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Bis(2-ethylhexyl) 2,3,4,5-tetrabromophthalate (TBPH) has been used as a replacement in some commercial flame-retardant mixtures. It is widely used in industrial products, so the probability of human exposure to TBPH is high. Yet, little is known about how it is metabolized or its toxicity. To this end, we investigated what effect oral exposure of Balb/c mice to TBPH at concentrations of 200 mg kg−1 had on hepatic damage. Staining results showed liver injury in the mice exposed to TBPH. Oxidative stress markers and endoplasmic reticulum stress associated proteins were altered in the TBPH exposed mice, and these changes could be attenuated by administration of curcumin at 25 mg kg−1. Overall, TBPH induces hepatic damage via increasing oxidative stress, and curcumin plays a protective role in alleviating the TBPH-mediated histopathological alterations in the liver.

The purpose of this study was to evaluate the hepatoprotective activity of cubebin isolated from Syringa oblata Lindl., Oleaceae, on hepatic damage in mice caused by carbon tetrachloride. Mice were divided into six groups and treated for 7 days as follows: the negative control and model group (CCl4 only) received 0.5% CMC-Na solution; the positive control group received bifendate (150 mg/kg); and the three experimental groups received daily doses of cubebin (150, 75, and 37.5 mg/kg, respectively) by gavage for 7 days. After the treatment, all groups were given 0.5% CCl4 olive oil solution (10 ml/kg) to evoke hepatic damage in mice, except for the negative control group. The hepatoprotective effects of cubebin were assessed using liver histopathology and biochemical parameters. Hepatotoxicity was assessed by measuring serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and hepatic levels of malondialdehyde, superoxide dismutase, and glutathione peroxidase. Cubebin treatment (150 mg/kg) exhibited significant hepatoprotective effects by improving CCl4-induced alterations of the biochemical and physiological indexes of serum and hepatic tissue. Histopathological observation showed that CCl4 causes substantial liver damage compared with untreated mice, whereas the administration of cubebin (150 mg/kg) notably prevents pathological damage of liver tissue. Hence, the therapeutical use of cubebin to protect from liver intoxication could be further explored.

The tropical fruit sapodilla (Manilkara zapota syn. Achras zapota) is a rich source of nutrients, minerals and a myriad of bioactive phytochemicals such as flavonoids and catechins. Pharmacologically, sapodilla has been shown to exhibit anti-bacterial, anti-parasitic, anti-fungal, antiglycative, hypocholesterolemic and anti-cancer effects. However, its influence on hepatic tissue and serum lipids remains obscure. To address this, we used an in vivo model of liver damage to elucidate the effect of lyophilized sapodilla extract (LSE) treatment in carbon tetra chloride (CCl4) intoxicated rats. Exposure of CCl4 resulted in elevation of serum biomarkers of liver damage (aspartate transaminase, alanine aminotransferase, γ-glutamyl transferase and alkaline phosphatase), bilirubin and dysregulation of serum lipid profile (cholesterol and triglycerides). These effects were significantly and dose-dependently reversed by LSE treatment (250 and 500 mg/kg). Administration of LSE also reduced the structural damage caused by CCl4 in the liver. Furthermore, determination of oxidative stress parameters (malondialdehyde and non-protein sulfhydryls) revealed that LSE treatment mitigated CCl4-triggered modulation of both molecules. LSE also showed a strong antioxidant activity in 2,2-diphenyl-1-picrylhydrazyl (DPPH) and β-carotene-linoleic acid assays. In conclusion, the present study discloses the hepatoprotective and lipid-lowering effects of lyophilized sapodilla extract against CCl4-induced liver damage, an effect, at least in part, mediated by its antioxidant activity.

The present study examined the protective effects of curcuminoid isolates from Curcuma longa against carbon tetrachloride (CCL4)-induced hepatic injury in rats. The hepatoprotective effect of the crude extract (150, 300 and 600 mg/kg bw) and curcuminoids (75, 150 and 300 mg bw) was evident by significant increases in the serum antioxidative defence capacities (super oxide dismutase, reduced glutathione, catalase) and reduction in biomarker enzymes of liver integrity (aspartate transaminase, alanine transaminase and alkaline phosphatase) in comparison to the results obtained in the CCL4-untreated animals. Some of these parameters were completely restored by pre-treatments with curcuminoids. Similarly, the curcuminoids increases the concentrations of total proteins, albumins and ameliorated histological changes observed in CCL4 injured rats. Therefore, curcuminoid could be considered a novel candidate for the development of new drug against liver diseases.

This study evaluated the prospective molecular and biochemical mechanisms behind the hepatoprotective effects of curcumin in Wistar rats exposed to KBrO3. Techniques for assessment of hepatic oxidative injury and histological biomarkers were used. The concentrations of proteins connected with inflammation (e.g. tumor necrosis factor-alpha (TNF-α), interleukins 1β (IL-1β) and C-reactive protein (CRP)) were estimated by enzyme-linked immunosorbent assay (ELISA) techniques. Results showed that, curcumin administered orally at a dose of 20 mg/kg for 28 days significantly suppressed the activities of serum transaminases and alkaline induced by KBrO3 administration (20 mg/kg, twice weekly) and protected the integrity of the liver tissue. Also, curcumin at the tested dose abridged the KBrO3-induced increase in hepatic malondialdehyde (MDA) levels and reversed KBrO3 mediated reduction in activities of hepatic antioxidant molecules including reduced glutathione (GSH), total thiol (TSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD). In addition, curcumin significantly assuaged inflammatory response in KBrO3-lesioned liver as revealed by the decrease in inflammatory biomarkers. This study suggests that curcumin exhibits a protective effect via induction of hepatic detoxification proteins and inhibition of inflammatory proteins in addition to its antioxidative ability in KBrO3- induced hepatic injury in rats.

The study was design to evaluate the antioxidant and anti-inflammatory effect of snack bars that made of black glutinous rice and pumpkin powder and study on the male Sprague Dawley rats. Twenty-five male rats in between the age of 2 and 3 months were selected and randomly divided into 5 groups, which were positive control, negative control, group with sylimarin treatment, snack bars A and snack bars B. Carbon tetrachloride was used to induce hepatic damage. The results showed that group with CCl4 treatment has 3.04 ± 0.16 μmol/L MDA while group with Sylimarin, snack bars A, snack bars B were 0.49 ± 0.05; 0.54 ± 0.05; and 1.15 ± 0.16 μmol/L MDA, respectively. The snack bars had the capacity to decline the damage in liver as much as Sylimarin (standardized natural medicine for hepatotoxicity). The SGPT (Serum Glutamin Pyruvic Transaminase) of the two treatment was 22.24 ± 0.80 U/I for Sylimarin and 22.33 ± 1.03 U/I for snack bars while SGOT (Serum Glutamic Oxaloacetic Transaminase) was 40.78 ± 0.77 U/I for Sylimarin and 40.88 ± 1.25 U/I for snack bars A. Snack bars B has a significantly different value on final SGOT and SGPT.

Hepatic ischemia/reperfusion injury (IRI) is aggravated by steatosis and is a main risk factor in fatty liver transplantation. Adenosine receptors (ARs) are emerging as therapeutic targets in liver diseases. By using cellular and in vivo systems of hepatic steatosis and IRI, here we evaluated the effects of pharmacological A2AR and A1R activation. The A2AR agonist CGS21680 protected the primary steatotic murine hepatocyte from IR damage and the activation of ASK1 and JNK. Such an effect was attributed to a phosphatidylinositol-3-kinase (PI3K)/Akt-dependent inhibition of ASK1. By contrast, the A1R agonist CCPA enhanced IR damage, intracellular steatosis and oxidative species (OS) production, thereby further increasing the lipid/OS-dependent ASK1-JNK stimulation. The CGS2680 and CCPA effects were nullified by a genetic ASK1 downregulation in steatotic hepatoma C1C7 cells. In steatotic mice livers, CGS21680 protected against hepatic IRI and ASK1/JNK activation whereas CCPA aggravated hepatic steatosis and IRI, and enhanced ASK1 and JNK stimulation. These results evidence a novel mechanism of CGS21680-mediated hepatoprotection, i.e., the PI3K/AKT-dependent inhibition of ASK1, and they show that CGS21680 and CCPA reduces and enhances the IRI of fatty liver, respectively, by preventing or increasing the activation of the cytotoxic ASK1/JNK axis. They also indicate the selective employment of A2AR agonists as an effective therapeutic strategy to prevent IRI in human fatty liver surgery.

Jaundice is a yellow pigmentation of the skin, the conjunctival membrane over the sclera and other mucous membrane caused by hyperbilirubinemia (increase level of bilirubin in blood). Today’s lifestyle with unhygienic and poor dietary habit and alcoholic habits, etc. which are responsible factor to promote hepatic damage which clinically reflect as kamala In this case study 25 years male patient having kamala who was suffering from pain in abdomen, weakness, anorexia, burning maturation and fever on and off, the patient was treated with shodhan chikitsa (Virechan with panchatikta ghrita) followed by shaman chikitsa. Patient got significant result as per the values of bilirubin with symptomatic relief in complaints within 30 days, Kamala can be successfully managed by shodhan and shaman chikitsa , the effect of ayurvedic treatment was assessed in relation to improvement in overall clinical sign and symptoms and biochemical investigations. Further study will be needed as per different assessment criteria.

The rodenticidal effect of crude argel (Gomphocarpus sinaicus Boiss) leaves was carried out on Norway rat under laboratory and field circumstances with zinc phosphide in Menofyia Governorate. The laboratory results proved that non-choice also, free - choice feeding tests gave the same trend; a bait 1% either zinc phosphide and argel ethanolic extract excepted 100% mortality for Norway rat as well as shorter time to death for zinc phosphide treatment. Argel ethanolic extract bait was more accepted than zinc phosphide with 57.1 and 34.5%, respectively. Also cleared that zinc phosphide more toxic than argel ethanolic leaves extract whereas the acute oral LD50 values were 0.255 and 85.78mg/kg b.w respectively, for rattus norvegicus. Oral administration of sub-leathal dose (¼ LD50) of each compound induced a noticeable disfunction in (AST), (ALT) enzymes and TP levels as they increased in plasma at 24 and 48 hours after treatment indicating a hepatic damage. Aprolongation of the prothrombin time (PT) had occurred following administration of Argel leaves ethanolic extract indicating disorders in blood coagulation mechanism but no effect on (PT) was observed with zinc phosphide treatment. Under the field conditions, zinc phosphide caused 70.6% population reduction, While Argel leaves ethanol extract reduced 68.0% of Norway rat, Rattus norvegicus population, while the water extract gave the lowest value (11.3%).

The authors have withdrawn this preprint due to author disagreement.

The present study investigated the combinatorial effect of gallic acid and catechin (GC) on some biochemical and inflammatory parameters in CCl4-mediated hepatic damage to rats. Male Wistar rats were distributed equally into five groups. Group A (control) received distilled water orally and olive oil intraperitoneally (ip), group B rats were intoxicated with CCl4 {1.25 ml/kg in olive oil, ip) only, while Groups C, D and E were induced with CCl4, thereafter they were administered 50 mg/kg body weight of silymarin, combined dose of gallic acid and catechin (50 and 100 mg/kg bw, 1:1) for 7 days respectively. After 7 days of treatment, the rats were sacrificed, and the fasting blood sample was collected by cardiac puncture for biochemical analyses. Findings from our results show that there were significant increases (p ˂ 0.05) in serum hepatic enzyme markers (ALT, AST, ALP, and GGT activities), bilirubin, albumin, and malondialdehyde (MDA) concentrations, but a significant decrease in GSH, SOD and CAT activities. It was also observed that the antioxidant genes coding for SOD and CAT were down-regulated or suppressed, while the inflammatory cytokines (IL-1B, IL-6, COX 2, and TNF α) were activated in rats intoxicated with CCl4 when compared to the control group. Administration of the combined dose of GC and silymarin drug attenuated the toxic insult of CCl4 at the biochemical and molecular levels. Our findings confirm that a combination of gallic acid and catechin may have exhibited a synergistic hepatoprotective activity against CCl4 induced liver damage.

Cryptosporidiosis has been proposed to be one of the major causes of diarrhoeal disease in humans worldwide that possesses zoonotic concern. Thereby, this study investigated the potential effects of s-Methylcysteine (SMC) on the parasite in vivo followed by the measurement of cytokines, oxidative stress parameters, and an investigation of the major histopathological changes. Sixty male Swiss albino mice weighing 20&ndash, 25 g were allocated equally into five groups and orally administered saline only (control), SMC only (SMC50) (50 mg/kg b.w.), and 104Cryptosporidium parvum oocysts per mouse via an esophageal tube (C + ve untreated). The fourth and fifth groups (C + SMC25, C + SMC50) administrated 104C. parvum oocysts combined with SMC25 (low dose) and 50 (high dose) mg/kg b.w., respectively. At days 7 and 14 post-infection (PI), the feces was collected from each group in order to count C. parvum oocysts. After two weeks of treatment, the animals were euthanized and the serum was collected for biochemical analysis. Next, the intestinal, spleen, and liver sections were dissected for histopathological examination. The results revealed lower oocyst numbers in the C + SMC25 and C + SMC50 groups compared to the infected untreated group. Moreover, higher doses of SMC treatment significantly reduced the enteritis induced by C. parvum in a dose-dependent manner. The hepatic lesions were also mitigated as demonstrated in C + SMC25 and C + SMC50 groups unlike the infected group via lowering the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes and increasing albumin and globulin serum levels. SMC administration also reduced cytokines production (SAP, TNF-&alpha, IL-6, and IFN-&gamma, ) mediated by Cryptosporidium infection in contrast to the infected untreated group. There were marked lymphoid depletion and amyloidosis observed in the infected untreated group, while the treated groups showed obvious increase in the lymphoid elements. Moreover, the scoring of intestinal parasites, hepatic, and splenic lesions in the SMC-treated groups exhibited significantly lower pathological lesions in different organs in a dose-dependent manner, compared to the infected untreated group. Our results also revealed a significant change in the malondialdehyde content with an elevation of glutathione and superoxide dismutase in the intestines collected from C + SMC25 and C + SMC50 mice relative to the untreated group. Taken together, our results indicated that SMC could be a promising effective compound for treating and declining C. parvum infestation via restoring structural alterations in different tissues, enhancing antioxidant enzymes, and suppressing the cytokines liberation.

Liver fibrosis occurs due to liver injuries and toxins. Silymarin (SMR) extracted by the milk thistle seeds, is widely used such as herbal drug for its hepatoprotective properties. The purpose of this study to assess the properties of an optimized dose of encapsulated crude SMR on antidiabetic activity and liver fibrosis induced by paracetamol in male albino rat. Hepatic fibrosis was assessed by measuring liver enzymes. Results revealed that the consumption of encapsulated SMR, can effectively affluence the target and avoid the degradation of bioactive compound. Body weight of animal also significantly increased in each group during all the period. According to our optimized study, the long-term induction of SMR (300 mg/kg) significantly amplified survival time of rats with paracetamol induced hepatic injuries. The changes of liver fibrosis and the significant increase of hepatic enzyme biomarkers were also observed. In conclusion, the results suggest that SMR acts as a hepatoprotective agent by inhibiting the fibrogenisis and apoptosis in liver, as well as insulin resistance.

The production of chestnut (Castanea sativa Miller) is mostly concentrated in Europe. Chestnut is recognized by its high content of antioxidants and phytosterols. This work aimed to evaluate the effects of dietary chestnut consumption over physiological variables of FVB/n mice. Eighteen FVB/n male 7-month-old mice were randomly divided into three experimental groups (n = 6): 1 (control group) fed a standard diet, 2 fed a diet supplemented with 0.55% (w/w) chestnut, and 3 supplemented with 1.1% (w/w) chestnut. Body weight, water, and food intake were recorded weekly. Following 35 days of supplementation, the mice were sacrificed for the collection of biological samples. Chestnut supplementation at 1.1% reduced abdominal adipose tissue. Lower serum cholesterol was also observed in animals supplemented with chestnut. There were no significant differences concerning the incidence of histological lesions nor in biochemical markers of hepatic damage and oxidative stress. These results suggest that chestnut supplementation may contribute to regulate adipose tissue deposition.

Introduction: In this study, we aimed to evaluate the protective effects of Descurainia sophia seed extract on paracetamol-induced oxidative stress and acute liver injury in mice. Methods: Sixty male Swiss albino mice were divided into 6 groups, group I: as control group received NaCl 9%. Group II: as paracetamol group received paracetamol intraperitoneally (i.p.) (500 mg/kg). Groups III to VI as treatment groups received different doses of D. sophia seed extract (T1 = 50, T2 = 100, T3 = 200 and T4 = 300 mg/kg, respectively). Twenty-four hours after the paracetamol administration, the mice were sacrificed under mild anesthesia and their blood samples were collected to estimate serum alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin and malondialdehyde (MDA) levels. Their livers were also removed for histopathological examinations. Results: Pretreatment of mice with D. sophia seed extract, significantly prevented the paracetamol induced elevation in the levels of serum ALT, AST and ALP, total bilirubin and MDA (P < 0.05). The results of histopathologic studies were consistent with the above findings. Conclusion: Descurainia sophia seed extract has a protective effect against paracetamol induced oxidative damage and acute hepatotoxicity in mice.

For many years, fluorosis has been known as a worldwide disease which seriously diminishes quality of life through skeletal embrittlement and hepatic damage. Aiming to develop novel drugs for simultaneous fluorosis diagnosis and therapy, in this work we explore the feasibility of a novel pyrogallic acid-titanium(iv) complex-modified upconversion nanoprobe (UCNP-PA-Ti) for F- capture and real-time quantification. Utilizing the strong interaction between Ti4+ and F-, the modified PA-Ti decomposes in F--containing solution, which not only weakens the FRET but results in upconversion luminescence (UCL) recovery. Both in vitro and in vivo experiments demonstrate a highly sensitive F- UCL response and therapeutic efficiency, which was promising for successful UCL image monitoring and the therapeutic process. Long blood circulation time and low toxicity ensured their safe application for fluorosis theranostics. Our work provides a new possibility for F- concentration detection within fluorosis therapeutic periods and encourages the development of novel drugs for fluorosis theranostics.

The nutritional characteristics and bioactive compound content in purees elaborated with guava-strawberry, guava-blackberry, guava-soursop or guava-passion fruit were evaluated as well as their effect on biochemical markers of hyperglycemic and hypercholesterolemic rats. Over a 4-week period, the effects of each puree were examined. All purees presented a high content of indigestible fraction (70.6–82.3 g/100 g), vitamin C (500–534.6 mg/100 g), soluble polyphenols (32.8–33 mg/g) and antioxidant capacity. Several phenolic acids and flavonoids were identified. The addition of purees in the diet increased the body weight of hyperglycemic rats (∼7%), but decreased the body weight of hypercholesterolemic rats (∼15%). All the purees decreased the levels of plasma glucose, urea and creatinine in hyperglycemic rats, as well as the total cholesterol and triacylglycerol levels in hypercholesterolemic rats. The hepatic damage was reduced for all purees. These guava-purees represent a therapeutic alternative for individuals with diet-related diseases problems such as hyperglycemia and hypercholesterolemia.

The aim of this study was to investigate the toxic effects of gossypol from cottonseed meal on the growth performance, serum characteristics and tissue gossypol residues in Shanshui White Ducklings. A total of 750 1-d-old ducklings (375 males and 375 females) was randomly divided into 5 dietary treatments with 5 replicate pens per treatment and 30 birds in each pen (15 males and 15 females). The experimental diets were formulated with raw cottonseed meal, de gossypol cottonseed meal and cottonseed powder as free gossypol (FG) sources. The final FG concentrations in the 5 diets were 0, 80, 160, 240 and 320 mg/kg feed. Feeding the diet with 320 mg FG/kg decreased ( P 0.0003) body weight (BW), average daily gain (ADG) and average daily feed intake (ADFI) of ducklings during the periods of d 1–10 and 1–21, and increased ( P 0.0003) feed: gain ratio (F:G) of ducklings during the period of d 1–10. Gossypol concentration in liver and muscle of ducklings measured at d 10 and 21 linearly increased ( P 0.001) with the increase of dietary FG levels. Notably, the diet containing 320 mg FG/kg increased ( P 0.05) liver index and serum alanine aminotransferase and aspartate aminotransferase activities at d 10, as well as decreased ( P 0.05) thymus index and serum total protein and albumin contents at d 10 and the body protein deposition at d 21. Our results indicated that ducklings fed the diet with 320 mg FG/kg resulted in an accumulation of gossypol in liver and then induced hepatic damage in the ducklings at d 10. Subsequently, the serum total protein concentrations and body protein deposition were reduced and growth rate were depressed in the ducklings at d 10 and 21 (or from d 10 to 21). Therefore, dietary FG concentration should be controlled at below 320 mg/kg to prevent an economic loss from the toxicity of FG in Shanshui White ducklings from 1 to 21 d of age.

The present study was undertaken to investigate the cisplatin (cDDP) induced oxidative damage in hepatic tissue of wistar rats and mechanisms of protection by quercetin. A total of 24 wistar rats were randomly divided into four groups with six animals in each. Group I served as control, group II received cDDP (12 mg kg−1 body weight) and group III quercetin (50 mg kg−1 body weight) intra-peritoneally. Group IV received quercetin 6 h prior to cDDP administration intra-peritoneally. Administration of cDDP in rats resulted in significant (P

Fig leaves (Ficus carica Linn.) belonged to the family Moraceae and used as a source of medicines for the ailment of diseases. The present study was conducted to evaluate the hepatoprotective activity against the carbon tetrachloride induced toxic chemical in rats. The petroleum ether, ethyl acetate and methanol extract of Ficus carica leaves was prepared, and evaluated for phytochemical screening. The serum level of glutamic oxaloacetate transaminase (SGOT), glutamic pyruvic transaminase (SGPT) and bilirubin were investigated for the assessment of hepatoprotective activity of ethyl acetate extract. Additionally, the histological changes in liver were observed. Preliminary phytochemical investigations of the extracts of leaves of Ficus carica revealed the presence of flavonoids, tannins, phenolic compounds, alkaloids, glycosides, fats and carbohydrates. Pre-treatment with ethyl acetate extract of Ficus carica led to significant (p

Trang To (Ixora duffii) belongs to the genus Ixora in the family Rubiaceae. The in vitro total antioxidant and anti-inflammatory capacity of the methanol extract of Trang To leaf was investigated using the phosphomolypdenum method and the bovine serum albumin denaturation test, respectively. The results showed that the methanol extract of Trang To leaf possessed relatively high antioxidant activity (OD0,5 = 15,551 ± 0,344 μg/mL) compared to that of the standard, trolox (OD0,5=2,315±0,083 μg/mL). The anti-inflammatory effect using bovine serum albumin denaturation test showed that the activity of the methanol extract of Trang To leaf (EC50= 6,03±0,12 μg/mL) was comparable to that of the reference drug, diclofenac sodium (EC50=0,57±0,21µg/mL). To evaluate the hepatoprotective activity of the methanol extract of Trang To leaf, the liver damage was induced in mice given with carbon tetrachloride (CCl4) mixed in olive oil (1: 4) at a dose of 2.5 mL/kg body weight/day. As a control, the standard hepatoprotective agent, silymarin, was used at the dose of 16 mg/kg body weight for 4 consecutive weeks. Trang To leaf extract was given at three different doses 100, 200 and 400 mg/kg body weight. The results showed the effective dose-dependent reduction of transaminase enzyme (ALT and AST) levels in sera. In addition, Trang To leaf extract also improved the oxidative stress status of the liver through effective reduction of MDA level and increase of GSH level in the liver. Histopathological examination of the liver tissue revealed that the mice treated with Trang To leaf extract showed significant improvement of liver tissue damages similar to silymarin treatment compared to the non-treated control group. The present results demonstrated that Trang To leaf extract has potent antioxidant and hepatoprotective activity.

Hepatotoxicity implies chemical-driven liver damage. Liver disease is still a worldwide health problem. Traditional drugs for the treatment of liver diseases are at times inactive and can have adverse effects. So there is a worldwide trend to go back to traditional medicinal plants. The present investigation was aimed for a comparative study of conventional histopathological examination with modern electronic image processing studies with respect to evaluating the hepatoprotective action of ethanolic extract of Melia azedarach (MAE) and Piper longum (PLE) with their combination biherbal extract (BHE) against carbon tetrachloride (CCl4) induced hepatic damage in rats. The three ethanolic extracts at a dose level of 50 mg/kg body weight each were administered to three different groups of rats orally once daily for 14 days. The hepatoprotective effect of the biherbal extract (BHE) was assessed by histopathological photograph of the cells.

Little is known about the pathogenesis of high fructose corn syrup (HFCS) induced hepatic toxicity. We investigated hepatic lesions induced by chronic HFCS consumption and the protective effects of alpha-lipoic acid (ALA) on liver pathology. We used 24 rats allocated randomly into three groups of eight. The HFCS group was given in drinking water for 10 weeks. The ALA + HFCS group was given the same dose of HFCS and ALA also was administered during the last 6 weeks of the experiment. The control group was untreated. The rats were euthanized at the end of 10 weeks and 24 h after the last ALA administration. A significant increase was observed in the serum aspartate aminotransferase (AST) level of the HFCS group compared to controls. Tissue malondialdehyde (MDA) levels also increased significantly and catalase (CAT) activity decreased significantly in the HFCS group. Caspase-3 expression increased significantly in the HFCS group compared to controls. In the ALA treated group, the levels of MDA, CAT and caspase-3 returned to near control levels. HFCS caused hepatic toxicity by increasing oxidative stress and apoptosis. ALA administration ameliorated the pathological changes. © 2018, © 2018 The Biological Stain Commission.

This study investigated the effect of ethanol leaf extract of Spilanthes filicaulis on liver indices and selected biochemicals on carbon tetrachloride induced hepatic damage in wistar rats. A total of thirty (30) rats comprising of five (5) rats per group (90-130 g), were used for the study. Groups 1-3, served as normal, negative (CCl4 induced 1 mL/kg, 1:1 i.p.) and positive (CCl4 induced and administered with silymarin 50 mg/kg) controls respectively. Groups 4-6 were the extract treated groups administered with 250 mg/Kg bw, 500 mg/Kg bw and 750 mg/Kg bw respectively for 14 days. The results of the liver marker enzymes showed a significant decrease (p 0.05) in all treated groups when compared to the negative control group. Catalase (CAT) and Superoxide Dismutase (SOD) levels were significantly increased (p 0.05) in all treated groups when compared to the negative control. The study showed that the ethanol leaf extract of Spilanthes filicaulis has potential of restoring hepatic liver damage.

Liver cirrhosis results from chronic hepatic damage and is characterized by derangement of the organ architecture with increased liver fibrogenesis and defective hepatocellular function. It frequently evolves into progressive hepatic insufficiency associated with high mortality unless liver transplantation is performed. We have hypothesized that the deficiency of critical nutrients such as essential omega-3 fatty acids might play a role in the progression of liver cirrhosis. Here we evaluated by LC-MS/MS the liver content of omega-3 docosahexaenoic fatty acid (DHA) in cirrhotic patients and investigated the effect of DHA in a murine model of liver injury and in the response of hepatic stellate cells (HSCs) (the main producers of collagen in the liver) to pro-fibrogenic stimuli. We found that cirrhotic livers exhibit a marked depletion of DHA and that this alteration correlates with the progression of the disease. Administration of DHA exerts potent anti-fibrogenic effects in an acute model of liver damage. Studies with HSCs show that DHA inhibits fibrogenesis more intensely than other omega-3 fatty acids. Data from expression arrays revealed that DHA blocks TGFβ and NF-κB pathways. Mechanistically, DHA decreases late, but not early, SMAD3 nuclear accumulation and inhibits p65/RelA-S536 phosphorylation, which is required for HSC survival. Notably, DHA increases ADRP expression, leading to the formation of typical quiescence-associated perinuclear lipid droplets. In conclusion, a marked depletion of DHA is present in the liver of patients with advanced cirrhosis. DHA displays anti-fibrogenic activities on HSCs targeting NF-κB and TGFβ pathways and inducing ADPR expression and quiescence in these cells. This study was supported by European FEDER funding and grants from the Ministry of Economy (SAF2015-70971-R), Gobierno de Navarra 0011-1365-2016-000308, Fundación Echevano, Fundación Unicaja, and Fondo de Investigación Sanitaria (PI16/02081), financed by the Instituto de Salud Carlos III.

The present study was aimed to evaluate the hepatoprotective activity of methanol extract against carbon tetrachloride (CCl4) induced hepatic damage in rats. CCl4 caused liver damage in rats manifested by significant rise in serum enzyme levels. To examine the effect of the extract male albino rats were used and extract was administered orally at a dose of 300 mg/kg once daily. The results obtained showed that there were reductions in the activities of serum SGOT, SGPT, ALP, total protein, total bilirubin from 97.67±1.78, 275.67±2.86, 934 ± 1.41, 1.13±0.227 and 7.50±0.707 in animals treated with toxic doses of CCl4 to 78.33±1.08, 53±1.41, 870±0.707, 0.67±0.04 and 6.47±0.356 in animal treated with extract before CCl4 intoxication. The extract could also repair the abnormal lipid profile. From these results, it is concluded that methanol extract of Alpina nigra leaves has hepatoprotective activity in CCl4-induced hepatic damage in rats.

The present study investigated the preventive effect of polyphenols in Liubao tea (PLT) on carbon tetrachloride (CCl4)-induced liver injury in mice. The mice were initially treated with PLT, followed by induction of liver injury using 10 mL/kg CCl4. Then liver and serum indices, as well as the expression levels of related messenger RNAs (mRNAs) and proteins in liver tissues were measured. The results showed that PLT reduces the liver quality and indices of mice with liver injury. PLT also downregulates aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglycerides (TGs), and malondialdehyde (MDA), and upregulates superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the sera of mice with liver injury. PLT also reduces serum levels of interleukin-6 (IL-6), interleukin-12 (IL-12), tumor necrosis factor- &alpha, (TNF- &alpha, ), and interferon- &gamma, (IFN- &gamma, ) cytokines in mice with liver injury. Pathological morphological observation also shows that PLT reduces CCl4-induced central venous differentiation of liver tissues and liver cell damage. Furthermore, qPCR and Western blot also confirm that PLT upregulates the mRNA and protein expressions of Gu/Zn-SOD, Mn-SOD, catalase (CAT), GSH-Px, and nuclear factor of &kappa, light polypeptide gene enhancer in B-cells inhibitor- &alpha, (I &kappa, B- &alpha, ) in liver tissues, and downregulates the expression of cyclooxygenase 2 (COX-2) and nuclear factor &kappa, light-chain-enhancer of activated B cells (NF- &kappa, B). Meanwhile, PLT also raised the phosphorylated (p)-NF- &kappa, B p65 and cytochrome P450 reductase protein expression in liver injury mice. The components of PLT include gallic acid, catechin, caffeine, epicatechin (EC), epigallocatechin gallate (EGCG), gallocatechin gallate (GCG), and epicatechin gallate (ECG), which possibly have a wide range of biological activities. Thus, PLT imparts preventive effects against CCl4-induced liver injury, which is similar to silymarin.

Acute, or chronic, ethanol consumption leads to the formation of free radicals in the liver, which is related to hepatic damage. Among these radicals 1-hydroxyethyl, •CH(OH)CH3, is the most abundant one. Thus, efficient •CH(OH)CH3 scavengers are likely candidates to offer liver protection after ethanol consumption. In the present work ergosterol and homogentisic acid (HGA), which are found in edible mushrooms, were investigated as potential candidates to that purpose. The investigation was carried out following the QM-ORSA protocol, and using the density functional theory (DFT). The overall rate constants calculated for the •CH(OH)CH3 radical scavenging activity of ergosterol in lipid and ethanol media are 1.34 × 107 and 1.86 × 107 M-1 s-1, respectively. For homogentisic acid the overall rate constant in lipid, ethanol and aqueous media are 4.33 × 108, 2.74 × 106, and 3.62 × 107 M-1 s-1, respectively. Accordingly, both compounds are predicted to efficiently scavenge the •CH(OH)CH3 radical. Thus, the results from this investigation support the antioxidant capability of edible mushrooms, their potential beneficial effects against ethanol hepatotoxicity, and the nutraceuticals properties of ergosterol and homogentisic acid.

In the last years, the agricultural expansion has led to an increased use of pesticides, with glyphosate as the most widely used worldwide. This is also the situation in Argentina, where glyphosate formulations are the most commercialized herbicides. It is known that glyphosate formulations are much more toxic than the active ingredient, and this difference in toxicity can be attributed to the adjuvants present in the formula. In this context, the aim of the present study was to evaluate and compare sub-lethal histological effects of the glyphosate formulation Roundup Ultramax and glyphosate active ingredient on Leptodactylus latrans tadpoles at Gosner-stage 36. Semi-static bioassays were performed using 96 h of exposure with Roundup Ultramax formulation (RU; 0.37–5.25 mg a.e./L), glyphosate (GLY; 3–300 mg/L), and a control group. RU exposure showed an increment in the melanomacrophagic cells (MMc) and melanomacrophagic centers (MMCs) from 0.37 mg a.e./L. GLY exposure showed a significant increment in the number of MMc from 15 mg/L, and of MMCs from 3 mg/L. Also, histopathological lesions were observed in the liver of tadpoles exposed to both, GLY and RU. These lesions included: lipidosis and hepatic congestion, but only RU showed significant differences respect to control, with a LOEC value of 2.22 mg a.e./L for both effects. In sum, this study represents the first evidence of adverse effects of glyphosate and RU formulation on the liver of anuran larvae at concentrations frequently found in the environment. Fil: Bach, Nadia Carla. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús). Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús); Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Química. Centro de Investigaciones del Medio Ambiente; Argentina Fil: Marino, Damian Jose Gabriel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Química. Centro de Investigaciones del Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina Fil: Natale, Guillermo Sebastian. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Química. Centro de Investigaciones del Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina Fil: Somoza, Gustavo Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús). Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. Instituto de Investigaciones Biotecnológicas "Dr. Raúl Alfonsín" (sede Chascomús); Argentina

Tartrazine (TAZ) is one of the most commonly used artificial dyes for foods and drugs. We determined the effect of TAZ on fetal development by examining morphological, visceral, and skeletal malformations in rat fetuses following daily oral administration of TAZ to pregnant Wistar rats at the 6th-15th day of gestation. TAZ at 0.45 and 4.5 mg/kg induced 6.0 and 7.1% fetal resorptions, as well as 10.0 and 10.5% fetal mortality, respectively. Fetal body weight and length were significantly lower in the groups treated with TAZ at 0.45 (3.97 ± 0.21 g and 27.3 ± 0.54 mm, respectively) and 4.5 mg/kg (3.48 ± 0.15 g and 23.22 ± 1.02 mm, respectively) than in the control group (4.0 ± 0.15 g and 30.01 ± 0.42 mm, respectively). TAZ at 0.45 and 4.5 mg/kg induced hepatic damage (20 and 33.3%, respectively), dark brown pigmentation due to hemosiderin in the splenic parenchyma (16.7 and 21.7%, respectively), as well as destructed and necrotic renal tubules (16.7 and 26.7%, respectively) in the fetuses. Moreover, TAZ at 0.45 and 4.5 mg/kg caused one or more missing coccygeal vertebrae (20 and 40%, respectively), missing sternebrae (6 and 10%, respectively), missing hind limbs (24 and 4%, respectively), and irregular ribs (16 and 20, respectively) in the fetuses. We concluded that TAZ has embryotoxic and teratogenic potentials in rats.

Hepatic fibrosis is a worldwide health problem with significant morbidity and mortality. Currently, there is no effective therapy for hepatic fibrosis. The present study was aimed to evaluate the possible regenerative effect of platelet-rich plasma (PRP) against thioacetamide (TAA)-induced hepatic damage. Eighty albino rats were included; 40 were used for PRP preparation and 40 were randomly divided into 4 groups: group I (control group); group II (PRP control); group III (TAA-intoxicated by a dose of 200 mg/kg body mass, intraperitoneally, twice weekly for 7 weeks), and group IV (TAA intoxicated + PRP treated). Macrophage inflammatory protein-1α (MIP-1α) and cyclic adenosine monophosphate (cAMP) were immunoassayed in addition to peroxinitrite level, NADPH-quinone oxidoreductase-1 (NQO1) enzyme activity, and liver function. PRP treatment showed significant improvement in hepatic function, and decreased MIP-1α and peroxinitrite levels. Meanwhile, significant increase in NQO1 enzyme activity and cAMP level were observed. The histopathological results confirmed the laboratory results with improvement of hepatic architecture except for some inflammatory cellular infiltrates. This study shows that PRP has the ability to protect against TAA-induced liver damage, possibly by improving redox status, liver histopathological architecture, and disruption of the inflammatory and fibrotic response induced by TAA.

Liver, the most important metabolic organ of the body, is also the major organ for the detoxification of the blood stream. If the accumulation of toxins is faster than their removal by liver, hepatic damage occurs. Although synthetic drugs are available in the market, long-term use of such drugs has consequential side effects. Therefore, the growing need to find safe, cost-effective drugs devoid of adverse effects is spawning extensive research. Mushrooms are rising as a major medicinal food and pharmaceuticals. This review summarizes the medicinal value of different edible mushrooms on free radical–, xenobiotic-, and drug-induced hepatotoxicity.

Systemic inflammation is accompanied by an increased production of reactive oxygen species (ROS) and by either fever or hypothermia (or both). To study aseptic systemic inflammation, it is often induced in rats by the intravenous administration of bacterial lipopolysaccharide (LPS). Knowing that bilirubin is a potent ROS scavenger, we compared responses to LPS between normobilirubinemic Gunn rats (heterozygous, asymptomatic; J/+) and hyperbilirubinemic Gunn rats (homozygous, jaundiced; J/J) to establish whether ROS mediate fever and hypothermia in aseptic systemic inflammation. These two genotypes correspond to undisturbed versus drastically suppressed (by bilirubin) tissue accumulation of ROS, respectively. A low dose of LPS (10 μg/kg) caused a typical triphasic fever in both genotypes, without any intergenotype differences. A high dose of LPS (1,000 μg/kg) caused a complex response consisting of early hypothermia followed by late fever. The hypothermic response was markedly exaggerated, whereas the subsequent fever response was strongly attenuated in J/J rats, as compared to J/+ rats. J/J rats also tended to respond to 1,000 μg/kg with blunted surges in plasma levels of all hepatic enzymes studied (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase), thus suggesting an attenuation of hepatic damage. We propose that the reported exaggeration of LPS-induced hypothermia in J/J rats occurs via direct inhibition of nonshivering thermogenesis by bilirubin and possibly via a direct vasodilatatory action of bilirubin in the skin. This hypothermia-exaggerating effect might be responsible, at least in part, for the observed tendency of J/J rats to be protected from LPS-induced hepatic damage. The attenuation of the fever response to 1,000 μg/kg could be due to either direct actions of bilirubin on thermoeffectors or the ROS-scavenging action of bilirubin. However, the experiments with 10 μg/kg strongly suggest that ROS signaling is not involved in the fever response to low doses of LPS.

This study was to investigate the preventive effect of taemyeongcheong (TMC, a Korean traditional health drink) on acetaminophen (APAP, 800 mg/kg BW)-induced hepatic damage in ICR mice. TMC is prepared from Saururus chinensis, Taraxacum officinale, Zingiber officinale, Cirsium setidens, Salicornia herbacea, and Glycyrrhizae. A high dose of TMC (500 mg/kg BW) was found to decrease APAP-induced increases in serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase. TMC pretreatment also increased the hepatic levels of hepatic catalase, superoxide dismutase, glutathione peroxidase, and glutathione, and reduced serum levels of the inflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 in mice administered APAP (P

The present study examined the protective effects of seabuckthorn seed oil (Hippophae rhamnoidesL seed oil., SBT) on acute alcoholic-induced hepatic damage in male SD rats. Our results showed that oral administration of SBT seed oil at doses of 0.167, 0.333 and 0.500 g/kg for 45 days significantly reduced the changed levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, and the level of triglyceride (TG) and malondialdehyde (MDA) in liver, which were induced by alcoholic-induced in rats. Moreover, the treatment of SBT seed oil was also found to significantly increase the activities of sglutathione peroxidase (GSH-Px) in liver. Our study found that the optimal dose of SBT seed oil was 0.333 g/kg, as the minimum amount exhibiting the greatest hepatoprotective effects on alcoholic-induced liver injury, which have been supported by the evaluation of the liver histopathology in rats. In conclusion, it has been found the hepatoprotective effect of SBT seed oil at all tested doses.

The events of 9/11 caused a unique health hazard by creating a large dust cloud and debris fires that burned for months. The combination of collapsed buildings and fires released many chemicals including a variety of carcinogens and the potential for pulmonary injury and inhalational exposure. Analyses of the spatial-temporal aspects of the dust cloud suggest very high levels of inhalation exposure to first responders and residents in lower Manhattan and western Brooklyn. Of particular, concern are asbestos, titanium, polycyclic aromatic hydrocarbons, dioxins, and chlordane pesticides. Beyond carcinogenicity and the potential for acute lung injury, many of the identified chemicals are implicated in cardiovascular disease. Furthermore, renal and hepatic damage may occur. Healthcare providers treating exposed persons should be aware of increased risk of contracting these sundry diseases.

The hepatoprotective activity of the EtOH–water extract of Ziziphus jujuba leaves was evaluated against CCl4-induced hepatic damage in mice. The EtOH–water extract significantly alleviated liver damage as indicated by the decreased levels of serum ALT and AST and the decreased MDA content, the increased levels of SOD, GSH and GSH-Px, and the reduced pathological tissue injury induced by CCl4. A quantitative analysis of fifteen major constituents (1–15) of the EtOH–water extract of the leaves of Z. jujuba was conducted by HPLC-DAD. Based on our research results, it can be concluded that the EtOH–water extract of the leaves of Z. jujuba is efficacious for prevention and treatment of CCl4-induced hepatic injury in mice. Flavonoids might be the active ingredients responsible for the biological and pharmacological activities towards hepatoprotection.

The aim of the present study was to determine the preventive effect of the traditional Chinese medicine, Dendrobium candidum Wall ex Lindl. (D. candidum), on CCl4-induced hepatic damage in mice. The CCl4-induced hepatic damage mice were treated with D. candidum, and the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), triglyceride (TG) and total cholesterol (TC) were determined. In addition, serum cytokine levels of interleukin (IL)-6, IL-12, tumor necrosis factor (TNF)-α and interferon (IFN)-γ were analyzed with kits, while liver tissues were analyzed using hematoxylin and eosin staining and reverse transcription polymerase chain reaction (RT-PCR). Furthermore, the contents of D. candidum were determined by nuclear magnetic resonance (NMR). D. candidum was demonstrated to successfully prevent hepatic damage in mice. The serum levels of AST, ALT and LDH were significantly decreased when the mice were treated with 200 and 400 mg/kg D. candidum, as compared with the control mice (P

The administration of vitamin A (10000 IU/kg b.w), vitamin A, C and E (10000 IU/kg, 100 mg/kg 100 mg/kg b.w), penicillin (50000 IU/kg b.w), penicillin + vitamin A, penicillin + vitamin A, C and E, streptomycin (50 mg/kg b.w), streptomycin + vitamin A, streptomycin + vitamins A, C and E for 30 days caused a significant increase in the levels of AST, ALT and ALP, and also caused a significant decrease in the levels of total protein and albumin in penicillin and streptomycin treated groups. However, co-administration of penicillin and streptomycin with vitamin A alone or in combination with vitamins C and E ameliorated the harmful effects of penicillin and streptomycin in most of the tested parameters. Vitamin A, either alone or in combination with vitamin C and E, has a protective effect on the histological changes of liver tissues induced either by penicillin or streptomycin administration. The result of the present work reveals for the first time that vitamin A alone or in combination with vitamin C and E plays an important role as cytoprotective compounds on hepatic damage in guinea pigs. Hence, further studies on the possible uses of vitamins as protective compounds during treatment with antibiotics are needed.