Liver Function Marker Enzymes Research Articles

Acetaminophen-induced Liver Injury: Protective Effect of <i>Laportea aestuans</i> Aqueous Leaf Extract in Experimental Mice Model

Acetaminophen commonly referred to as paracetamol is an analgesic and antipyretic drug commonly available as over the counter medications. Indiscriminate use of acetaminophen for management of pain and fever causes liver damage. The study evaluated the hepatoprotective effect of the Laportea aestuans aqueous leaf extract in acetaminophen-treated mice. Group 1: control, Group 2: APAP treated, Group 3, 4, 5, 6 and 7 received 25, 50, 100, 200 and 400 mg/kg bw of the extract for 7 days and then treated with 300 mg/kg bw APAP respectively, Group 8: silymarin group. Biochemical parameters were analyzed. Activities of liver function marker enzymes (gamma- glutamyl transferase, alkaline phosphatase, lactate and glutamate dehydrogenases, aspartate, and alanine aminotransferases) were significantly (p< 0.05) lower in the serum of acetaminophen-treated mice pre-administered with the Laportea aestuans aqueous leaf extract extract when compared to the acetaminophen-treated control mice. Activities of antioxidant enzymes significantly (p<0.05) increased in groups pre-administered with the extract or silymarin. Histological micrographs also showed that the hepatic architectures of the preadministered mice were maintained following treatment with APAP. Pre-administration of 100 mg/kg bw of Laportea aestuans aqueous leaf extract gave the best protective effect against APAP-induced hepatotoxicity. Findings from this study showed that L. aestuans leaf extract evidently protects mice against acetaminophen-induced liver injury, exhibiting antioxidant and hepatoprotective properties. This study supports the ethnobotanical use of L. aestuans for the prevention and treatment of liver diseases.

Implication of Lupeol in compensating Sorafenib-induced perturbations of redox homeostasis: A preclinical study in mouse model

AimsCancer chemotherapeutic drugs can potentially cause several adverse effects that influence a patient's general well-being. Sorafenib, an approved drug used in clinics against multiple cancers whose overall efficacy suffered a serious setback due to various side effects, leading to its frequent discontinuation. Lupeol has recently been considered an important prospective therapeutic agent due to its low toxicity and enhanced biological efficacy. Hence, our study aimed to evaluate whether Lupeol can perturb the Sorafenib-induced toxicity. Main methodsTo test our hypothesis, we studied DNA interaction, level of cytokines, LFT/RFT, oxidant/antioxidant status, and their influences on genetic, cellular, and histopathological changes using both in vitro and in vivo models. Key findingsThe Sorafenib-treated group showed a marked increase in reactive oxygen and nitrogen species (ROS/RNS), an increase in liver and renal function marker enzymes, serum cytokines (IL-6, TNF-α, IL-1β) macromolecular damages (protein, lipid, and DNA), and a decrease in antioxidant enzymes (SOD, CAT, TrxR, GPx, GST). Moreover, Sorafenib-induced oxidative stress caused marked cytoarchitectural damage in the liver and kidney and increased p53 and BAX expression. Interestingly, combining Lupeol with Sorafenib improves all the examined toxic insults caused by Sorafenib. In conclusion, our findings suggest that Lupeol can be used in combination with Sorafenib to reduce ROS/RNS-induced macromolecule damage, which might result in hepato-renal toxicity. SignificanceThis study presents the possible protective effect of Lupeol against Sorafenib-induced adverse effects by perturbing redox homeostasis imbalance and apoptosis leading to tissue damage. This study is a fascinating finding that warrants further in-depth preclinical and clinical studies.

Evaluation of hypolipidemic, antioxidant, atherogenic index and cardiac risk suppressing effects of unpolished maniki madhuri rice extract and HPLC analysis of phenolics compounds

Intake of whole grain has received huge consideration in recent times. This study aimed to investigate the hypolipidemic, antioxidant, and cardiac risk suppressing effect of whole rice extract of maniki madhuri joha rice (GI tagged) of Assam, India. In vitro antioxidant, HMG-CoA reductase enzyme inhibition assay, cholesterol esterase (CEase) inhibitory assay and antilipase activities of extracts of maniki madhuri were performed. Hyperlipidemia in experimental rats was induced by administering a high fat-high sugar diet for 45 days. Ethanol extract of whole rice (EtOH-MM) and atorvastatin were given orally to the animals in designated groups, and biochemical parameters were evaluated. Further, the presence of phenolic compounds was also estimated using the HPLC method. Extracts displayed concentration-dependent in vitro antioxidant, HMG-CoA reductase inhibitory and pancreatic lipase inhibitory activity. EtOH-MM exhibited strong CEase inhibitory activity (IC50 = 91.60 μg/ml). EtOH-MM at the dose of 200 and 400 mg/kg significantly ameliorated lipid parameters and the level of liver function marker enzymes to near normal. The lactate dehydrogenase and creatine kinase-NAC levels in EtOH-MM (400 mg/kg) group were 680.1 and 360.3 U/L, significantly less than the disease control group. C-reactive protein and lipoprotein a were significantly reduced in EtOH-MM treated group Ratio of ApoB/ApoA1 increased in the disease control group, which was reduced significantly in the standard and EtOH-MM treated group. The atherogenic index, atherogenic coefficient and cardiac risk ratio were decreased, while the cardioprotective index was increased in EtOH-MM treated group. Ten phenolic compounds i.e., gallic acid, caffeic acid, ferulic acid, p-coumaric acid, sinapic acid, o-coumaric acid, t-coumaric acid, rosamarinic acid, chlorogenic acid, phytic acid is quantified in maniki madhuri rice. The present study provided important evidence that consuming unpolished whole-grain of MM might be beneficial in managing hyperlipidemia and preventing associated cardiac complications.

Assessment of Antidiabetic Potential and Phytochemical Profiling of Viscum album, a Traditional Antidiabetic Plant

The traditional antidiabetic plant Viscum album (V. album) was collected from the oak plant in the wild at Maidan, Khyber District, of Pakistan, for assessment of its antidiabetic potential and phytochemical profile. Lowering of blood glucose level, antioxidant effect, lipids profile, liver function marker enzymes, and kidney function markers were evaluated in extract and glibenclamide treated groups, in normal as well as in diabetic control groups. An elevated level of blood glucose level, lipids (Cholesterol, TG, LDL), liver function marker enzymes (ALT, AST, ALP), and kidney function markers (bilirubin, creatinine, urea) were observed in alloxan-induced diabetic rats; however, a HDL level was decreased. Administration of V. album hydroalcoholic extract for 28 days renovated significantly ( p < 0.05 ) all the above biochemical parameters. The antioxidant enzymes SOD, CAT, and GPX were also considerably restored. In vitro, antioxidant assay indicated that the extract of 2,000 µg/mL scavenges free radicals of DPPH 68.4%, ABTS 69.5%, and H2O2 50.6%. The extracts revealed the presence of saponins, flavonoids, alkaloids, terpene, tannins, phenols, protein, amino acids, sterols, and glycosides. The extract has shown phenolic contents 421 ± 4.8 mg GAE/100 g d. w and flavonoids content 127 ± 1.4 mg equiv. Rut/100 g d. w. The findings of this research recommend V. album could be a potent source of natural antidiabetic constituents.

Cytokine profile as biomarker of COVID-19 and its correlation with liver function enzymes and other markers of inflammation

Introduction and Aim: Various hematological and biochemical parameters are assessed as biomarkers of COVID-19, caused by the SARS-CoV-2. In this study, efforts were made to identify the correlation of cytokines (IL-6, TNF-?, IL-1?, and IL-1?) with the liver function enzyme markers, LDH, CRP, Ferritin, and D-dimer. We also assessed the correlation of cytokines with severity of COVID-19. Materials and Methods: We analyzed 53 serum samples of RT-PCR-positive patients admitted to the hospital. Cytokines (IL-6, TNF-?, IL-1?, and IL-1?) were analyzed with sandwich ELISA. The levels of cytokines were compared between mild, moderate, and severe cases of COVID-19, and the correlation among cytokines, liver function marker enzymes, LDH, CRP, D-dimer, and ferritin were analyzed. Results: Along with CRP, LDH and ferritin, IL-6 showed significant difference between mild, moderate, and severe COVID groups. significant correlation between IL-6 & LDH (p -.002), IL-6 & D-Dimer (p- .010), IL-6 & IL-1? (p- .027), IL-1? & D-Dimer (p- .010), IL-1? & LDH (p-.027), and IL-1? & TNF-? & (p-.000). Conclusion: Cytokines especially IL-6 correlated with disease severity. Assaying the profile of cytokines could be of immense value in diagnosis, prognosis, and management of COVID-19.

The modulatory effect of taurine on benzo (a) pyrene-induced hepatorenal toxicity.

Toxicities linked with Benzo (a) pyrene B[a]P exposure, particularly in liver and kidney have been reported in both animals and humans. Taurine (2-aminoethane sulfonic acid) is an intracellular β-amino acid reported to elicit hepatorenal protective functions. However, the modulatory effect of taurine on hepatorenal toxicity associated with exposure to B[a]P has not been reported. This study evaluated the effects of taurine on the hepatorenal toxicities induced in cohorts of rats exposed to B[a]P. Experimental rats were treated as follows: B[a]P (10mg/kg); co-treated cohorts -B[a]P (10mg/kg) plus taurine (100 or 200mg/kg) for 4 successive weeks. Results show that co-dosing with taurine significantly (P<0.05) improved B[a]P-induced distortion of oxidative stress markers (catalase, superoxide dismutase, glutathione S-transferase, glutathione peroxidase, total sulphydryl, reduced glutathione, lipid peroxidation and xanthine oxidase), renal function (urea and creatinine) and liver function marker enzymes (alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase and gamma glutamyl transferase). Moreover, taurine effectively mitigated increase in myeloperoxidase activity, levels of reactive oxygen and nitrogen species, nitric oxide and interleukin-1β in kidney and liver of rats treated with B[a]P. In conclusion, taurine modulates hepatorenal toxicity in B[a]P-exposed rats by suppressing hepatic and renal damage indices, oxidative injury and inflammatory stress.

Antiarthritic activity of synthesized silver nanoparticles from aqueous extract of Moringa concanensis Nimmo leaves against FCA induced rheumatic arthritis in rats

Background and Objective: The rheumatoid arthritis is autoimmune disease and it is a major health issues among the peoples in worldwide. People affected by rheumatism have double risk of heart disease, lungs and chest infections, which causes 10-20% of deaths in individuals. The present research work was aimed to evaluate the antiarthritic potential of synthesized silver nanoparticles from the aqueous extract of M.concanensis leaves.&#x0D; Material and Methods: The arthritis was induced by complete freund’s adjuvant method and the rats was treated with synthesized silver nanoparticles from aqueous extract of M.concanensis leaves. The body weight, paw volume, hematological parameters, liver function marker enzymes and the renal function markers of the arthritic rats and nanoparticles treated rats was analyzed by the standard methods.&#x0D; Results: The results of the present study were made the new findings in antiarthritic activity of silver nanoparticles from M.concanensis leaves. The nanoparticles showed a noteworthy antiarthritic activity against FCA induced rheumatoid arthritis in experimental rats.&#x0D; Conclusion: Based on the above results, it was concluded as the present work are states the better understand on the antiarthritic activity of silver nanoparticles of Moringa concanensis Nimmo leaves.

Hepatoprotective efficacy of edible macrofungi Dacryopinax spathularia (Schwein) and Schizophyllum commune (Fries) against Carbon tetrachloride induced hepatotoxicity in albino Wistar rats

In the present study the hepatoprotective efficacy of two edible macrofungi Dacryopinax spathularia and Schizophyllum commune has been assessed against CCl4-induced hepatotoxicity in albino wistar rats. The administration of CCl4(1ml/Kg) resulted into significant (p&lt;0.05) rise in the levels of liver function marker enzymes Alanine Transaminase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP) and bilirubin and decrease in the levels of total protein and albumin in blood. On administration of low dose (250mg/Kg) and high dose (500mg/Kg) of both macrofungal extracts in different hepatotoxic group of rats, the serum levels of AST, ALT, ALP and bilirubin significantly (p&lt;0.05) lowered down and the levels of total protein and albumin significantly (p&lt;0.05) increased in comparison to the hepatotoxic group of rats, reflecting the hepatoprotective impact of both the extracts.

Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats: roles of adenosine deaminase and xanthine oxidase activities

Nutritional challenges and androgen excess have been implicated in the development of gestational diabetes and poor fetal outcome, but the mechanisms are not well delineated. The effects of short chain fatty acid (SCFA) on glucose dysmetabolism and poor fetal outcome induced by gestational androgen excess is also not known. We tested the hypothesis that blockade of androgen receptor (AR) and suppression of late gestational androgen excess prevents glucose dysmetabolism and poor fetal outcome through suppression of adenosine deaminase (ADA)/xanthine oxidase (XO) pathway. Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SCFA (sodium acetate; 200 mg/kg; p.o.) or AR blocker (flutamide; 7.5 mg/kg; p.o.) between gestational days 14 and 19. The results showed that late gestational androgen excess led to glucose deregulation, poor fetal outcome, increased plasma and hepatic free fatty acid and lactate dehydrogenase, liver function marker enzymes, malondialdehyde, uric acid, ADA and XO activities. Conversely, gestational androgen excess resulted in reduced body weight gain, visceral adiposity, plasma and hepatic anti-oxidant defenses (glutathione peroxidase, reduced glutathione/glutathione disulphide ratio, glucose-6-phosphate dehydrogenase, adenosine and nitric oxide). However, all these effects were ameliorated by either sodium acetate or flutamide treatment. The study demonstrates that suppression of testosterone by SCFA or AR blockade protects against glucose deregulation and poor fetal outcome by improvement of anti-oxidant defenses and replenishment of hepatic oxidative capacity through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome.

Olive oil and leaf extract prevent fluoxetine-induced hepatotoxicity by attenuating oxidative stress, inflammation and apoptosis

Olive oil and leaf extract have several health benefits; however, their beneficial effect against fluoxetine-induced liver injury has not been investigated. The present study aimed to scrutinize the impact of fluoxetine on the liver of rats and to evaluate the protective effects of olive oil and leaf extract. Rats received fluoxetine orally at dose of 10 mg/kg body weight for 7 consecutive days. The fluoxetine-induced rats were concurrently treated with olive oil or leaf extract. At the end of the experiment, blood and liver samples were collected for analysis. Fluoxetine administration significantly increased circulating ALT, AST, ALP and the pro-inflammatory cytokines TNF-α and IL-1β levels in rats. Histological analysis showed several alterations, such as inflammatory cells infiltration, hepatocyte vacuolation and dilated sinusoids in the liver of fluoxetine-induced rats. Concurrent supplementation of olive oil and olive leaf extract significantly reduced circulating liver function marker enzymes and pro-inflammatory cytokines, and prevented fluoxetine-induced histological alterations. Both olive oil and leaf extract significantly decreased liver lipid peroxidation and nitric oxide, and ameliorated liver glutathione, superoxide dismutase, catalase and glutathione peroxidase. In addition, olive oil and leaf extract prevented fluoxetine-induced apoptosis in the liver of rats as evidenced by decreased expression of Bax and caspase-3, and up-regulated expression of Bcl-2. In conclusion, olive oil and leaf extract protect against fluoxetine-induced liver injury in rats through attenuation of oxidative stress, inflammation and apoptosis.

Hesperidin protects against chemically induced hepatocarcinogenesis via modulation of Nrf2/ARE/HO-1, PPARγ and TGF-β1/Smad3 signaling, and amelioration of oxidative stress and inflammation

Hesperidin is a plant-derived bioflavonoid with promising antitumor efficacy, though the underlying mechanisms of action remain poorly elucidated. Thus, we evaluated the in vivo chemopreventive effect of hesperidin against diethylnitrosamine (DEN)-induced hepatocarcinogenesis. We demonstrated the modulatory effect of hesperidin on Nrf2/ARE/HO-1, PPARγ and TGF-β1/Smad3 signaling. Hepatocarcinogenesis was initiated with DEN and promoted with carbon tetrachloride (CCl4). DEN/CCl4-induced rats were treated with 50 and 100 mg/kg hesperidin throughout the experiment. The results revealed that hesperidin significantly reduced circulating liver function marker enzymes, bilirubin, tumor markers and tumor necrosis factor alpha. Hesperidin prevented liver morphological damage, proliferating cell nuclear antigen (PCNA) expression and oxidative stress as evidenced by the reduced lipid peroxidation and enhanced antioxidant defenses. Liver NF-κB and TGF-β1 expression, and Smad3 phosphorylation were significantly up-regulated in DEN/CCl4-induced rats. Hesperidin dramatically abolished NF-κB and TGF-β1/Smad3 signaling as well as collagen deposition in the liver of DEN/CCl4-induced rats. In addition, hesperidin markedly up-regulated the expression of Nrf2, HO-1 and PPARγ in the liver of DEN/CCl4-induced rats. In conclusion, hesperidin can inhibit hepatocarcinogenesis by suppressing oxidative stress, inflammation, cell proliferation, TGF-β1/Smad3 signaling and collagen deposition. These effects are suggested to be mediated by activating Nrf2/ARE/HO-1 and PPARγ pathways.

Berberine ameliorates methotrexate-induced liver injury by activating Nrf2/HO-1 pathway and PPARγ, and suppressing oxidative stress and apoptosis in rats

Berberine (BBR) is a natural isoquinoline alkaloid with very impressive health benefits. It is one of the most effective natural supplements available; however, its ameliorative mechanism against methotrexate (MTX)-induced liver injury is not well defined. This study investigated the protective effect of BBR against MTX hepatotoxicity, focusing on its ability to attenuate oxidative stress and apoptosis and to activate nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling and peroxisome proliferator activated receptor gamma (PPARγ). Rats received BBR (25 and 50mg/kg) orally for 7days before MTX injection. Other groups received MTX followed by BBR (25 and 50mg/kg) orally for 7 days. MTX-induced rats showed significant body weight loss, increased serum liver function marker enzymes, bilirubin and tumor necrosis factor alpha (TNF-α). Liver lipid peroxidation, nitric oxide (NO) and caspase-3 were significantly increased following MTX administration. BBR supplemented either before or after MTX significantly ameliorated body weight, liver function markers, TNF-α, lipid peroxidation, NO and caspase-3. BBR increased serum albumin and liver antioxidant defenses in MTX-induced rats. Histological and immunohistochemical examination showed improved histological structure and decreased expression of Bax in liver of MTX-induced rats treated with BBR. In addition, BBR up-regulated Nrf2, HO-1 and PPARγ expression in the liver of MTX-induced rats. In conclusion, BBR attenuated MTX-induced oxidative stress and apoptosis, possibly through up-regulating Nrf2/HO-1 pathway and PPARγ. Therefore, BBR can protect against MTX-induced liver injury.

Curative effect of &lt;em&gt;Plumbago indica&lt;/em&gt; root extract on thioacetamide induced hepatotoxicity in experimental rats

&lt;p&gt;The root parts of &lt;em&gt;Plumbago indica&lt;/em&gt; is widely used in the Indian Ayurvedic traditional system. The study was designed to evaluate the hepato curative activity Plumbago&lt;em&gt; Indica&lt;/em&gt; (PLBM) methanolic root extracts at different doses (100 and 200 mg/kg bw) against thioacetamide induced liver damage in albino wistar rats. Liver damage was induced by administration of Thioacetamide (100 mg/kg bw) and was assessed by evaluating the activity of liver-function marker enzymes, antioxidant enzymes and lipid peroxidation. The liver sections were evaluated for histopathological changes. PLBM significantly (&lt;em&gt;p &lt;/em&gt;≤ 0.05) reversed the elevation of serum liver enzymes and hepatic levels of antioxidant markers. Histopathological findings also confirmed the curative effect of &lt;em&gt;Plumbago Indica&lt;/em&gt; in a dose dependent manner. Thus this study scientifically rationale the use of &lt;em&gt;Plumbago indica &lt;/em&gt; root as a promising drug against various liver disorders.&lt;/p&gt;

Commiphora molmol resin attenuates diethylnitrosamine/phenobarbital-induced hepatocarcinogenesis by modulating oxidative stress, inflammation, angiogenesis and Nrf2/ARE/HO-1 signaling

The objective of the current study was to investigate the possible chemopreventive activity of Commiphora molmol resin (myrrh) extract using a rat model of diethylnitrosamine (DEN)/phenobarbital (PB)-induced early stage hepatocarcinogenesis. Here, we pointed to the modulatory effect of myrrh on oxidative stress, angiogenesis, inflammation and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Hepatocarcinogenesis was induced in Wistar rats using DEN for initiation and PB as a promoting agent. The rats received 125 or 250 mg/kg C. molmol resin extract throughout the experiment. Both doses of myrrh improved liver function marker enzymes and prevented oval cells proliferation and the distortion of hepatic architecture. The pro-inflammatory cytokine interleukin-6, tumor markers, angiogenesis markers, lipid peroxidation and nitric oxide (NO) were significantly increased in DEN/PB-induced rats. In addition, the antioxidant defenses showed marked reduction in the liver of DEN/PB-induced rats. Oral administration of C. molmol extract to DEN/PB-induced rats significantly decreased circulating markers of inflammation, tumor proliferation and angiogenesis, and liver lipid peroxidation and NO. In addition, C. molmol markedly ameliorated the antioxidant defenses and up-regulated Nrf2 and hemeoxygenase (HO)-1 in the liver of DEN/PB-induced rats. In conclusion, these results provide evidence that C. molmol resin has a potent chemopreventive activity, possibly by up-regulating the Nrf2/HO-1 signaling and attenuation of inflammation, angiogenesis and oxidative stress.

Methotrexate hepatotoxicity is associated with oxidative stress, and down-regulation of PPARγ and Nrf2: Protective effect of 18β-Glycyrrhetinic acid

18β-glycyrrhetinic acid (18β-GA) is a bioactive component of licorice with promising hepatoprotective activity. However, its protective mechanism on methotrexate (MTX) hepatotoxicity in not well defined. We investigated the hepatoprotective effect of 18β-GA, pointing to the role of peroxisome proliferator activated receptor gamma (PPARγ) and the redox-sensitive nuclear factor erythroid 2-related factor 2 (Nrf2). Wistar rats were orally administered 18β-GA (50 and 100 mg/kg) 7 days either before or after MTX injection. MTX induced significant increase in circulating liver function marker enzymes and bilirubin with concomitant declined albumin levels. Serum pro-inflammatory cytokines, and liver malondialdehyde and nitric oxide were significantly increased in MTX-induced rats. Treatment with 18β-GA significantly reduced serum enzymes of liver function, bilirubin and pro-inflammatory cytokines. 18β-GA attenuated MTX-induced oxidative stress and restored the antioxidant defenses. In addition, 18β-GA improved liver histological structure and decreased the expression of Bax whereas increased Bcl-2 expression. MTX-induced rats showed significant down-regulation of Nrf2, hemoxygenase-1 and PPARγ, an effect that was markedly reversed by 18β-GA supplemented either before or after MTX. In conclusion, 18β-GA protected against MTX-induced liver injury, possibly by activating Nrf2 and PPARγ, and subsequent attenuation of inflammation, oxidative stress and apoptosis. Therefore, 18β-GA can provide protection against MTX-induced hepatotoxicity.

Evaluation of Antioxidant and Hepatoprotective Activity of Fruit Rind Extract of Garcinia dulcis (Roxburgh) Kurz.

Background:Garcinia spp. belongs to the family Clusiaceae has been traditionally used for the treatment of many ailments including the liver damage. Garcinia dulcis found in North Eastern region of Assam; India can be a potential candidature to combat different ailments. Objective: The present work has been designed in such a way to appraisal the antioxidant and hepatoprotective activity of fruit rind extract of this plant.Materials and Methods:The antioxidant activity was investigated through the various in vitro models, namely, 2,2-diphenyl-1-picrylhydrazine, 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid, nitrite oxide. Phytochemical investigation for total phenolic and flavonoids contents were carried out by standard protocol. For the evaluation of hepatoprotective activity, albino Wistar rats were divided into five groups, five animals per group and activity was determined by measuring the contents of liver function marker enzymes such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (ALP), and biochemical parameter, that is, Bilirubin and total protein. Histopathology observation of liver sections was conducted.Results:Phytochemical investigation revealed the presence of both phenolic and flavonoid groups in the extract in a significant amount. Antioxidant activity of the plant extract was observed in all models and percentage of inhibition was dose-dependent. Intoxicated with carbon tetrachloride, elevated the liver function enzymes, bilirubin, and suppressed the production of total protein. Pretreatment with the extract decreased the SGOT, SGPT, ALP, and bilirubin level significantly and increased the production level of total protein in a dose-dependent manner. The histopathological observation supported the hepatoprotective potentiality of the extract.Conclusion:The results indicate that fruit rind part of G. dulcis is nontoxic and the plant can utilize as an antioxidant source. The plant has a protective agent for liver damages and other diseases caused by free radicals.SUMMARY In vitro antioxidant and in vivo hepatoprotective activity was evaluatedMethanolic extract was subjected to quantify the both phenolic and flavonoid contents. The extract showed the significant amount of both phenolic and flavonoids contents. The extract showed the free radical scavenging activity in 2,2-diphenyl-1-picrylhydrazine, 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid and nitrite oxide modelsThe extract was administrated against the carbon tetrachloride intoxicated animal models to evaluate the hepatoprotective activity by determining the level of liver marker enzymes such as serum glutamate pyruvate transaminase, SGOT, alkaline phosphatase and biochemical parameter such as protein and bilirubin. Pretreatment with the extract reversed the elevated level of the enzymes and increased the protein level in a dose-dependent mannerThe histopathological observations of the liver sections supported the hepatoprotective activity of the extractThe present study revealed that the Garcinia dulcis extract is a good candidature for preventing liver damage and other disease caused by free radicals. Abbreviations Used: DPPH: 2,2-diphenyl-1-picrylhydrazine, ABTS: 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid, SGOT: Serum glutamate oxaloacetate transaminase, SGPT: Serum glutamate pyruvate transaminase, ALP: Serum alkaline phosphatase.

Formulation and characterization of an apigenin-phospholipid phytosome (APLC) for improved solubility, in vivo bioavailability, and antioxidant potential

The apigenin-phospholipid phytosome (APLC) was developed to improve the aqueous solubility, dissolution, in vivo bioavailability, and antioxidant activity of apigenin. The APLC synthesis was guided by a full factorial design strategy, incorporating specific formulation and process variables to deliver an optimized product. The design-optimized formulation was assayed for aqueous solubility, in vitro dissolution, pharmacokinetics, and antioxidant activity. The pharmacological evaluation was carried out by assessing its effects on carbon tetrachloride-induced elevation of liver function marker enzymes in a rat model. The antioxidant activity was assessed by studying its effects on the liver antioxidant marker enzymes. The developed model was validated using the design-optimized levels of formulation and process variables. The physical-chemical characterization confirmed the formation of phytosomes. The optimized formulation demonstrated over 36-fold higher aqueous solubility of apigenin, compared to that of pure apigenin. The formulation also exhibited a significantly higher rate and extent of apigenin release in dissolution studies. The pharmacokinetic analysis revealed a significant enhancement in the oral bioavailability of apigenin from the prepared formulation, compared to pure apigenin. The liver function tests indicated that the prepared phytosome showed a significantly improved restoration of all carbon tetrachloride-elevated rat liver function marker enzymes. The prepared formulation also exhibited antioxidant potential by significantly increasing the levels of glutathione, superoxide dismutase, catalase, and decreasing the levels of lipid peroxidase. The study shows that phospholipid-based phytosome is a promising and viable strategy for improving the delivery of apigenin and similar phytoconstituents with low aqueous solubility.

Ellagic acid rich Momordica charantia fruit pulp supplementation prevented oxidative stress, fibrosis and inflammation in liver of alloxan induced diabetic rats

The present study was undertaken to investigate the hepatoprotective effect of Momordica charantia in alloxan induced diabetic rats. The experimental rats were randomly divided into four groups. Oral glucose tolerance test (OGTT) and biochemical analysis for oxidative stress parameters and liver function marker enzymes were analyzed for each group of rats. Moreover, histological staining was also performed on liver sections. Momordica charantia supplementation prevented the rise of blood glucose level and improved oral glucose tolerance test in alloxan induced diabetic rats. Liver marker enzymes such as aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) activities were increased in alloxan induced rats which were normalized in Momordica charantia supplemented group. In addition, elevated level of oxidative stress markers were also observed in alloxan induced diabetic rats. Momordica charantia supplementation significantly restored the superoxide dismutase (SOD), catalase (CAT) enzymes activities and increased reduced glutathione (GSH) concentration in diabetic rats. Histological assessments confirm the mononuclear cell infiltration and fibrosis in liver of alloxan induced diabetic rats which were ameliorated by Momordica charantia supplementation. The present investigation suggests the hepatoprotective nature of Momordica charantia in diabetic rats probably by attenuating oxidative stress and improving the antioxidant competence in hepatic tissues.

Green chicken without antibiotics produced by replacing the methanol extract of alfalfa (Medicago sativa) and remove antibiotics and effects on liver function enzymes and poultry performance in terms of weight gain

Abstract. In recent years, due to prohibitions and restrictions on the use of antibiotics as feed additives in poultry nutrition additives such Fytobiotics as healthy additives, poultry industry is concerned. Method: A total of 60 male Ross broiler chicks were randomly divided into three treatment. Treatments including : control, alfalfa0.1%, alfalfa 0.15%. The None type of antibiotic that is used in the project and at the end of the period of function indicators of liver enzymes (AST, ALT, ALP) was determined and the Body weight was measured. The results: Treatments for liver function marker enzymes have been shown to increase. But ALP enzyme at P<0/01was significant and the other two enzymes AST, ALT did not showed a significant increase. In terms of weight gain in all groups compared with control Group, a significant increase showed in the level of P<0/001. The conclusion: By replacing the alcoholic extract of alfalfa in the dose listed can without the use of antibiotics, to gain weight, without any metabolic particular problem found during the rearing broiler chickens.

The Influence of Pesticides on Hepatic and Renal Functions in Occupational Sprayers of Rural Malihabad, Lucknow (India)

Pesticides affect several human organs, resulting in a wide variety of physiological changes. In context with the occupational pesticide sprayers it is important to understand the influence of toxic exposure on human health. The present study is a comparative analysis of hematologic parameters, hepatic and renal function in the occupationally exposed pesticide sprayers of mango plantation of rural Malihabad, Lucknow. This area is predominantly a mango cultivation belt in North India. The select group of study comprises of sixty (60) pesticide sprayers [study group] and the control group included thirty (30) pesticides-unexposed normal healthy persons engaged in normal usual agricultural work [age group 20 to 45 years corresponding to age group of select subject group] from rural Malihabad, Lucknow [India]. Blood samples were collected from both groups. Questionnaire, interview and observation were employed to obtain demographic, occupational, dietary and clinical data. The sprayers as compared with control participants showed significantly increased serum C reactive protein, liver function marker enzymes, serum bilirubin, creatinine, blood glucose, and blood urea; whereas the acetyl cholinesterase activity and the level of serum cholesterol declined. No significant alteration was observed in the serum total protein, globulin, and the albumin/globulin ratio; however, a slight downfall in the level of serum albumin was recorded. Compared with the control group, hematologic parameters significantly decreased in pesticide sprayers. It is suggested that a high degree of pesticide absorption in occupationally exposed pesticides sprayers is responsible for decrease in the level of serum acetyl cholinesterase and consequently there is impairment of liver and kidney functions and slightly altered hematologic parameters. The present study suggests the toxic effect of pesticides on the occupational sprayer and precautionary measures must be taken to ameliorate their health status. It also suggests that restrain must be imposed on the indiscriminate use of lethal pesticides as it affects the ecosystem.