scholarly journals Probiotic Bacillus Spores Protect Against Acetaminophen Induced Acute Liver Injury in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 632 ◽  
Author(s):  
Maria Adriana Neag ◽  
Adrian Catinean ◽  
Dana Maria Muntean ◽  
Maria Raluca Pop ◽  
Corina Ioana Bocsan ◽  
...  

Acetaminophen (APAP) is one of the most used analgesics and antipyretic agents in the world. Intoxication with APAP is the main cause of acute liver toxicity in both the US and Europe. Spore-forming probiotic bacteria have the ability to resist harsh gastric and intestinal conditions. The aim of this study was to investigate the possible protective effect of Bacillus (B) species (sp) spores (B. licheniformis, B. indicus, B. subtilis, B. clausii, B. coagulans) against hepatotoxicity induced by APAP in rats. A total of 35 rats were randomly divided into seven groups: group I served as control; group II received silymarin; group III received MegaSporeBioticTM (MSB); group IV received APAP and served as the model of hepatotoxicity; group V received APAP and silymarin; group VI received APAP and MSB; group VII received APAP, silymarin and MSB. The livers for histopathological examination and blood samples were collected on the last day of the experiment. We determined aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total antioxidant capacity (TAC) levels and zonula occludens (ZO-1), tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) expression. APAP overdose increased AST and ALT. It slowly decreased TAC compared to the control group, but pretreatment with silymarin and MSB increased TAC levels. Elevated plasma concentrations were identified for ZO-1 in groups treated with APAP overdose compared with those without APAP or receiving APAP in combination with silymarin, MSB or both. The changes were positively correlated with the levels of other proinflammatory cytokines (TNF-α, IL-1β). In addition, histopathological hepatic injury was improved by preadministration of MSB or silymarin versus the disease model group. Bacillus sp spores had a protective effect on acute hepatic injury induced by APAP. Pretreatment with MSB resulted in a significant reduction in serum AST, ALT, TNF-α, IL-1β, ZO-1, TAC and also hepatocyte necrosis, similar to the well-known hepatoprotective agent—silymarin.

2014 ◽  
Vol 92 (6) ◽  
pp. 490-497 ◽  
Author(s):  
Doaa Ibrahim Mohamed ◽  
Ahmed Abdel salam Mohamed Elmelegy ◽  
Lubna Foaad A. El-Aziz ◽  
Hala Salah Abdel kawy ◽  
Abeer Ahmed AbdEl-Samad ◽  
...  

Tumor necrosis factor alpha (TNF-α) plays an important role in the pathogensis of hepatitis C virus (HCV) infection induced liver injury. This study aimed to evaluate the effects of TNF-α inhibition with pentoxifylline (PTX) on concanavalin A (Con A)-induced hepatic injury in rats. The rats were distributed among 3 groups: (i) control group (1 mL saline·week–1 by intravenous injection (i.v.)); (ii) Con A treatment group (20 mg Con A·(kg body mass)–1·week–1, i.v.), and (iii) rats treated with Con A and with PTX (200 mg PTX·(kg body mass)–1·day–1, per oral) group. Blood samples and livers were collected at the end of weeks 1, 2, 4, and 8 of Con A treatment. Portal pressure (PP) was measured at the end of week 8. The administration of PTX was found to confer significant protection against the injurious effects of Con A on the liver, by reducing serum levels of aspartate aminotransferase, alanine aminotransferase, hepatic TNF-α, and malondialdehyde. Histopathological examination revealed that treatment with PTX significantly suppressed early inflammation, reduced alpha smooth muscle actin, and the apoptosis of hepatocytes induced by Con A. Moreover, PTX significantly (P < 0.05) reduced PP, and quantitative analyses of the area of fibrosis induced by treatment with Con A showed a significant reduction at the end of week 8. We conclude that rats treated with PTX revealed a more or less normal hepatocyte architecture as well as marked improvement in fibrosis and PP.


2020 ◽  
Vol 19 (7) ◽  
pp. 1465-1471
Author(s):  
Osama Abdelaziz Hassan ◽  
Entesar Farghally Amin ◽  
Rabab Ahmed Moussa

Purpose: To study the possible mitigating effect of erdosteine (ERD) against methotrexate (MTX)-induced liver toxicity.Methods: Male albino Sprague-Dawley rats were randomly assigned to four groups of 8 rats each, viz, vehicle control, MTX (20 mg/kg i.p.), MTX (20 mg/kg i.p.) + ERD (300 mg/kg) and ERD (300 mg/kg) groups. Serum levels of alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were determined by enzymatic colorimetric commercial kits while Hepatic tissue content of malondialdehyde (MDA), reduced glutathione (GSH), SOD and catalase (CAT) were also evaluated. In addition, measurement of the inflammatory cytokine, TNF-α, as well as histopathological  examination and histochemical assessment were carried out.Results: The results indicate that, compared to the control group, MTX group showed a remarkable elevation in oxidative stress as indicated by significantly lower levels of SOD, CAT and reduced glutathione, and increased tissue malondialdehyde (p < 0.05). MTX group exhibited significantly higher blood activities of ALT, AST and TNF-α, reflective of hepatocyte damage and inflammation (p < 0.05). In MTX group, significant hepatic degenerative changes were detected on histological examination, while marked apoptotic alternations were observed following  immunohistochemical analysis of caspase-3 expression, when compared to control group. However, administration of ERD to rats ameliorated thechanges in these parameters (p < 0.05).Conclusion: Treatment with ERD in rats produced alleviation in hepatic oxidative stress, apoptosis, inflammation, and histological damage, when compared to MTX group. This study is the first to demonstrate the potentially protective effect of ERD-pretreatment against hepatotoxicity associated with MTX. Keywords: Erdosteine, Methotrexate, Hepatotoxicity, Oxidant, Anti-oxidant                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            


2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.


2002 ◽  
Vol 36 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Daniel Klintman ◽  
Gunnar Hedlund ◽  
Henrik Thorlacius

2017 ◽  
Vol 9 (2) ◽  
pp. 196 ◽  
Author(s):  
Hamed R. Takruri ◽  
Maha S. Shomaf ◽  
Saida F. Shnaigat

This research was conducted to study the protective effect of bee honey on the 7,12-dimethylbenz(a)anthracene (DMBA)- induced breast cancer in rat model. The study consisted of three groups: honey group, positive control group (PC), and negative control group (NC) to which the carcinogen was not administered. All rats were fed the diet recommended by the American Institute of Nutrition for growing rats (AIN-93G), with addition of honey (50 g/kg diet) to the honey group. All Rats were fed their diets ad libitum on 12 hours dark/light cycle. At the age of 50 days all rats in the honey and PC groups were gavaged once by the carcinogen DMBA with a dose of 80 mg/kg body Wt. After three weeks of carcinogen administration, rats were palpated weekly to detect any tumor growth. After 18 weeks, all rats were sacrificed. The palpable structures and the mammary glands along with associated lymph nodes were removed and fixed in saline formalin and prepared for histopathological examination. The results revealed that the honey group diet significantly (p < 0.05) reduced the incidence rate of mammary cancer, palpable tumor multiplicity, tumor size and weight compared to the PC group. In conclusion, multi floral honey has a protective effect against DMBA- induced mammary cancer in the initiation, promotion, and progression stages of DMBA-induced mammary carcinogenesis. However, further research is needed to reveal the mechanisms that might have contributed to the preventive effect of honey against mammary cancer.


2017 ◽  
Vol 43 (2) ◽  
pp. 644-659 ◽  
Author(s):  
Azza H. Abd Elwahab ◽  
Basma K. Ramadan ◽  
Mona F. Schaalan  ◽  
Amina M. Tolba

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the alarmingly rising clinical problems in the 21st century with no effective drug treatment until now. Taurine is an essential amino acid in humans that proved efficacy as a non-pharmacological therapy in a plethora of diseases; however, its impact on NAFLD remains elusive. The aim of the current study is to evaluate the protective mechanism of taurine in experimental steatohepatitis induced by junk food given as cafeteria-diet (CAF-D) in male albino rats. Methods: Forty adult male albino rats of local strain between 8-10 weeks old, weighing 150 ± 20 g, were divided into four equal groups: Group I (control group), Group II (Taurine group), Group III (CAF-D for 12 weeks) and Group IV (CAF-D +Taurine). CAF-D was given in addition to the standard chow for 12 weeks, where each rat was given one piece of beef burger fried in 15 g of sunflower oil, one teaspoonful of mayonnaise, and one piece of petit pan bread, weighing 60g/ piece. In the serum, liver function tests; ALT, AST, ALP, GGT and the lipid profile; TG, TC, HDL-C added to reduced glutathione (GSH) were assessed colorimetrically, while fibroblast growth factor (FGF)-21, adiponectin & interleukin (IL)-6 via ELISA. The same technique was used for the assays of the hepatic levels of FGF-21, silent information regulator (SIRT1), malondialdehyde (MDA),IL-10, tumor necrosis factor-α (TNF-α) as well as the apoptotic markers; caspase-3 and B-cell lymphoma (Bcl-2). Results: The cafeteria-diet induced steatohepatitis was reflected by significantly increased body and liver weight gain, elevation of liver enzymes; ALT, AST, ALP and GGT added to the dyslipidemic panel, presented as increased TC, TG, LDL-C and decreased HDL-C levels. The steatosis-induced inflammatory milieu, marked by elevated serum levels of FGF-21, IL-6, hepatic TNF-α, as well as reduced IL-10 and adiponectin, was associated with steatosis- induced hepatic oxidative stress, reflected by increased hepatic MDA and decreased GSH levels, along with stimulated caspase-3 and decline in BcL-2 hepatic levels. These pathological disturbances were significantly ameliorated by taurine supplementation and evidenced histopathologically. The cross talk between hepatic FGF-21 and SIRT1 and their association to the induced perturbations are novel findings in this study. Taurine's efficacy in restoration of hepatic structure and function is partially via the increase in SIRT1 and associated reduction of FGF-21. Conclusion: The findings of the current study prove the protective role of taurine in NAFLD via a novel role in the amelioration of FGF-21/ SIRT1 axis, which could be considered a new therapeutic target.


Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 308 ◽  
Author(s):  
Ahmed Eleojo Musa ◽  
Dheyauldeen Shabeeb ◽  
Haider Saadoon Qasim Alhilfi

Background and Objectives: Radiation enteritis is a common side effect after radiotherapy for abdominal and pelvic malignancies. The aim of the present study was to investigate the protective effect of melatonin, known for its free radical scavenging ability, against radiotherapy-induced small intestinal oxidative damage. Materials and Methods: Thirty male Wistar rats were randomly assigned to six groups (5 rats in each) as follows: Group I (control group) rats received neither radiation nor melatonin; group II rats received only 8 Gy single dose of gamma radiation to their abdomen and pelvis regions; group III (administered with only 50 mg/kg melatonin); group IV (administered with only 100 mg/kg melatonin); group V (50 mg/kg melatonin + 8 Gy radiation), group VI (100 mg/kg melatonin + 8 Gy radiation). All rats were sacrificed after 5 days for biochemical assessments of their intestinal tissues. Results: Treatment with melatonin post irradiation significantly reduced malondialdehyde (MDA) levels as well as increased both superoxide dismutase (SOD) and catalase (CAT) activities of the irradiated intestinal tissues. In addition, melatonin administration with different doses pre irradiation led to protection of the tissues. Moreover, the 100 mg/kg dose was more effective compared to 50 mg/kg. Conclusions: The results of our study suggest that melatonin has a potent protective effect against radiotherapy-induced intestinal damage, by decreasing oxidative stress and increasing antioxidant enzymes. We recommend future clinical trials for more insights.


Biomedicines ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 39
Author(s):  
Sahar Youssef ◽  
Marwa Salah

Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.


2015 ◽  
Vol 49 (6) ◽  
Author(s):  
A. Hajalshaikh ◽  
M. J. Al-Hassan ◽  
H. E. Mohamed

The objective of this study was to test the effects of sodium selenite (SS) injection on semen characteristics and testosterone plasma concentrations in male Aardi goats. Fifteen animals were assigned into three groups; control (group I, with no supplemental SS); group II; injected intramuscular with 0.1 mg/kg SS body weight; group III injected 0.05 mg/kg SS body weight. Blood samples were collected once weekly (week 0 and four weeks after treatment) in the morning (at 8 am). Semen was collected by electro-ejaculator on a weekly basis post SS supplementation. Sperm count, motility %, progressive motility characteristic; average path velocity (VAP), straight line velocity (VSL), curvilinear velocity (VCL), straightness (STR) and linearity (LIN) were analyzed. Significant differences were found between the two treated-groups and control after week four for motility and progressive motility. After five weeks, significant differences were found between groups, for motility and progressive motility. The live % showed significant differences after five weeks between treated and control groups. After five weeks, significant differences were found between the three groups, for motility and progressive motility. The live % showed significant differences after 5 weeks between different treatments. However, VAP, VSL, VCL, STR, and LIN showed non-significant differences, suggesting that bucks might already have a good motility characteristic. No significant effects of SS supplementation on testosterone plasma levels, and the reported values were 1.28; 1.35, and 1.36 ng/ml for control; group 1, and group 2; respectively. In conclusion, SS improved reproduction in goats <italic>via</italic> the enhancement of semen quality in Aardi goats.


1979 ◽  
Vol 91 (3) ◽  
pp. 553-563 ◽  
Author(s):  
H. K. Kley ◽  
H. G. Solbach ◽  
J. C. McKinnan ◽  
H. L. Krüskemper

ABSTRACT The concentration of sex hormones and their binding in the plasma were measured in male patients (20–40 years old), who weighed 140–170 % (I), 170–200 % (II) and > 200 % (III) of their ideal weight. Correlated to body weight, there is a reduction in the total concentration of testosterone, which, in the very obese patients, amounts to 41 % (in group I: 85 % in group II: 68 % P < 0.001) of that found in an age-matched healthy control group of subjects of "normal" body weight (90–115 % of the ideal body weight; n: 20). Androstenedione values show only a trend downwards (from 0.94 to 0.72 ng/ml plasma), while the oestrogen values increase significantly; oestrone increases by a factor of 1.09 (I), 1.43 (II; P < 0.001) and 1.69 (III; P < 0.001) and oestradiol by 1.13, 1.43 P < 0.001) and 1.76 (P < 0.001), respectively. Despite the fall in testosterone there are no clinical signs of hypogonadism, as SHBG (from 5.1 ± 0.8 in the controls to 2.4 ± 0.6 ×10−8 Mol/l in the very obese patients of group III) and the protein-bound fraction of testosterone also decrease. As a result the concentration of free testosterone remains constant (120 pg/ml), except in the very obese (93 pg/ml). Because of the different affinity of the binding proteins for testosterone and oestradiol the ratio of free oestradiol: free testosterone shifts less strongly in favour of the feminizing hormone (11.1 × 10−3 in group III as compared to 4.1 × 10−3 in the controls), than is suggested by the total hormone concentrations. A disturbance in the gonadal function of the pituitary gland or the testes is not present, since the concentration of LH is normal and the testicular response to HCG in very obese patients adequate (increase of testosterone by a factor of 3.11 as compared to 2.23 in the controls). The cause of the decrease in testosterone and SHBG is unknown, while the increase of plasma oestrogens is likely to be due to the increased conversion of androgens to oestrogens in the adipose tissue, which clearly plays an important role for plasma concentrations of sex hormones in obese patients.


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