium_sensu_stricto_1 and lower the abundance of harmful Escherichia–Shigella in cecal and colonic digesta (p < 0.05). Our results demonstrated TTO benefits on improving growth performance of weaned pigs and further proved that encapsulation of TTO was superior to its unencapsulated counterpart at multiples. Encapsulated TTO was similar to the PC group and could be potentially an alternative of feed antibiotics for weaned pigs.

Atherogenic index and lipid profiles in albino rats fed with surface modified Hibiscus sabdariffa cellulose

Despite the several applications of modified cellulose, there is limited information on their safety, and antidyslipidemic functions, which are the focus of this study. To address this, cellulose isolated from Hibiscus sabdariffa cellulose was surface modified using nitrilotriacetic acid to produce nitrilotriacetic acid modified Hibiscus sabdariffa cellulose (HSNT). It was characterized using Fourier transformed infrared spectroscopy (FTIR), X-ray diffraction (XRD), thermogravimetric (TGA) analysis, scanning electron microscopy (SEM) and carbon, hydrogen, nitrogen, sulfur/oxygen (CHNS/O) analyzer. The study further investigated the safety of HSNT at the doses of 50, 100, and 150 mg kg−1 body weight in albino rats after a 7-day uninterrupted oral gavage. Histology of cardiac and hepatic tissues was observed, in addition to estimation of clinico-biochemical parameters such as atherogenic index of plasma (AIP), Castelli's risk index (CRI-1), total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), albumin (ALB), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). FTIR revealed peaks corresponding to the synthesis of HSNT, while XRD showed HSNT to have a crystallinity index of 53.20% with a type I cellulose crystal. HSNT had no significant effect on the absolute heart and liver weights, heart and liver organo-somatic indices, TG, AST, and ALB. Exposure to HSNT-50 caused a significant decrease in AIP levels. However, administration of HSNT-100 and 150 significantly reduced ALT, total cholesterol, and CRI-1 levels but caused a significant elevation in HDL-C levels. Cardiac histology revealed mild inflammatory and fatty infiltration of the myocardium, while the significant indications of the hepatic morphology included congestion of vessels and mild focal periportal infiltration at the HSNT-100 and HSNT-150 doses. Our preliminary data seem to indicate the potential of HSNT modification to resolve blood lipid abnormalities and make a case for an expanded study on its cardio-hepatic effects as well as study to understand the causes of congestion in hepatic vessels.

Alcohol overuse increases susceptibility to malaria and its complications: a pilot study

Malaria has remained a dangerous disease that has been posing great burden to man and his wellbeing. Several factors influence the susceptibility to this disease including genetic and environmental determinants. The role of alcohol on malaria parasite infection and its complications is not well-defined. It is established that malaria infection and alcohol independently influence the immune system of man and other animals. Therefore, it is logical to reason that their combined influence may be additive. The aim of this study was to investigate the effect of alcohol on determinants of malaria infection in mice. Nine groups of mice (n = 5) were used with group one serving as normal control, group 2 (alcohol control) received 12 g/kg b.w/d. of 50% absolute ethanol p.o only for 7 days and group 3 was parasitized only (parasite control). Groups 4-6 received 12 g/kg b.w/d. of 10, 30 and 50% ethanol, respectively for 7 days prior to parasite inoculation. Similarly, groups 7-9 were parasitized and thereafter received 12 g/kg b.w/d. of 10, 30 and 50 % ethanol, respectively 24-h after parasite inoculation till the next 7 days. In each case, malaria infection was confirmed 72-h post-inoculation. Thereafter, overnight fasted blood samples were analyzed for malaria parasitemia (malaria parasite density), hematological indices (hemoglobin concentration, packed cell volume and erythrocyte and leukocyte counts), lipid profile (total cholesterol, triacylglycerol, low and high density lipoproteins), and liver (alanine and aspartate aminotransferases and total bilirubin) and kidney (urea and creatinine) status using standard methods. The results of various analyzed parameters in alcohol exposed mice infected with malaria parasite were compared with mice exposed to alcohol and malaria parasite alone using one-way analyses of variance. The result showed that parasitized alcohol-treated mice had higher malaria parasitemia (34.33 ± 2.53, 39.49 ± 1.71 and 54.12 ± 2.76 x104 parasites/μL, respectively for 10, 30 and 50 % ethanol) relative to parasitized mice not treated with alcohol (22.01 ± 1.35 x104 parasites/μL). In addition, concentration-based reduction in hematological status (packed cell volume, hemoglobin concentration, and erythrocyte and leukocyte counts) was observed in alcohol-fed parasitized mice relative to parasite only and alcohol only controls. Furthermore, biochemical status indicating dyslipidemia as characterized by the elevation in total cholesterol, low density lipoprotein and triacylglycerol concentrations and decrease in high density lipoprotein level, hypoglycemia, renal and hepatic dysfunctions as indicated by increase in liver function markers as well as creatinine and urea levels in serum were observed in infected mice treated with alcohol relative to parasite only and alcohol only controls. In conclusion, this observation suggests that alcohol overuse exacerbates malaria parasitemia and suppresses immune response to malaria parasites, in a concentration-dependent manner, thereby promoting the progression and severity of complications associated with malaria. Further study to investigate the mechanism behind this preliminary observation is warranted.

Impacts of dietary zinc on growth performance, haematological indicators, transaminase activity and tissue trace mineral contents of soft‐shelled turtle ( Pelodiscus sinensis )

A 12-week growth trial was conducted to investigate the impacts of dietary zinc on growth performance, whole-body composition, haematological parameters, liver aspartate aminotransferase and alanine transaminase activity and tissue trace mineral contents of soft-shelled turtle (Pelodiscus sinensis). Approximately 4 g of turtles were fed fishmeal-based diets with 35.43, 46.23, 55.38, 66.74, 75.06 and 85.24 mg Zn/kg. Respiratory burst, red blood cells and intestine somatic index enhanced with escalating dietary Zn concentrations up to 55.38 mg/kg and then kept constant beyond this level. Escalating dietary Zn inclusion up to 66.74 mg/kg improved weight gain, survival rate, feed intake, albumin, haemoglobin, liver aspartate aminotransferase and alanine transaminase activity, carapace ratio and crude protein of turtles, beyond which they decreased. Osmolality, hepatosomatic index and crude lipid of turtles firstly declined with elevating dietary zinc levels from 35.43 to 55.38 mg/kg diet and then increased at a higher zinc level. Liver and muscle Zn concentrations enhanced with escalating dietary zinc inclusion, whereas Cu and Fe concentrations reduced. In summary, the optimal dietary zinc requirements for turtles were 61.27, 60.46 and 60.03 mg/kg diet, based on quadratic regression analysis derived from weight gain, aspartate aminotransferase and alanine transaminase activity, respectively.

Вплив тяжкості стеатозу підшлункової залози на перебіг неалкогольної жирової хвороби підшлункової залози в дiтей

Актуальність. Неалкогольна жирова хвороба підшлункової залози — надлишкове накопичення жиру в підшлунковій залозі, асоційоване з ожирінням, при виключенні вторинної етіології стеатозу. Неалкогольна хвороба печінки може мати прогредієнтний перебіг. Чи супроводжується прогресування неалкогольної жирової хвороби підшлункової залози специфічними структурними та лабораторними змінами, залишається неясним. Мета: встановити особливості сонологічних та лабораторних змін у дітей iз неалкогольною жировою хворобою підшлункової залози залежно від ступеня стеатозу. Матеріали та методи. Ми спостерігали 93 дітей віком від 7 до 17 років, середній вік 11,87 ± 2,82 року. Ступінь стеатозу підшлункової залози оцінювали за допомогою ультрасонографії. Пацієнтам проводили зсувнохвильову еластографію і стеатометрію (кількісну оцінку ступеня загасання ультразвуку з визначенням середнього коефіцієнта загасання ультразвуку (КЗУ)) підшлункової залози за допомогою апарату Ultima PA Expert («Радмір», Україна). Фіброз та стеатоз печінки були діагностовані з використанням апарату FibroScan 502 Touch (Франція) з функцією контрольованого параметра ультразвукового загасання (КПУЗ). Діти були розділені на наступні групи: 1-ша група — 50 пацієнтів зi стеатозом підшлункової залози й ожирінням/надмірною вагою; ця група була розділена на підгрупи: S1 — 20 осіб iз 1-м ступенем стеатозу підшлункової залози; S2 — 22 пацієн­ти з 2-м ступенем стеатозу підшлункової залози, S3 — 8 хворих iз 3-м ступенем стеатозу підшлункової залози; 2-га група — 30 пацієнтів без стеатозу підшлункової залози з ожирінням/надмірною вагою, 3-тя (контрольна) група — 13 дітей iз нормальною вагою. Пацієнтам були проведенi загальноклінічний аналіз крові з визначенням швидкості осідання еритроцитів (ШОЕ), біохімічна гепатограма (аланінамінотрансфераза (AЛТ), аспартатамінотрансфераза (АСТ), гамма-глутамілтранспептидаза (ГГТП), амілаза крові). Рівень інсуліну визначали за допомогою імуноферментного аналізу з розрахунком індексу інсулінорезистентності HOMA. Статистичний аналіз проводився з використанням програмного забезпечення Statistica 7.0 за допомогою дисперсійного аналізу (ANOVA) з наступним post hoc аналізом. Результати. У дітей групи S3 порівняно з контрольною групою продемонстровано більш високий рівень ШОЕ — в 1,86 раза (р = 0,01), АЛТ — в 1,86 (р = 0,006), АСТ — в 1,96 (р = 0,00019), ГГТП — в 2,10 раза (р = 0,0001). Ми виявили, що пацієнти зi стеатозом підшлункової залози мали більш високий рівень інсуліну порівняно з контрольною групою (підгрупа S1 — 18,38 ± 5,07 мкОД/мл, S2 — 30,76 ± 3,92 мкОД/мл, S3 — 33,70 ± 5,37 мкОд/мл; 2-га група — 18,70 ± 2,98 мкОд/мл; 3-тя група — 9,480 ± 5,067 мкОд/мл (р = 0,00262)). Також у пацієнтiв зi стеатозом підшлункової залози відмічено більш високий індекс HOMA порівняно з конт­рольною групою (S1 — 4,04 ± 0,87, S2 — 7,11 ± 0,96, S3 — 7,99 ± 1,35; 2-га група — 3,81 ± 0,73; 3-тя група — 1,94 ± 0,92 (p = 0,00156)). КПУЗ був підвищеним у дітей зi стеатозом підшлункової залози порівняно з конт­рольною групою (підгрупа S1 — 234,50 ± 9,94 дБ/м, S2 — 239,05 ± 8,99 дБ/м, S3 — 245,33 ± 17,21 дБ/м; 2-га група — 197,87 ± 7,70 дБ/м; 3-тя група — 172,754 ± 12,170 дБ/м (p = 0,00156)). КЗУ сягав максимальних рівнів у дітей підгрупи S3 (S1 — 2,55 ± 0,08 дБ/см, S2 — 2,56 ± 0,09 дБ/см, S3 — 2,74 ± 0,14 дБ/см; 2-га група — 2,26 ± 0,08 дБ/см; 3-тя група — 1,72 ± 0,15 дБ/см (р = 0,00001)). Пацієнти зі стеатозом підшлункової залози мали вищий рівень жорсткості печінки та підшлункової залози, проте значущість відмінностей була недостатньою. Висновки. Дослідження показало, що неалкогольна жирова хвороба підшлункової залози в дітей супроводжується стеатозом печінки, зростанням рівня маркерів запалення та інсулінорезистентності, що збільшуються при зростанні ступеня ­стеатозу.

Biochemical and Histopathological effects of Acetaminophen and Protective Effects of Naringin on Liver Rats

This study was conducted to find out liver protective activity of naringin (NRG) 40-80 mg/kg body weight(b.w.) against acetaminophen (ACN) 2g/kg induced liver damage in rats. Thirty two male rats were dividedinto four groups : group1: negative control, (1 ml/kg Saline orally) group II: positive control ACN (2g/kg), orally as single dose at first day, group III: ACN (2g/kg), orally as single dose at first day , plus NRG(40 mg//kg) orally for (8) consecutive days, group IV: ACN (2g/kg), orally as single dose at first day , plusNRG (80 mg//kg) orally for (8) consecutive days. All the rats were anesthetized to collect blood then killedon the (9) day of the experiment to take the liver samples. ACN induced liver damage was proved by asignificant (P&lt;0.01) reduction in the body weight , total protein (TP) , albumin (AB) , superoxide dismutase(SOD) and catalase (CAT) enzymes and a significant (P&lt;0.01) increased in liver weight, serum aspartatetransaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), total bilirubin (TB), directbilirubin (DB) , malondialdehyde enzyme (MAD) and histopathological changes. Protective liver toxicityeffect and oxidative damage caused by ACN significantly (P&lt;0.01) increasing in body weight, TP, AB ,SODand CAT and significantly (P&lt;0.01) decreasing in liver weight , AST, ALT, ALP, TB, DB and MAD andimproving tissue morphology by a meliorative in NRG 40 , 80 mg/kg b.w. These results confirm that NRGantioxidant effects can protect ACN induced hepatic toxicity in rats.

Berberine ameliorates nonalcoholic fatty liver disease by decreasing the liver lipid content via reversing the abnormal expression of MTTP and LDLR

The global incidence of nonalcoholic fatty liver disease (NAFLD) is increasing. The present study explored the effect and mechanism of berberine (BBR) on NAFLD in rats. Thirty-five Sprague-Dawley rats were randomly divided into the control and NAFLD groups, which were fed a normal diet or high-fat diet, respectively, for 8 weeks. Hematoxylin and eosin staining was performed on liver tissues and establishment of the NAFLD model was confirmed by microscopy. NAFLD rats were subsequently randomly subdivided and treated with saline or BBR for 8 weeks. The liver wet weight of rats in each group was measured, the liver tissue structure was observed by microscopy, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), fasting blood glucose (FBG), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) levels were detected using a semi-automatic biochemical detector. Reverse transcription-quantitative PCR and western blotting were performed to determine the mRNA and protein expression levels of microsomal triglyceride transfer protein (MTTP), apolipoprotein B and low-density lipoprotein receptor (LDLR). Compared with the control group, the liver wet weight of the NAFLD rats was higher; the liver showed obvious fatty degeneration and liver TG levels increased significantly, as did serum levels of ALT, AST, TC, TG, FBG, HDL and LDL, while expression of MTTP and LDLR significantly decreased. Compared with the saline-treated NAFLD rats, the BBR-treated rats had reduced liver wet weight, improved liver steatosis and a significant decrease in liver TG levels, while ALT, AST, TC, TG, and LDL serum levels significantly decreased and MTTP levels were significantly upregulated. In conclusion, BBR treatment ameliorated the fatty liver induced by a high-fat diet in rats. Furthermore, BBR reversed the abnormal expression of MTTP and LDLR in rats with high-fat diet induced-NAFLD. The present findings suggest that fatty liver could be improved by BBR administration, via reversing the abnormal expression of MTTP and LDLR and inhibiting lipid synthesis.

Protective effect of vitamin D in mice with acute liver failure

Objective: To explore the protective effect of vitamin D in acute liver failure through a mouse model. Methods: Acute liver failure was induced by combining D-galactosamine (D-GalN) lipopolysaccharide (LPS) to observe the effect of long-term vitamin D deficiency on liver injury and inflammatory signals in a mouse model. Acute liver failure was induced by thioacetamide (TAA) to observe the effect of vitamin D deficiency on the survival rate, and further high-dose of vitamin D supplementation protective effect was determined in a mouse model. Liver function was evaluated by measuring serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver inflammation by hematoxylin-eosin staining. The expressions of tumor necrosis factor (TNF-α), interleukin (IL) -1β, NOD-like receptor family, pyrin domain containing 3 (NLRP-3), chemokines (CCL2, CXCL1 and CXCL2), etc. in liver tissues were detected by RT-qPCR. The quantitation of macrophages in liver tissue was detected by immunohistochemistry. The comparison between groups were performed by t-test. The survival curve was analyzed by log-rank (Mantel-Cox) test. Results: Long-term vitamin D deficiency had increased acute liver failure sensitivity in mice, which was manifested by increased blood cell extravasation, massive necrosis of parenchymal cells, up-regulation of TNF-α, IL-1β, and NLRP-3 mRNA expression (P < 0.05), and increased macrophages quantitation (P < 0.05) in liver tissues. At the same time, vitamin D deficiency had increased the mice mortality rate because of liver injury (P < 0.01). On the contrary, pre-administration of high dose of vitamin D (100 IU/g) had significantly reduced liver injury, inhibited ALT and AST rise (P < 0.01), alleviated liver necrosis, and down-regulated the mRNA expression of inflammatory factors in liver tissues (P < 0.05). Conclusion: Mouse model shows that long-term vitamin D deficiency can aggravate drug-induced acute liver failure and reduce survival rates. Furthermore, high-dose of vitamin D has a certain hepatoprotective effect, which can significantly improve liver necrosis condition and inhibit inflammation. Therefore, adequate vitamin D can retain liver physiological balance to resist liver injury.

Effects of evodiamine on carbon tetrachloride-induced liver fibrosis mice based on modulating gut microbiota

Objective: To access the effects of evodiamine on carbon tetrachloride (CCl(4)) -induced liver fibrosis mice and study the mechanism based on modulating gut microbiota. Methods: From August 2019, 30 SPF male C57BL/6 mice were randomly divided into normal, model and evodiamine groups. Mice in control group received intraperitoneal injection of olive oil (2 ml/kg, twice per week) for 6 weeks. Mice in model and evodiamine groups received intraperitoneal injection of 20% CCl(4) (2 ml/kg, twice per week) for 6 weeks to induce liver fibrosis mice. Then, mice in evodiamine group received orally of evodiamine (18 mg/kg) for 4 weeks. The levels of serum alanine aminotransferase (ALT) , aspartate aminotransferase (AST) , albumin (ALB) and total protein (TP) were detected. The pathological changes of liver tissue were observed. The effects of evodiamine on the abundance and diversity of intestinal microflora in liver fibrosis mice were determined. The mRNA and protein expression levels of inflammatory factors[interleukin-6 (IL-6) , interleukin-1β (IL-1β) , and tumor necrosis factor α (TNF-α) ] in liver tissue were measured. Results: Compared with the normal group, the body weight, serum ALB and TP levels of the model group were decreased, the liver index, ALT and AST levels were increased, and the intestinal flora Shannon and Simpson indexes were decreased (P<0.01) . Compared with the normal group, the abundance of Lactobacillus, Akkermansia and Bacteroides in the feces of the model group decreased, while the abundance of Enterococcus and Lachnoclostridium increased (P<0.01) . Compared with the normal group, the mRNA and protein expressions levels of IL-6, IL-1β, and TNF-α in the liver tissue of the model group were significantly increased (P<0.01) . Compared with the model group, evodiamine could reduce liver index and serum ALT and AST levels, increase ALB and TP levels (P<0.05) , improve inflammatory cell infiltration and fibrosis degree in liver tissue, and up regulate intestinal flora Shannon and Simpson indexes in liver fibrosis mice (P<0.05) . Compared with the model group, evodiamine could increase the abundance of Lactobacillus, Akkermansia, Bacteroides, and reduce the abundance of Enterococcus and Lachnoclostridiun (P<0.05) . Compared with the model group, evodiamine could reduce the mRNA and protein levels of IL-6, IL-1β and TNF-α in liver tissue of liver fibrosis mice (P<0.05) . Conclusion: Evodiamine can ameliorate CCl(4)-induced liver fibrosis through modulating gut microbiota and inhibiting the inflammatory response in liver.

The Accumulative Effect of Heavy Metals on Liver and Kidney Functions

Some of the heavy metals exist in the outer layer of the earth, which is utilized for different economic andmanufacturing objectives. As some of these minerals impact humans in several ways, which are direct andindirect, others like Cadmium and Zinc are needed for several body activities, such as organ functions andbiological chemical processes. Within these tests, we employed analysis of liver enzyme, urea, and creatinine,to discover the damaged tissue causing after exposure to heavy metals. Results of liver function enzymes,Aspartate aminotransferase (AST), Alanine transaminase (ALT), and Alkaline phosphatase (ALP), wereregistered a significantly increasing (P?0.05) for control, Cadmium treatment and zinc treatment groups,with (32.1, 39.3, and 30.5) IU/ml, (9.6, 16.0, and 8.4) IU/ml, and (1.6, 2.5 and 2.12) IU/ml, respectively.Cadmium administration was significantly reduced (P?0.05) in serum creatinine concentration (1.26) IU/ml, compared to the control group (2.02) IU/ml. While the average serum creatinine concentration increasedto (4.99) IU/ml after giving rat group Zinc solution. Moreover, the urea concentration was significantlydecreased to (18.85) IU/ml in the Cadmium treatment group than values of control and Zinc group (30.61,and 35.97) IU/ml, respectively.

高タンパク質摂取によるRat肝臓Aspartate Transaminaseの誘導 Aspartate Transaminaseタンパク質はrat肝臓細胞質の SDS-PAGEで確認できる

高タンパク質摂取によるRat肝臓Aspartate Transaminaseの誘導 Aspartate Transaminaseタンパク質はrat肝臓細胞質の SDS-PAGEで確認できる

Knockout of calpain-1 protects against high-fat diet-induced liver dysfunction in mouse through inhibiting oxidative stress and inflammation.

The present study was designed to investigate the significance of calpain‐1 in the high‐fat diet (HFD)‐induced liver dysfunction and to explore the possible mechanism. C57 mice and calpain‐1 knockout (KO) mice were fed with standard diet (SD) or HFD, respectively, for 16 weeks. The activities of calpain, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and superoxide dismutase (SOD) in serum and/or liver of mouse were measured. Lipid profiles in the serum and liver were examined. Contents of oxidized low‐density lipoprotein (oxLDL), malondialdehyde (MDA), tumor necrosis factor (TNF‐α), and interleukin‐6 (IL‐6) in serum or/and liver were detected. The results showed that compared with C57 mice fed with SD, HFD‐fed C57 mice showed the increased activities of AST and ALT in the serum, which was decreased in calpain‐1 KO mice fed with HFD. In addition, knockout of calpain‐1 decreased the contents of oxLDL, MDA, TNF‐α, and IL‐6, while increased SOD activity, in serum and/or liver. However, knockout of calpain‐1 had no effects on lipid profiles in both serum and liver. When fed with SD, all these parameters of C57 and calpain‐1 KO mice were comparable except for decreased calpain activity in the liver of calpain‐1 KO mice. The results suggested that knockout of calpain‐1 protects against HFD‐induced liver dysfunction through inhibiting oxidative stress and inflammation.

The Effect of Lecithins Coupled Decorin Nanoliposomes on Treatment of Carbon Tetrachloride-Induced Liver Fibrosis.

This study aimed to investigate the effect of bile duct-targeting lecithins- (PC-) coupled decorin (DCN) (PC-DCN) nanoliposomes against liver fibrosis in vitro and in vivo. We prepared PC-DCN nanoliposomes by using rat astrocytes, HSC-T6, to verify the antifibrosis effect of PC-DCN in vitro. First, we established a rat model of carbon tetrachloride-induced fibrosis. PC-DCN nanoliposomes were then injected into fibrotic rats via the portal vein or bile duct. The EdU assay was performed to analyze cell proliferation. Immunofluorescence staining was used to detect α-smooth muscle actin (α-SMA) expression. Western blot was performed to examine the expression of α-SMA, collagen type I alpha 1 (COL1A1), and transforming growth factor-β (TGF-β) protein. The levels of aspartate transaminase (AST), alanine transaminase (ALT), and total bilirubin (TBIL) were examined by enzyme-linked immunosorbent assay (ELISA) analysis. Hematoxylin and eosin (H&E) staining and Masson trichrome staining were used to determine liver tissue lesions and liver fibrosis. Compared with TGF-β group, PC-DCN treatment could significantly reduce cell proliferation. Western blot analysis indicated that the expression of α-SMA, COL1A1, and TGF-β was downregulated after treatment with PC-DCN in vitro and in vivo. Immunofluorescence staining confirmed that α-SMA expression was reduced by PC-DCN. Furthermore, H&E staining and Masson trichrome staining showed that the administration of PC-DCN nanoliposomes via the bile duct could reduce the extent of liver fibrosis. PCR analysis showed that PC-DCN administration could reduce proinflammatory cytokines IL-6, TNF-α, and IL-1β expression via the bile duct. The administration of PC-DCN nanoliposomes also significantly downregulated liver function indicators ALT, AST, and TBIL. The results of our study indicated that PC-DCN could effectively reduce the extent of liver fibrosis.

Dietary choline requirement of juvenile Chinese sucker (Myxocyprinus asiaticus)

An 8-week growth experiment was conducted to quantify the appropriate dietary choline requirement of juvenile Chinese sucker (Myxocyprinus asiaticus). Each of seven semi-purified diets containing choline at a level of 44.79 (basal), 164.95, 278.70, 574.29, 1076.52, 2124.29 or 4477.72 mg/kg diet was fed to three replicates with 30 fish (5.52 g per fish). The results showed that weight gain and specific growth rate increased significantly with the increase of dietary choline levels from 44.79–574.29 mg/kg, and then decreased above these levels. Fish fed the basal diet had the lowest survival rate and feed efficiency. Choline contents in whole body and muscle tissues showed an increasing trend and then stabilized with increasing dietary choline supplementation. Dietary choline had no significant effects on whole-body moisture, crude protein, crude lipid and ash contents, but had a significant effect on muscle crude lipid content. Liver aspartate aminotransferase and alanine aminotransferase activities increased firstly and then decreased with the increase in dietary choline levels, whereas the changes in liver triglyceride content exhibited an opposite trend. Broken-line regression analysis showed that dietary choline requirement for juvenile Chinese sucker was 493.8 and 549.7 mg/kg based on specific growth rate and muscle choline content, respectively.

Therapeutic effects of chitin from Pleurotus eryngii on high-fat diet induced obesity in rats.

Recent shifts in lifestyles and diets have caused the incidence of obesity to increase rapidly, resulting in a serious threat to modern human health. There is a growing interest the use of plant or fungi derived supplements as a safe and effective means to treat obesity. In recent times, edible-medicinal fungi have garnered attention as therapeutics owing to their biocompatibility and effectiveness. Attempts to determine the therapeutic effects of these fungi have become a prime focus in drug discovery programs. Therefore, this study aimed to determine the anti-obesity effects of P. eryngii chitin in rats with obesity induced by administration of a high fat diet. To investigate the therapeutic effects of chitin from Pleurotus eryngii on high fat diet-induce obesity, we treated obese rats with different concentrations of chitin from P. eryngii for 4 weeks, using Lipitor as positive control. The living condition, food intake, body weight, perirenal adipose tissue, periepididymal adipose tissue, adipose tissue coefficient, serum lipid levels, including total cholesterol (TC), total glyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), were measured, and levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), themalonaldehyde (MDA), and superoxide dismutase (SOD) activity in liver were determined. The rats were also monitored for pathological changes in the liver and aorta. These studies indicated that administration of chitin from P. eryngii could significantly decrease obese rat food utilization rates and accumulation of adipose tissue in the body, thus preventing development of increased body weight. The treatment also significantly reduced serum lipid levels, including levels of TC, TG and LDL-C. Treatment with P. eryngii-derived chitin also enhanced ALT and AST enzymatic activity, enhanced SOD enzymatic activity, and reduced the MDA content of the liver, as well as significantly reducing the liver index and alleviating liver steatosis and aortic atherosclerosis resulting from obesity. In conclusion, chitin from P. eryngii had therapeutic effects on hyperlipidemia, fatty liver, and aortic atherosclerosis resulting from obesity in rats.