scholarly journals Hepatoprotective effect of essential oils of Nepeta cataria L. on acetaminophen-induced liver dysfunction

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Juan Tan ◽  
Jing Li ◽  
Jilei Ma ◽  
Feng Qiao
Keyword(s):  
Liver Injury ◽  
Essential Oils ◽  
Liver Damage ◽  
Animal Experiments ◽  
Intermediate Formation ◽  
Uridine Diphosphate ◽  
Phase Ii Enzymes ◽  
Nepeta Cataria ◽  
Hepatoprotective Agent ◽  
Increase Mrna Expression

Abstract Nepeta cataria L. has long been used in folk food and medicine for several functions. Essential oils (EOs) were extracted from Nepeta cataria L. by supercritical fluid extraction. The results of animal experiments showed that EOs from Nepeta cataria L. significantly attenuated acetaminophen-induced liver damage. Further study confirmed that EOs were able to increase mRNA expression of uridine diphosphate glucuronosyltransferases (UGTs) and sulfotransferases (SULTs), as well as inhibit CYP2E1 activities, and thereby suppressed toxic intermediate formation. Nrf-2 activation might be involved in EOs-induced up-regulation of Phase II enzymes. Collectively, our data provide evidence that EOs protect the liver against acetaminophen-induced liver injury mainly by accelerating acetaminophen harmless metabolism, implying that EOs can be considered as a potential natural resource to develop hepatoprotective agent.

Risk for death increasing with cardiovascular chronic gout patients associated with febuxostat

2020 ◽  
Vol 10 (1) ◽  
pp. 14-17
Author(s):  
Ramachandran K ◽  
Rajesh Yadav ◽  
Sumitra Devkota
Keyword(s):  
Liver Injury ◽  
Associate Degree ◽  
Medical Attention ◽  
Uridine Diphosphate ◽  
Therapeutic Result ◽  
Pyrimidine Synthesis ◽  
Chronic Gout ◽  
Excretory Organ ◽  
Outcomes Study ◽  
Coronary Failure

Febuxostat used for the treatment of patients with arthritis littered with Hyperuricemia and is utilized in its Chronic Management. a number of the internal organ adverse effects have diode to the employment of febuxostat replaced with with allopurinol drug. Febuxostat, associate degree compound accelerator matter, achieves its therapeutic result by decreasing humour acid. At therapeutic concentrations it is not expected that Febuxostat will inhibit different enzymes which are involved in purine and pyrimidine synthesis and their metabolism. Metabolism of Febuxostat is done by conjugation via uridine diphosphate glucuronosyltransferase (UGT) enzymes and also by UGT1A1, UGT1A3, UGT1A9, and UGT2B7 and reaction via hemoprotein P450 (CYP) enzymes as well as CYP1A2, 2C8 and 2C9 and non-P450 enzymes. Febuxostat is eliminated primarily through each viscus and excretory organ pathways. Febuxostat could cause heart issues that may result in coronary failure, could cause issues within the blood vessels that visit your brain. this could conjointly result in stroke, urarthritis flare-ups and Liver injury. Some facet effects of febuxostat could occur that sometimes don't would like medical attention. We conclude from our review, vessel Death urarthritis patients with established vessel (CV) illness treated with febuxostat had a better rate of CV death compared to those treated with allopurinol drug in a very CV outcomes study.

scholarly journals BML-257, a small molecule that protects against drug induced liver injury in zebrafish

2022 ◽  
Author(s):  
Urmila Jagtap ◽  
Sandeep Basu ◽  
Lavanya Lokhande ◽  
Nikhil Bharti ◽  
Chetana Sachidanandan
Keyword(s):  
Liver Injury ◽  
Small Molecule ◽  
Liver Damage ◽  
Protective Action ◽  
Damage Model ◽  
Akt Inhibitor ◽  
Drug Induced ◽  
Specific Expression ◽  
Drug Induced Liver Injury ◽  
Chemical Screen

The use of many essential drugs is restricted due to their deleterious effects on the liver. Molecules that can prevent or protect the liver from drug induced liver injury (DILI) would be valuable in such situations. We used hepatocyte-specific expression of bacterial nitroreductase in zebrafish to cause temporally controlled liver damage. This transgenic line was used to run a whole organism based chemical screen in zebrafish larvae. In this screen we identified BML-257, a potent small molecule AKT inhibitor, that protected the liver against metronidazole-induced liver injury. BML-257 also showed potent prophylactic and pro-regenerative activity in this liver damage model. BML-257 also showed remarkable protective action in two independent toxicological models of liver injury caused by acetaminophen and Isoniazid. This suggests that BML-257 may have the potential to protect against multiple kinds of drug induced liver injury.

Protective and Therapeutic Effects of Curcuma xanthorrhiza on Hepatotoxin-induced Liver Damage

1995 ◽  
Vol 23 (03n04) ◽  
pp. 243-254 ◽  
Author(s):  
Song-Chow Li ◽  
Chun-Ching Lin ◽  
Yun-Ho Lin ◽  
S. Supriyatna ◽  
Chao-Wei Teng
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Damage ◽  
Intraperitoneal Administration ◽  
Therapeutic Effects ◽  
Acute Liver Damage ◽  
Liver Injuries ◽  
Acute Elevation ◽  
Serum Transaminases ◽  
Hepatoprotective Agent ◽  
Curcuma Xanthorrhiza

Curcuma xanthorrhiza Roxb. (Zingiberaceae family, commonly known as temu lawak or Javanese turmeric in Indonesia), which is found both wild and cultivated in Indonesia, has been traditionally used for medicinal purposes. C. xanthorrhiza is also used as a tonic in Indonesia. The aim of the present study is to clarify whether C. xanthorrhiza treatment may prevent acute liver damage induced by acetaminophen and carbon tetrachloride in mice. The results clearly indicated that extract of C. xanthorrhiza could reduce significantly the acute elevation of serum transaminases levels induced by the two kinds of hepatotoxins, and alleviated the degree of liver damage at 24 hours after the intraperitoneal administration of two hepatotoxins. It may be concluded that C. xanthorrhiza can protect the liver from various hepatotoxins, hence C. xanthorrhiza could be useful in the treatment of liver injuries and has promise as a kind of broad spectrum hepatoprotective agent.

Drugs and liver damage

2010 ◽  
pp. 2527-2537
Author(s):  
J. Neuberger
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Pulmonary Tuberculosis ◽  
Liver Damage ◽  
Case History ◽  
Genetic Component ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Almost All

Case History—A 22 yr old man, being treated for pulmonary tuberculosis, now presenting with confusion and jaundice. Drug-induced liver injury (DILI) is relatively uncommon but can very rarely be fatal. Almost all patterns of liver disease can be induced by drugs, and some drugs may be associated with more than one type of reaction. Some cases of DILI have a genetic component. Most cases present with jaundice and/or hepatitis....

scholarly journals Cell-specific regulatory effects of CXCR2 on cholestatic liver injury

2019 ◽  
Vol 317 (6) ◽  
pp. G773-G783 ◽  
Author(s):  
Takanori Konishi ◽  
Rebecca M. Schuster ◽  
Holly S. Goetzman ◽  
Charles C. Caldwell ◽  
Alex B. Lentsch
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Liver Damage ◽  
Chemokine Receptor ◽  
Therapeutic Target ◽  
Bile Duct Ligation ◽  
Wild Type ◽  
Neutrophil Accumulation ◽  
Duct Ligation ◽  
Cholestatic Liver Injury

The CXC chemokine receptor 2 (CXCR2) is critical for neutrophil recruitment and hepatocellular viability but has not been studied in the context of cholestatic liver injury following bile duct ligation (BDL). The present study sought to elucidate the cell-specific roles of CXCR2 on acute liver injury after BDL. Wild-type and CXCR2−/− mice were subjected BDL. CXCR2 chimeric mice were created to assess the cell-specific role of CXCR2 on liver injury after BDL. SB225002, a selective CXCR2 antagonist, was administrated intraperitoneally after BDL to investigate the potential of pharmacological inhibition. CXCR2−/− mice had significantly less liver injury than wild-type mice at 3 and 14 days after BDL. There was no difference in biliary fibrosis among groups. The chemokines CXCL1 and CXCL2 were induced around areas of necrosis and biliary structures, respectively, both areas where neutrophils accumulated after BDL. CXCR2−/− mice showed significantly less neutrophil accumulation in those injured areas. CXCR2Liver+/Myeloid+ and CXCR2Liver−/Myeloid− mice recapitulated the wild-type and CXCR2-knockout phenotypes, respectively. CXCR2Liver+/Myeloid+ mice suffered higher liver injury than CXCR2Liver+/Myeloid− and CXCR2Liver−/Myeloid+; however, only those chimeras with knockout of myeloid CXCR2 (CXCR2Liver+/Myeloid− and CXCR2Liver−/Myeloid−) showed reduction of neutrophil accumulation around areas of necrosis. Daily administration of SB225002 starting after 3 days of BDL reduced established liver injury at 6 days. In conclusion, neutrophil CXCR2 guides the cell to the site of injury, while CXCR2 on liver cells affects liver damage independent of neutrophil accumulation. CXCR2 appears to be a viable therapeutic target for cholestatic liver injury. NEW & NOTEWORTHY This study is the first to reveal cell-specific roles of the chemokine receptor CXCR2 in cholestatic liver injury caused by bile duct ligation. CXCR2 on neutrophils facilitates neutrophil recruitment to the liver, while CXCR2 on liver cells contributes to liver damage independent of neutrophils. CXCR2 may represent a viable therapeutic target for cholestatic liver injury.

scholarly journals Bamboo Stems (Phyllostachys nigra variety henosis) Containing Polyphenol Mixtures Activate Nrf2 and Attenuate Phenylhydrazine-Induced Oxidative Stress and Liver Injury

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 114 ◽  
Author(s):  
Ji Hye Yang ◽  
Moon-Hee Choi ◽  
Chang-Su Na ◽  
Sam Seok Cho ◽  
Jae Hoon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Iron Overload ◽  
Liver Damage ◽  
Hepg2 Cells ◽  
Hepatoprotective Effect ◽  
Glutathione Depletion ◽  
Related Factor ◽  
Nrf2 Target Gene ◽  
Phyllostachys Nigra

This study was designed to investigate the hepatoprotective effect of bamboo stems using in vitro and in vivo experimental liver damage models. Ethyl acetate fraction of 80% ethanol extract of Phyllostachys nigra stem (PN3) containing polyphenols had a higher NQO1-ARE reporter gene activity as monitored by the activity of the NF-E2-related factor (Nrf2) antioxidant pathway in cells in comparison to extracts from other species and under other conditions. The Nrf2 was translocated from the cytosol to the nucleus in response to PN3, followed by induction of the Nrf2 target gene expression, including HO-1, GCL, and NQO-1 in HepG2 cells. Phosphorylation of Nrf2 in HepG2 cells was enhanced in PN3, which was mediated by PKCδ, ERK, and p38 MAPK. Consequently, PN3 inhibited arachidonic acid (AA) + iron-induced reactive oxygen species generation and glutathione depletion, and, thus, highlighted their role in cytotoxicity. Treatment with major polyphenols of PN3, including catechin, chlorogenic acid, caffeic acid, and p-coumaric acid, also improved AA + iron-mediated oxidative stress and, thus, improved cell viability. Treatment with phenylhydrazine in mice, i.e., the iron overload liver injury model, increased plasma alanine aminotransferase and aspartate aminotransferase levels and changed histological features in mice—a response that was almost completely blocked by PN3 administration. Moreover, PN3 extract mitigated phenylhydrazine-induced oxidative stress and inflammatory responses. Conclusively, PN3 can exert a hepatoprotective effect against iron overload-induced acute liver damage due to its antioxidant properties.

scholarly journals Antibacterial and Cytotoxic Activity of Nepeta Cataria L., N. Cataria Var. Citriodora (Beck.) Balb. and Melissa Officinalis L. Essential Oils

2007 ◽  
Vol 2 (12) ◽  
pp. 1934578X0700201 ◽  
Author(s):  
Ulrike Suschke ◽  
Frank Sporer ◽  
Jürgen Schneele ◽  
Heinrich Konrad Geiss ◽  
Jürgen Reichling
Keyword(s):  
Respiratory Tract ◽  
Essential Oils ◽  
Cytotoxic Activity ◽  
Clinical Isolates ◽  
Melissa Officinalis ◽  
Bronchial Epithelial ◽  
Lemon Balm ◽  
Nepeta Cataria ◽  
Tract Infections ◽  
Reference Strains

The aim of the present study was to investigate the susceptibility of bacteria that play a role in respiratory tract and skin infections to the essential oils of catnip (Nepeta cataria), lemon catnip (N. cataria var. citriodora) and lemon balm (Melissa officinalis) with regard to their chemical composition. In addition, we wanted to assess whether antibiotic-resistant and -sensitive strains differ in their susceptibility to the oils and if there are cross resistances between standard antibiotics and essential oils. To evaluate the safety of topical application, cytotoxicity of the oils was studied in human keratinocyte and bronchial epithelial cell lines and irritation threshold concentrations were determined in ovo using the HET-CAM-test. The composition of the essential oils was analyzed by GC and GC-MS. Their MICs and MBCs were determined by a broth microdilution method against both reference strains from culture collections and clinical isolates with different susceptibility to standard antibiotics. Cytotoxicity was assessed by the MTT assay. Except for P. aeruginosa (MIC ≥2%), all reference strains tested were susceptible to catnip and lemon balm oils with MIC values ranging from 0.016 % to 0.25% (v/v). The clinical isolates were as susceptible to the oils (± 1 serial dilution) as the corresponding reference strains, regardless of their origin and resistance to standard antibiotics. The oils were cytotoxic to both keratinocytes and bronchial epithelial cells at CC50 values from 0.0012% to 0.015% (v/v). Lemon balm oil, whose main components were monoterpene aldehydes, exhibited the highest antibacterial and cytotoxic activity, followed by lemon catnip oil, which contained mainly monoterpene alcohols, and catnip oil, which was characterized by nepetalactones. Our results provide a rationale for the use of catnip, lemon catnip and lemon balm oils in the complementary topical treatment of respiratory tract infections, as the oils show a high antibacterial activity against respiratory tract pathogens, including clinical isolates with reduced susceptibility to standard antibiotics. However, cytotoxicity must be considered in topical therapy.

Liver asialoglycoprotein receptor levels correlate with severity of alcoholic liver damage in rats

2004 ◽  
Vol 96 (1) ◽  
pp. 76-80 ◽  
Author(s):  
Carol A. Casey ◽  
Benita L. McVicker ◽  
Terrence M. Donohue ◽  
Melinda A. McFarland ◽  
Robert L. Wiegert ◽  
...  
Keyword(s):  
Liver Injury ◽  
Oral Administration ◽  
Liver Damage ◽  
Medium Chain Triglyceride ◽  
Asialoglycoprotein Receptor ◽  
Mrna Levels ◽  
Liver Pathology ◽  
Medium Chain ◽  
Ethanol Group ◽  
Liver Changes

It has been demonstrated that the oral administration of ethanol (Lieber-DeCarli liquid diet) to rats results in a decreased expression and content of the asialoglycoprotein receptor (ASGP-R) in the resultant fatty liver. In the present study, we wanted to determine whether the extent of impaired receptor content was correlated with the severity of liver pathology by using the intragastric feeding model. When ASGP-R protein and mRNA levels were measured in animals infused with ethanol or dextrose in the presence of fish oil (FO) or medium-chain triglyceride as the source of fat, more significant impairments to the ASGP-R were observed in the FO-ethanol group compared with the medium-chain triglyceride-ethanol group. Furthermore, only the FO-ethanol group showed pathological liver changes. These results demonstrate that a correlation exists between the progression of alcohol-associated liver injury, as defined by the severity of liver pathology, and an ethanol-induced decline in ASGP-R content.

The chemokine scavenging receptor D6 limits acute toxic liver injury in vivo

2009 ◽  
Vol 390 (10) ◽  
Author(s):  
Marie-Luise Berres ◽  
Christian Trautwein ◽  
Mirko Moreno Zaldivar ◽  
Petra Schmitz ◽  
Katrin Pauels ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Damage ◽  
Immune Modulation ◽  
Scavenger Receptor ◽  
Wild Type ◽  
Protein Levels ◽  
Inflammatory Chemokines ◽  
Toxic Liver Injury ◽  
Acute Toxic

Abstract The chemokine decoy receptor D6 is a promiscuous chemokine receptor lacking classical signaling functions. It negatively regulates inflammation by targeting CC chemokines to cellular internalization and degradation. Here we analyze the function of D6 in acute CCl4-induced liver damage in constitutive D6-/- and wild-type mice. The degree of liver injury was assessed by liver histology, serum transaminases, IL-6, and TNFα mRNA expression. Protein levels of D6 ligands (CCL2, CCL3, CCL5) and the non-D6-ligand CXCL9 within the livers were determined by ELISAs. The intrahepatic infiltration of immune cells was characterized by FACS. Genetic deletion of D6 led to prolonged liver damage after acute CCl4 administration. The augmented liver damage in D6-/- mice was associated with increased protein levels of intrahepatic inflammatory chemokines CCL2, CCL3, and CCL5 after 48 h, whereas CXCL9 was not different between knockout and wild-type mice. Functionally, increased intra-hepatic CC chemokine concentrations led to increased infiltration of CD45+ leukocytes, which were mainly identified as T and NK cells. In conclusion, the chemokine scavenger receptor D6 has a non-redundant role in acute toxic liver injury in vivo. These results support the importance of post-translational chemokine regulation and describe a new mechanism of immune modulation within the liver.

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