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Hepatoprotective - Science topic

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I am currently working on the hepatoprotective effect of pomegranate by CCl4-induced liver injury in C57 mice. This is my final year research project for my BS(hon).
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Good luck
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Hello !!!
I am working on the hepatoprotective effect of some medicinal plants and, i want to use the ccl4 induced acute liver injury ( 7days protocole)
there are a plenty of articles that treat the subject, and each one use differente concentration !!
so according to your experience what is the best and most used ccl4 concentration to induce mice acute liver injury ??
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We got the best resalts using 0.5 ml/kg CCl4 to induce fibrosis
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Dear Bioscientists,
ALT is a biomarker of liver damage, generally used to investigate hepatoprotective activities. Usually this marker is quantified in plasma/serum, but sometimes, it can also been assessed in liver homogenates.
1- May you share with me some publications reporting ALT assay in liver homogenates, After a chemical injury ?
2- using apap as an example of hepatotoxicant, Do you think ALT values in liver should increase or decrease. Because I saw some conflicting publications on that.
Thanks in advance for your suggestions.
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After induced- paracetamol liver injuries, surely the levels of ALT increase.
i advise to you to assay livers antioxidative enzymes, such as SOD or superoxide dismotase, or malone dialdehyde.....
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Dear Researchers
I have done in vitro hepatoprotective activity of diff. conc. of my plant extract in HePG2 cell lines using Paracetamol as toxicity inducer and silymarin as reference drug. I am in confusion to use which method to use for statistical analysis of data. Whether two way ANNOVA, one way ANNOVA need to be used or independent t-test is sufficient for analysis? Please guide me regarding this.
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1. Independent t-test: compare untreated control to either one of your treatment group.
For instance: Paracetamol vs. Plant extract concentration 1 or, Silymarin vs. Plant extract concentration 1.
2. One way ANOVA with Dunnett's post-hoc test: compare untreated control to all the treatment group.
For instance: Untreated control (Normal control) vs. Plant extract concentration 1, 2, 3 and so forth.
OR,
One way ANOVA with Tukey's post-hoc test: compare all the treatment groups in your in vitro study.
3. Two way ANOVA - inappropriate in your scenario as what you mentioned doesn't need this analysis.
Hope it's helpful. All best luck!
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I am working on hepatoprotective activity. As a part of my study I have to conduct histopathological study of larvae. I went through different research papers. But each paper showing different procedure. Can any one share exact protocol for fixing zebrafish larvae by using 4 % PFA.
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Thank you Melissa Chernick, Daniel Turkewitz, Emmanuel Ifeanyi Obeagu for your guidance,
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Recently I have done with my hepatoprotective experiment where I used CCl4 to induce liver damage. While evaluating my hepatic marker, unfortunately I have got higher serum AST level in the reference control (222 U/L) than the hepatic control (156 U/L) group. The other marker is ok. How can I validate the data with my statics? Badly need some suggestions what to do?
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Use more animals in a group to take care of the errors. Normal control may have erroneously been fed CCl4.
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Hepatoprotective activity
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Herewith i am attaching a detailed paper on hepatoprotective activities paper.
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im working on the antioxidant and hepatoprotective potential of Azolla microphylla . please help me with the simplest method to synthesis the gold nanopareticles from azolla.
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In liver hepatoprotective studies, we use many animals and we incur high financial costs. Can we use ovo in the experiments of evaluating the efficacy of plant extracts in protecting the liver by injecting the extract into fertilized eggs and observing their effect on the fetus?
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Not suitable may plan on specific cells.
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we have some experiment about "hepatoprotective effect of some plant extract on mice" and we need to measure the mice blood pressure .  
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Hi Abdollah
May be the following paper will be helpful for you.
Non-invasive blood pressure measurement in mice. 
Abstract
Hypertension is a leading cause of heart attack, stroke, and kidney failure and represents a serious medical issue worldwide. The genetic basis of hypertension is well-established, but few causal genes have been identified thus far. Non-invasive blood pressure measurements are a critical component of high-throughput genetic studies to identify genes controlling blood pressure. Whereas this technique is fairly routine for blood pressure measurements in rats, non-invasive blood pressure measurement in mice has proven to be more challenging. This chapter describes an experimental protocol measuring blood pressure in mice using a CODA non-invasive blood pressure monitoring system. This method enables accurate blood pressure phenotyping in mice for linkage or mutagenesis studies, as well as for other experiments requiring high-throughput blood pressure measurement.
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Which are the best biomarkers to be study to check Hepatoprotective effect of a plant extract?
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AST, ALT, ALP, Albumin, Bilirubin are the best. 
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Seanol (Dieckol) has been reported to show various biological activities, such as anti-inflammatory, antioxidative, hepatoprotective, antidiabetic, anti-allergic, antiviral and anticancer activities. Moreover, it is intermediated agent which well disperses in polar solvents. How to conjugate Seanol (Dieckol) with the surface of porous silica nanoparticle or modified silica particle for biological applications ?
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Thank you so much, Professor.
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I have tested the hepatoprotective effect of a natural compound in cyclophosphamide-induced rats and I want to test it in vitro using HepG2 cell line. Because my main target is oxidative stress, I want to induce oxidative stress in HepG2 cells using cyclophosphamide. I found other models like CCl4, cyclosporine and hydrogen peroxide induced oxidative stress in HepG2, but I didn't found any about cyclophosphamide. Do you have any idea?
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Protein assay for heme oxygenase-1 (HO-1) induced by chemicals in HepG2 cells.
Miyamoto Y, Ohshida K, Sasago K.
Abstract
Levels of heme oxygenase-1 (HO-1), a stress response protein, were measured to examine oxidative stress induced by several chemicals in HepG2 cells with and without S9mix using an ELISA. CdCl(2), heme, and diclofenac sodium salt (diclofenac) were used as inducers of HO-1. Acetaminophen (AAP) and cyclophosphamide (CP) were used as oxidative stress inducers. Stannic mesoporphyrin (SnMP) was used as an inhibitor of HO activity. Cytotoxicity was determined, and HO-1 levels were measured in HepG2 cells exposed to chemicals other than CP with non-metabolic activation without S9mix, and to diclofenac, AAP and CP with metabolic activation with S9mix. HO-1 levels were increased by CdCl(2) (7.5 microM), heme (10, 100 microM), and stannic mesoporphyrin (SnMP) (10 microM), but were not changed by AAP, and were decreased by diclofenac. HO-1 levels were increased by diclofenac (300 microM), and CP (36 microM), but were unaffected by AAP because of low sensitivity in HepG2 cells. The induction of HO-1 expression was first observed in cultured HepG2 cells treated with CP under conditions involving metabolic activation. These results showed the measurement of HO-1 protein levels in this system is useful when assessing oxidative stress as a tool for detecting drug toxicity.
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I am investigating the hepatoprotective effect of some medicinal plant on chronic carbon tetrachloride induced liver injury. I observed that although some of the medicinal plants increased the antioxidant enzyme (SOD, CAT and GSH) level in rats co-exposed to CCl4 and the extracts while they also increased lipid peroxidation and markers of hepatic injury such as ALT and AST.Has anyone experienced something similar? If yes, what are the likely reasons why this happened?
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Dear Ifeoluwa T Oyeyemi
I am attaching literature on the anticancer properties. I hope they will be useful to you.
I recommend the fruit of Rhus coriaria L. (Anacardiaceae) for your research.
Good luck.
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We are evaluating the hepatoprotective effect of a plant extract against a chemical carcinogen. Following treatment of the induced rats with the plant extract, we observed increased serum albumin levels when compared with the control group. Interestingly, we found a significant increase in serum albumin compared to the NORMAL group. Is there any explanation?!
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There is a clinical study on Moringa Olifeira that observed:   '…the crude extract increased serum albumin by 15.22% (46-53 g/l). This value was also found to be statistically significant. It was concluded that the leaves of Moringa oleifera have definite hypocholesterolemic activity and that there is valid pharmacological basis for employing them..." The study is titled Hypocholesterolemic effects of crude extract of leaf of Moringa oleifera Lam in high-fat diet fed wistar rats.  You can access it at http://www.ncbi.nlm.nih.gov/pubmed/10661880.  I hope you find it useful.
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I have to carry out hepatoprotective screening of few ethnomedicinal plants using alcohol as hepatotoxicant. I went through several papers, but none has mentioned the alcohol percentage orally to be given to rats. Kindly help 
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Dear Nissar, do you mean single or chronic administration of ethanol - chronic seems to be not very convenient for the screening and single may not lead to necrosis (we used a single dose of 9 ml/kg as 30% sol. while modelling lipid metabolism disorders, and this dose have not lead even to an increase in cytolisis as evidenced by plasma ASaT and ALaT activity)
Regards,
Olga
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What is the role of hepatoprotective products in treatment/management of hepatitis B virus infection?
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The use of hepatoprotective products is useless in course of HBV infection since the liver damage is related to virus replication. 
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With concentration on (INH-Rifampicin , Acetaminophen , Alcohol , CCl4 , NSAIDs)
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miR-122 or Keratin 18..can you be more specific with the question, then would love to discuss ...
Also depending on the drug there can be changes..drug means the MOA of hepatotoxicity...cholestasis will have different signatures compared to hepatocellular..though mitochondrial tox can be a common feature for both of them...apart from Fas-induced apoptosis i think