OBJECTIVE:To investigate the effect of acupuncture of"Daimai"(GB26) on abdominal fat accumulation, lipid metabolism and hepatic oxidative stress in abdominal obese non-alcoholic fatty liver disease (NAFLD) rats.

METHODS:male SD rats were divided into 3 groups: normal diet (normal,＝8), high fat diet control (model) and acupuncture (＝8/group in the latter 2 groups). The abdominal obese NAFLD model was established by feeding the rats with high fat diet for 12 weeks. EA (2 Hz/15 Hz, 1.5 mA) was applied to bilateral GB26 for 20 min, once every other day for 8 weeks. Rats of the model group were also restrained for 20 min as those in the EA group. The body mass and abdominal circumference were measured weekly, the isolated adipose tissues around the bilateral kidney and epididymis and the fresh liver were weighed. The contents of serum cholesterol (TC), triglyceride (TG), alanine transaminase (ALT), glutamic oxaloacetic aminotransferase (AST) were detected by using an automatic biochemical analyzer. The abdominal visceral fat distribution was acquired by CT scanning. The oxidative stress indexes of the homogenated liver tissues, such as malondialdehyde (MDA) was assayed using sodium thiobarbital (TBA) method, and theactivity of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) were assayed by using hydroxylamine method and colorimetric method respectively. The histopathological changes of the liver were observed after staining with hematoxylin-eosin (HE).

RESULTS:Following modeling, the body mass and waist circumference, visceral fat weight of bilateral kidneys and testis (visceral fat weight), liver weight, serum ALT, AST, TG and TC and liver MDA contents, were significantly higher in the model group (<0.001，<0.05), while hepatic T-SOD and GSH-PX activity was considerably lower in the model group than those in the normal group (<0.001). After acupuncture intervention, the levels of all the above-mentioned indexes (modeling induced both increase and decrease) were reversed relevant to the model group (<0.05,<0.01). The results of CT scanning showed that the fat accumulation area in the abdomen was 8.67 cm18.51 cmand 13.75 cmin the normal, model and acupuncture groups, respectively, presenting a decrease after acupuncture. H．E. staining displayed that the degree of hepatic steatosis (including vague hepatic lobule boundary, disordered arrangement of hepatic cord, hepatocellular swelling, diffuse fatty degeneration, unequal-sized lipid droplets in the hepatocytes, nucleus excursion and dissolution after modeling) wasimproved after acupuncture.

CONCLUSION:Acupuncture can reduce body weight and abdominal fat accumulation in abdominal obese NAFLD rats, which may be related to its effects in inhibiting oxidative stress (lowering MDA level and increasing the activity of T-SOD and GSH-PX) and improving hepatic lipid metabolism.

The aim of the present study was to investigate the impact of the combined administration of Vitamin C and silymarin on lead toxicity. Male albino rats were subdivided into three groups: the first was a control group, the second received lead acetate in diet as 500 mg/kg diet daily, the third received the same lead acetate dose and supplemented with Vitamin C (1 mg/100g body weight) and silymarin (1 mg/100g body weight) by gastric tube three times per week. Blood samples were taken after 2, 4 and 6 weeks of treatment. Significant lead-induced elevations in serum ALT, AST, GGT and ALP activities were observed after different periods of treatment. However, serum LDLc was decreased. The intensities of RNA and apoptotic fragments of DNA were measured as optical density by Gel-pro program. Lead acetate decreased the intensity of DNA at 6 weeks and induced apoptotic DNA fragments reversibly with time. After 2 weeks of lead administration dilation and congestion of terminal hepatic veins and portal vein branches were observed. Lead also induced hepatocyte proliferation without any localized distribution among zones 1-3. Portal inflammatory infiltrate with disruption of the limiting plates (interface hepatitis), steatosis, apoptosis and mild fibrosis were detected especially by sixth week of lead administration. Combined treatment of lead-exposed animals with Vitamin C and silymarin showed marked improvement of the biochemical, molecular and histopathological findings. These experimental results strongly indicate the protective effect of Vitamin C and silymarin against toxic effects of lead on liver tissue.

Inonotus obliquus is a traditional mushroom well known for its therapeutic value. In this study, various solvent fractions of I. obliquus were preliminarily screened for their antioxidant,α-amylase and α-glucosidase inhibition properties. To improve the drug delivery, the active fraction (ethyl acetate fraction) of I. obliquus was synthesized into fungisome (ethyl acetate phophotidyl choline complex, EAPC) and its physical parameters were assessed using Fourier transform infrared spectroscopy (FTIR), High performance liquid chromatography (HPLC), Scanning electron microscope (SEM), and ς potential analysis. Then normal human hepatic L02 cells was used to evaluate the cytotoxicity of EAPC. The results showed that EA fraction possesses significant free radical scavenging, α-amylase and α-glucosidase inhibition properties. FTIR, SEM, and HPLC analysis confirmed the fungisome formation. The particle size of EAPC was 102.80 ± 0.42 nm and the ς potential was -54.30 ± 0.61 mV. The percentage of drug entrapment efficiency was 97.13% and the drug release rates of EAPC in simulated gastric fluid and simulated intestinal fluid were 75.04 ± 0.29% and 93.03 ± 0.36%, respectively. EAPC was nontoxic to L02 cells, however it could selectively fight against the HOinduced oxidative damage in L02 cells. This is the first study to provide scientific information to utilize the active fraction of I. obliquus as fungisome. PRACTICAL APPLICATIONS: Inonotus obliquus (IO) is a traditional medicinal fungus. The extracts of IO have obvious antioxidant and hypoglycemic activities. Ethyl acetate (EA) fraction of IO was encapsulated in liposomes to form EAPC. EAPC has a sustained-release effect. It has nontoxic to L02 cells and could protect L02 cells from oxidative damage caused by hydrogen peroxide. This study could provide new ideas for the treatment of diabetes.

Aldehyde reductase (AKR1A) plays a role in the biosynthesis of ascorbic acid (AsA), and AKR1A-deficient mice produce about 10-15% of the AsA that is produced by wild-type mice. We found that acetaminophen (AAP) hepatotoxicity was aggravated in AKR1A-deficient mice. The pre-administration of AsA in the drinking water markedly ameliorated the AAP hepatotoxicity in the AKR1A-deficient mice. Treatment of the mice with AAP decreased both glutathione and AsA levels in the liver in the early phase after AAP administration, and an AsA deficiency delayed the recovery of the glutathione content in the healing phase. While in cysteine supply systems; a neutral amino acid transporter ASCT1, a cystine transporter xCT, enzymes for the transsulfuration pathway, and autophagy markers, were all elevated in the liver as the result of the AAP treatment, the AsA deficiency suppressed their induction. Thus, AsA appeared to exert a protective effect against AAP hepatotoxicity by ameliorating the supply of cysteine that is available for glutathione synthesis as a whole. Because some drugs produce reactive oxygen species, resulting in the consumption of glutathione during the metabolic process, the intake of sufficient amounts of AsA would be beneficial for protecting against the hepatic damage caused by such drugs.

Seven new triterpenes, inonotusol A-G (1-7), one new diterpene, inonotusic acid (8), and 22 known compounds were isolated from Inonotus obliquus. Their structures were elucidated on the basis of spectroscopic analysis, including homonuclear and heteronuclear correlation NMR ((1)H-(1)H COSY, ROESY, HSQC, and HMBC) experiments. In in vitro assays, compounds 6 and 8-16 showed hepatoprotective effects against d-galactosamine-induced WB-F344 cell damage, with inhibitory effects from 34.4% to 81.2%. Compounds 7, 17, and 18 exhibited selective cytotoxicities against KB, Bel-7402, or A-549 cell lines. Compounds 16 and 17 showed inhibitory effects against protein tyrosine kinases, with IC50 values of 24.6 and 7.7μM, respectively.

The culinary and medicinal mushroom Hericium erinaceus is widely consumed in Asian countries, but apparently not in the United States, for its nutritional and health benefits. To stimulate broader interest in the reported beneficial properties, this overview surveys and consolidates the widely scattered literature on the chemistry (isolation and structural characterization) of polysaccharides and secondary metabolites such as erinacines, hericerins, hericenones, resorcinols, steroids, mono- and diterpenes, and volatile aroma compounds, nutritional composition, food and industrial uses, and exceptional nutritional and health-promoting aspects of H. erinaceus. The reported health-promoting properties of the mushroom fruit bodies, mycelia, and bioactive pure compounds include antibiotic, anticarcinogenic, antidiabetic, antifatigue, antihypertensive, antihyperlipodemic, antisenescence, cardioprotective, hepatoprotective, nephroprotective, and neuroprotective properties and improvement of anxiety, cognitive function, and depression. The described anti-inflammatory, antioxidative, and immunostimulating properties in cells, animals, and humans seem to be responsible for the multiple health-promoting properties. A wide range of research advances and techniques are described and evaluated. The collated information and suggestion for further research might facilitate and guide further studies to optimize the use of the whole mushrooms and about 70 characterized actual and potential bioactive secondary metabolites to help prevent or treat human chronic, cognitive, and neurological diseases.

The effect of broccoli extract (BE)-enriched diet was studied in order to evaluate its ability to counteract liver cholesterol oxidation products (COPs) induced by acute strenuous exercise in rats. Thirty-two female Wistar rats were randomly divided into four groups: control diet without exercise (C), BE-enriched diet without exercise (B), control diet with acute exhaustive exercise (S) and BE-enriched diet with acute exhaustive exercise (BS). The study lasted 45days and on the last day, rats of S and BS groups were forced to run until exhaustion on a treadmill. Glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT) and cholesterol oxidation products (COPs) were determined in liver. Exhaustive exercise was clearly responsible for tissue damage, as evidenced by the increase of lactate dehydrogenase (LDH) plasma activity in the S group. Moreover, the exercise protocol reduced CAT activity in liver, while it did not affect GST, GR and GPx. BE-enriched diet raised GST, GR and CAT activities in rats of BS group. The main COPs found were 7α-hydroxycholesterol, 7β-hydroxycholesterol, 7-ketocholesterol, cholestanetriol, 24-hydroxycholesterol and 27-hydroxycholesterol. The BE-enriched diet led to reduced cholesterol oxidation following exhaustive exercise; the highest level of COPs was found in the S group, whereas the BS rats showedthe lowest amount. This study indicates that the BE-enriched diet increases antioxidant enzyme activities and exerts an antioxidant effect towards cholesterol oxidation in rat liver, suggesting the use of phytochemicals in the prevention of oxidative damage and in the modulation of the redox environment.

Nonalcoholic fatty liver disease (NAFLD) is considered one of the most common and most important conditions affecting the liver, because of its increasing prevalence all over the world. It is usually associated with elevated liver enzymes and ranges from simple steatosis to liver cirrhosis. This study was conducted to compare the effects of electroacupuncture (EA) versus aerobic interval training (AIT) exercise and how they affect liver functions in people suffering from nonalcoholic fatty liver.This study was carried out on 50 female patients suffering from NAFLD with age ranging from 30 to 55 years; they were randomly divided into two equal groups: group A received (EA) stimulation at points of liver 3 (LR3), liver 14 (LR14), gall bladder 34 (GB34), and stomach 36 (ST36), whereas group B received AIT exercise. All patients in both groups A and B received 3 sessions per week for 6 weeks (receiving noninterrupted 18 sessions) in addition to their standard medications. Evaluation of all patients in both groups A and B was carried out before and after the treatment program by measuring the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TGs), and C-reactive protein (CRP).There is a significant decrease ( < 0.05) of ALT, AST, TGs, and CRP within each group, A and B, after 6 weeks of treatment sessions. A significant difference post-treatment was found between both groups in ALT, AST, and TGs ( < 0.05). However, there was no significant difference in CRP ( > 0.05) between both groups post-treatment.It can be concluded that both EA and AIT exercise are potent modalities that improve liver functions in people with NAFLD with better effect toward EA.

BACKGROUND:The use of devices emitted microwave radiation such as mobile phones, wireless fidelity (Wi-Fi) routers, etc. is increased rapidly. It has caused a great concern; the researchers should identify its effects on people's health. We evaluated the protective role of Vitamin C on the metabolic and enzymatic activities of the liver after exposure to Wi-Fi routers.

MATERIAL AND METHODS:70 male Wistar rats weighing 200-250 g were randomly divided into 7 groups (10 rats in each group).The first stage one -day test: Group A (received vitamin C 250 mg/kg/day orally together with 8- hour/day Wi-Fi exposure).Group B (exposed to Wi-Fi radiation). Group C (received vitamin C). Group D or Control (was neither exposed to radiation of Wi-Fi modem nor did receive vitamin C). The second phase of experiment had done for five consecutive days. It involved Group E (received vitamin C), Group F (exposed to Wi-Fi radiation), Group G (received vitamin C together with Wi-Fi radiation). The distance between animals' restrainers was 20 cm away from the router antenna. Finally, blood samples were collected and assayed the level of hepatic enzymes including alkaline phosphatase(ALP), alanine amino transferase(ALT) aspartate amino transferase (ASL), gamma glutamyl transferase (GGT) and the concentration of Blood Glucose, Cholesterol , Triglyceride(TG),High density lipoprotein (HDL)and low density lipoprotein (LDL).

RESULTS:Data obtained from the One day test showed an increase in concentration of blood glucose, decrease in Triglyceride level and GGT factor (P<0.05), however no observed significant difference on the Cholesterol , HDL , LDL level and hepatic enzymes activities in compare to control group. Groups of the five-day test showed reduction in the amount of blood glucose, elevation of cholesterol level and LDL relative to control group(P<0.05).

CONCLUSION:WiFi exposure may exert alternations on the metabolic parameters and hepatic enzymes activities through stress oxidative and increasing of free radicals, but the use of vitamin C protects them from changing induced. Also taking optimum dose of vitamin C is essential for radioprotective effect and maintaining optimum health.

Background and Aims. This study examined if exercise and omega-3 fatty acid (n3PUFA) supplementation is an effective treatment for hepatic steatosis in obese, hyperphagic Otsuka Long-Evans Tokushima Fatty (OLETF) rats.

Methods. Male OLETF rats were divided into 4 groups (n = 8/group): (1) remained sedentary (SED), (2) access to running wheels; (EX) (3) a diet supplemented with 3% of energy from fish oil (n3PUFA-SED); and (4) n3PUFA supplementation plus EX (n3PUFA+EX). The 8 week treatments began at 13 weeks, when hepatic steatosis is present in OLETF-SED rats.

Results. EX alone lowered hepatic triglyceride (TAG) while, in contrast, n3PUFAs failed to lower hepatic TAG and blunted the ability of EX to decrease hepatic TAG levels in n3PUFAs+EX. Insulin sensitivity was improved in EX animals, to a lesser extent in n3PUFA+EX rats, and did not differ between n3PUFA-SED and SED rats. Only the EX group displayed higher complete hepatic fatty acid oxidation (FAO) to CO(2) and carnitine palmitoyl transferase-1 activity. EX also lowered hepatic fatty acid synthase protein while both EX and n3PUFA+EX decreased stearoyl CoA desaturase-1 protein.

Conclusions. Exercise lowers hepatic steatosis through increased complete hepatic FAO, insulin sensitivity, and reduced expression of de novo fatty acid synthesis proteins while n3PUFAs had no effect.

The failure of Kupffer cells (KCs) to remove endotoxin is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, the effects of exercise training on KC function were studied in terms of in vivo endotoxin clearance and inflammatory responses. Mice were allocated into rest and exercise groups. KC bead phagocytic capacity and plasma steroid hormone levels were determined following exercise training. Endotoxin and inflammatory cytokine levels in plasma were determined over time following endotoxin injection. KC bead phagocytic capacity was potentiated and clearance of exogenously-injected endotoxin was increased in the exercise group. Inflammatory cytokine (TNF-α and IL-6) levels were lower in the exercise group. We found that only DHEA was increased in the plasma of the exercise group. In an in vitro experiment, the addition of DHEA to RAW264.7 cells increased bead phagocytic capacity and attenuated endotoxin-induced inflammatory responses. These resultssuggest that exercise training modulates in vivo endotoxin clearance and inflammatory responses in association with increased DHEA production. These exercise-induced changes in KC capacity may contribute to a slowing of disease progression in NAFLD patients.

BACKGROUND & AIMS:The burden of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. We performed a meta-analysis to determine the effectiveness of exercise-based lifestyle interventions on liver-specific endpoints in populations with NAFLD and underlying metabolic disorders such as obesity, type-2 diabetes, or the metabolic syndrome.

METHODS:We searched PUBMED-MEDLINE, EMBASE, and the Cochrane Central register, through 21st October, 2015 for randomized trials of exercise-based lifestyle interventions on endpoints such as intrahepatic lipid content and blood levels of alanine and aspartate aminotransferases. Effect sizes are reported as standardized mean difference and weighted mean difference values. To investigate heterogeneity, we performed sensitivity and meta-regression analyses. Results were reported according to the PRISMA statement.

RESULTS:We analyzed data from 28 trials. Physical activity, independently from diet change, was associated with a significant reduction in intra-hepatic lipid content (standardized mean difference, -0.69; 95% confidence interval [CI], -0.90 to -0.48) and with reductions in alanine aminotransferase (weighted mean difference, -3.30 IU/l; 95% CI, 5.57 to -1.04) and aspartate aminotransferase (weighted mean difference, -4.85 IU/l; 95% CI, -8.68 to -1.02). By meta-regression, we found individuals with increasing body mass index to be increasingly more likely to benefit from the intervention (beta coefficient = -0.10; P=.037). We recorded no effect modification by variables related to the intensity of the intervention.

CONCLUSIONS:In a meta-analysis of randomized trials, we found strong evidence that physical activity reduces intrahepatic lipid content and markers of hepatocellular injury in patients with NAFLD. This effect correlated with baseline body mass index.

AIMS:Supervised exercise reduces liver fat and improves endothelial function, a surrogate of cardiovascular disease risk, in non-alcoholic fatty liver disease (NAFLD). We hypothesised that after a 16-week supervised exercise program, patients would maintain longer-term improvements in cardiorespiratory fitness, liver fat and endothelial function.

MATHERIALS AND METHODS:Ten NAFLD patients [5/5 males/females, age 51±13years, BMI 31±3 kg.m(2) (mean±s.d.)] underwent a 16-week supervised moderate-intensity exercise intervention. Biochemical markers, cardiorespiratory fitness (VO2peak), subcutaneous, visceral and liver fat (measured by magnetic resonance imaging and spectroscopy respectively) and brachial artery flow-mediated dilation (FMD) were assessed at baseline, after 16 weeks supervised training and 12-months after ending supervision.

RESULTS:Despite no significant change in body weight, there were significant improvements in VO2peak [6.5 ml.kg(-1).min(-1) (95% CI 2.8, 10.1); P=0.003], FMD [2.9% (1.5, 4.2); P=0.001], liver transaminases (P<0.05) and liver fat [-10.1% (-20.6, 0.5); P=0.048] immediately after the 16-weeks supervised training. Nevertheless, 12-months after ending supervision, VO2peak [0.9 ml.kg(-1).min(-1) (-3.3 5.1); P=0.65], FMD [-0.07% (-2.3, 2.2); P=0.95], liver transaminases (P>0.05) and liver fat [1.4% (-13.0, 15.9); P=0.83] were not significantly different from baseline.

CONCLUSIONS:Twelve months following cessation of supervision, exercise-mediated improvements in liver fat and other cardiometabolic variables had reversed with cardiorespiratory fitness at baseline levels. Maintenance of high cardiorespiratory fitness and stability of body weight are critical public health considerations for the treatment of NAFLD.International Journal of Obesity accepted article preview online, 21 July 2016. doi:10.1038/ijo.2016.123.

Recent studies have demonstrated that repeated short-term nutrient withdrawal (i.e. fasting) has pleiotropic actions to promote organismal health and longevity. Despite this, the molecular physiological mechanisms by which fasting is protective against metabolic disease are largely unknown. Here, we show that, metabolic control, particularly systemic and liver lipid metabolism, is aberrantly regulated in the fasted state in mouse models of metabolic dysfunction. Liver transcript assays between lean/healthy and obese/diabetic mice in fasted and fed states uncovered"growth arrest and DNA damage-inducible"GADD45β as a dysregulated gene transcript during fasting in several models of metabolic dysfunction including ageing, obesity/pre-diabetes and type 2 diabetes, in both mice and humans. Using whole-body knockout mice as well as liver/hepatocyte-specific gain- and loss-of-function strategies, we revealed arole for liver GADD45β in the coordination of liver fatty acid uptake, through cytoplasmic retention of FABP1, ultimately impacting obesity-driven hyperglycaemia. In summary, fasting stress-induced GADD45β represents a liver-specific molecular event promoting adaptive metabolic function.

A two-arm randomized open labeled controlled clinical trial was conducted on 50 patients with non-alcoholic fatty liver disease (NAFLD). Participants were assigned to take either a lifestyle modification (LM), or LM +30 g/day brown milled flaxseed for 12 weeks. At the end of the study, body weight, liver enzymes, insulin resistance and hepatic fibrosis and steatosis decreased significantly in both groups (p< 0.05); however, this reduction was significantly greater in those who took flaxseed supplementation (p < 0.05). The significant mean differences were reached in hepatic markers between flaxseed and control group, respectively: ALT [-11.12 compared with -3.7 U/L; P< 0.001], AST [-8.29 compared with -4 U/L; p< 0.001], GGT [-15.7 compared with -2.62 U/L; p < 0.001], fibrosis score [-1.26 compared with -0.77 kPa; p = 0.013] and steatosis score [-47 compared with -15.45 dB/m; p = 0.022]. In conclusion, flaxseed supplementation plus lifestyle modification is more effective than lifestyle modification alone for NAFLD management.

A two-arm randomized open labeled controlled clinical trial was conducted on 50 patients with non-alcoholic fatty liver disease (NAFLD). Participants were assigned to take either a lifestyle modification (LM), or LM +30 g/day brown milled flaxseed for 12 weeks. At the end of the study, body weight, liver enzymes, insulin resistance and hepatic fibrosis and steatosis decreased significantly in both groups (p< 0.05); however, this reduction was significantly greater in those who took flaxseed supplementation (p < 0.05). The significant mean differences were reached in hepatic markers between flaxseed and control group, respectively: ALT [-11.12 compared with -3.7 U/L; P< 0.001], AST [-8.29 compared with -4 U/L; p< 0.001], GGT [-15.7 compared with -2.62 U/L; p < 0.001], fibrosis score [-1.26 compared with -0.77 kPa; p = 0.013] and steatosis score [-47 compared with -15.45 dB/m; p = 0.022]. In conclusion, flaxseed supplementation plus lifestyle modification is more effective than lifestyle modification alone for NAFLD management.

BACKGROUND:The prevalence of nonalcoholic steatohepatitis (NASH) in menopausal women is increasing, but current treatments have not been proven effective. The objective of this study was to investigate the treatment effects of genistein and running exercise in ovariectomized (OVX) rats with NASH.

METHODS:Thirty-six female Sprague-Dawley rats were divided into 6 groups, control; OVX with standard diet; OVX with high fat and high fructose (HFHF) diet for 4 weeks; OVX with HFHF and genistein treatment (16 mg/kg BW/day) for 5 weeks (OVX + HFHF+GEN); OVX with HFHF and moderate intensity exercise for 5 weeks (OVX + HFHF+EX); OVX with HFHF and combined treatments (OVX + HFHF+GEN + EX). Serum interleukin-6 (IL-6) levels, hepatic free fatty acid (FFA), hepatic glutathione (GSH), and hepatic malondialdehyde (MDA) levels were measured. Liver histology was examined to determine NASH severity.

RESULTS:OVX + HFHF group had the highest levels of hepatic FFA compared with OVX and control groups (5.92 ± 0.84 vs. 0.37 ± 0.01 vs. 0.42 ± 0.04 nmol/mg protein, respectively, p < 0.01). Serum IL-6 levels were significantly elevated in both OVX and OVX + HFHF groups as compared with controls (112.13 ± 6.50 vs. 121.47 ± 3.96 vs. 86.13 ± 2.40 pg/mL, respectively, p < 0.01). In OVX + HFHF group, hepatic MDA levels were higher, while GSH levels were lower than in OVX and control groups (MDA; 0.98 ± 0.04 vs. 0.82 ± 0.02 vs. 0.78 ± 0.03 nmol/mg protein, and GSH; 46.01 ± 0.91 vs. 55.21 ± 1.40 vs. 57.94 ± 0.32, respectively; p < 0.01 for both). Comparing with OVX + HFHF group, rats that received genistein, exercise and combined treatments demonstrated an improvement in liver histopathology, decreased levels of hepatic FFA (1.44 ± 0.21 vs. 0.45 ± 0.04 vs. 0.49 ± 0.05 nmol/mg protein, respectively, p < 0.01), serum IL-6 (82.80 ± 2.07 vs. 83.47 ± 2.81 vs. 94.13 ± 1.61 pg/mL, respectively, p < 0.01), and hepatic MDA (0.80 ± 0.03 vs. 0.76 ± 0.02 vs. 0.76 ± 0.03 nmol/mg protein, respectively, p < 0.01).

CONCLUSIONS:Genistein and moderate intensity exercise were effective in reducing the severity of NASH in OVX rats through the reduction in liver inflammation, oxidative stress and liver fat contents.

Historically, botanicals have been reported to possess good antioxidative activities as demonstrated by their free radical scavenging property rendering their usage in liver protection. In this study, we describe the potential use of MAP, a standardized blend comprising three extracts from Myristica fragrans, Astragalus membranaceus, and Poria cocos, in ameliorating chemically induced acute liver toxicities. Acetaminophen (APAP) and carbon tetrachloride (CCl)-induced acute liver toxicity models in mice were utilized. Hepatic functional tests from serum collected at T24, histopathology analysis, and merit of blending three standardized extracts were evaluated. MAP administered at doses of 150-400 mg/kg showed statistically significant and dose-correlated inhibitions of serum alanine aminotransferase (ALT) ranging from 30.8% (P ≤ .05) to 88.1% (P = .0001) in the APAP and 66.9% (P = .002) to 83.7% (P = .0002) in the CClmodels, respectively. Moreover, MAP resulted in up to 75.7%, 60.9%, and 33.3% reductions in serum aspartate aminotransferase (AST), bile acid, and total bilirubin, respectively. Mice treated with oral doses of composition of MAP at 300 mg/kg showed statistically significant reduction in hepatocyte necrosis when compared with vehicle control. Unexpected synergistic protection of liver damage was also observed. Therefore, the composition, MAP, could be potentially utilized as an effective hepatic detoxifying agent for the protection of liver damage.

The effect of carrot extract on carbon tetrachloride (CCl4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl4 administration. Increased activities of hepatic 5'-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl4-induced hepatocellular injury.