scholarly journals Diclofenac Synthesis

2021 ◽  
Author(s):  
Aymen Labidi
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Hepatic Injury ◽  
Liver Toxicity ◽  
Reactive Intermediates ◽  
The United States ◽  
Hepatocellular Injury ◽  
Hepatocellular Damage ◽  
Immune Mediated ◽  
Inflammatory Drugs

Diclofenac is an NSAID, Non-Steroidal Anti-Inflammatory Drugs, widely used clinically in the treatement of osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis, and has been available in the United States since 1988 (Banks et al. 1995). Diclofenac can cause hepatotoxicity, and despite the rare nature of these events, affects a large number of people due to its widespread usage. It is one of the most common drugs associated with idiosyncratic hepatic injury (Daly et al. 2007). From November 1988 to June 1991 the FDA received 180 cases of diclofenac-induced adverse hepatic injury of which 79% were female, 71% were elderly patients (above the age of 60), and 77% of the patients had osteoarthritis. In most of the cases the liver injury was characterized by hepatocellular damage or mixed hepatocellular injury, and there were some cases of cholestasis (Banks et al. 1995). The incidence of diclofenac hepatotoxicity has been reported to be 6.3 per 100 000 patients (DeAbajo et al. 2004). Bioactivation to reactive intermediates, their disposition, the production of oxidative stress, mitochondrial damage, and immune-mediated mechanisms have been suggested to play a role in diclofenac-mediated liver toxicity

Serum cytotoxin and oxidant stress markers in N-acetylcysteine treated thioacetamide hepatotoxicity of rats

1999 ◽  
Vol 18 (11) ◽  
pp. 669-676 ◽  
Author(s):  
A Akbay ◽  
K Ĉinar ◽  
Ö Uzunalimoglu ◽  
S Eranil ◽  
C Yurdaydin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxidant Stress ◽  
Serum Markers ◽  
Hepatocellular Injury ◽  
Rat Serum ◽  
Stress Markers ◽  
Hepatocellular Damage ◽  
Immune Mediated ◽  
Tnf Α ◽  
Clinical Conditions

N-acetylcysteine (NAC) is a glutathione precursor used to treat several clinical conditions where intracellular oxidant-antioxidant balance is disturbed, among which, acetaminophen induced hepatotoxicity may be counted. In this study, administering thioacetamide (TAA) as a hepatotoxic agent, a rat model of hepatotoxicity has been established, to investigate some of the immune mediated basic oxidant-antioxidant homeostatic mechanisms involved, and potential serum markers for follow-up of disease and treatment. To do this, four experimental groups receiving saline/saline, saline/NAC, saline/TAA and NAC/TAA as intraperitoneal injections, have been formed. Rat serum tumor necrosis factor-a (TNF-α), Interleukin1-β (IL1-β), malondialdehyde (MDA) as a measure of final oxidant damage and the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) have been assayed. Hepatocellular damage has been measured via the biochemical estimates ALT, AST and LDH as well as histopathological grading. It was found that both TNF-α and IL1-β were significantly elevated in saline/TAA receivers (P50.01) when compared to NAC/TAA receivers. Serum MDA was also increased in TAA receivers in addition to SOD (P50.05) and GSH-Px (P50.05). Serum nitrite levels have also been assayed to give an estimate of nitric oxide that is suggested as a counter-balancer of oxidant stress. NAC/saline receivers had the highest levels of nitrites in the serum (P50.05). Our results indicate that part of the hepatocellular injury to rat liver, induced by TAA is mediated by oxidative stress caused by the action of cytokines imparted by the enzymatic SOD and GSH-Px and non-enzymatic gaseous nitric oxide mechanisms causing an alleviation on administration of NAC. In addition, TNF-α,IL1-β,MDA, SOD, GSH-Px and nitrites are potential candidates of serum indicators for monitorization of pathophysiological stage of liver disease.

scholarly journals Choline and Cystine Deficient Diets in Animal Models with Hepatocellular Injury: Evaluation of Oxidative Stress and Expression of RAGE, TNF-α, and IL-1β

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juliana Célia F. Santos ◽  
Orlando R. P. de Araújo ◽  
Iara B. Valentim ◽  
Kívia Queiroz de Andrade ◽  
Fabiana Andréa Moura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Hepatic Steatosis ◽  
Hepatic Injury ◽  
Young Male ◽  
Thiobarbituric Acid ◽  
Hepatocellular Injury ◽  
Oxidative Stress Biomarkers ◽  
Tnf Α ◽  
Male Wistar Rats

This study aims to evaluate the effects of diets deficient in choline and/or cystine on hepatocellular injury in animal models (young male Wistar rats, aged 21 days), by monitoring some of the oxidative stress biomarkers and the expression of RAGE, TNF-α, and IL-1β. The animals were divided into 6 groups (n=10) and submitted to different diets over 30 days: AIN-93 diet (standard, St), AIN-93 choline deficient (CD) diet and AIN-93 choline and cystine deficient (CCD) diet, in the pellet (pl) and powder (pw) diet forms. Independently of the diet form, AIN-93 diet already led to hepatic steatosis and CD/CCD diets provoked hepatic damage. The increase of lipid peroxidation, represented by the evaluation of thiobarbituric acid reactive species, associated with the decrease of levels of antioxidant enzymes, were the parameters with higher significance toward redox profile in this model of hepatic injury. Regarding inflammation, in relation to TNF-α, higher levels were evidenced inCD(pl), while, for IL-1β, no significant alteration was detected. RAGE expression was practically the same in all groups, with exception ofCCD(pw)versusCCD(pl). These results together confirm that AIN-93 causes hepatic steatosis and choline and/or cysteine deficiencies produce important hepatic injury associated with oxidative stress and inflammatory profiles.

Polysaccharides from Enteromorpha prolifera protect against carbon tetrachloride-induced acute liver injury in mice via activation of Nrf2/HO-1 signaling, and suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (5) ◽  
pp. 4485-4498
Author(s):  
Fuchuan Guo ◽  
Xinyun Zhuang ◽  
Mengyuan Han ◽  
Wenting Lin
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Reactive Intermediates ◽  
Enteromorpha Prolifera ◽  
Hepatic Oxidative Stress

EPP protected against hepatic injury induced by CCl4-derived reactive intermediates through the suppression of hepatic oxidative stress, inflammation, and apoptosis.

Carbon Tetrachloride-Induced Hepatotoxicity: Protective Effect of 'Rocket' Eruca sativa L. in Rats

2010 ◽  
Vol 38 (01) ◽  
pp. 75-88 ◽  
Author(s):  
Saleh Alqasoumi
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Tissue ◽  
Hepatic Injury ◽  
Liver Toxicity ◽  
Elevated Serum ◽  
Ethanolic Extract ◽  
Albino Rats ◽  
Eruca Sativa ◽  
Protein Sulfhydryl

The hepatoprotective and antioxidant effect of an ethanolic extract of 'Rocket' Eruca sativa L. (EER), on liver injury induced by carbon tetrachloride ( CCl4 ) was investigated. Wistar albino rats were administered 250 and 500 mg/kg body weight extract orally for 10 consecutive days. Marker enzymes GOT, GPT, ALP, GGT and bilirubin were estimated in serum. Whereas, non-protein sulfhydryl (NP-SH), total protein (TP) and malondialdehyde (MDA) were estimated in liver tissue as markers for oxidative stress. Histopathological assessment was also done on liver tissue. CCl4 induced liver poisoning in all treated animals was evident by elevated serum GOT, GPT, ALP, GGT and bilirubin levels. Induction of oxidative stress in the liver tissue by CCl4 was evidenced by a fall in the levels of NP-SH and TP; and an increased level of MDA concentration. EER administration for 10 days prevented the CCl4 induced hepatic injury and oxidative stress. Furthermore, the extract also reduced the pentobarbital-induced prolongation of sleeping time in mice. The ability of rocket extract to protect the liver toxicity in rats was further confirmed by histological findings in the liver tissue. In conclusion, it was observed that Eruca sativa L. extract protects the liver against CCl4 induced hepatic injury through its potent antioxidant activity in rats.

scholarly journals Effect of combined treatment with Methotrexate and Non-steroidal anti-inflammatory drugs on plasma alpha-tocopherol level and Rheumatoid factor among Rheumatoid Arthritis patients

Mediscope ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. 80-86
Author(s):  
Farhana Pervin ◽  
Md Anwar Habib ◽  
Nazimuddin Ahmed ◽  
Md Mijanur Rahman Sardar
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Rheumatoid Factor ◽  
Combined Treatment ◽  
Alpha Tocopherol ◽  
Qualitative Assessment ◽  
Medical College ◽  
Tocopherol Level ◽  
Anti Oxidant ◽  
Inflammatory Drugs

Background: Oxidative stress might play a significant role in the pathogenesis of Rheumatoid Arthritis. Traditional therapies of Rheumatoid Arthritis are governed by different NSAIDs which improve symptoms of Rheumatoid Arthritis. But addition of Methotrexate (MTX) to Non-steroidal anti-inflammatory drugs (NSAIDs) has been found to be extra beneficial by halting the disease process. Objectives: To evaluate the status of anti-oxidant alpha-tocopherol and rheumatoid factor before and after treatment with MTX and NSAIDs for two months in Rheumatoid Arthritis patients. Methods: This quasi-experimental study was carried out in the Department of Pharmacology and Therapeutics of Rajshahi Medical College, Rajshahi between the periods of January 2011 to December 2011. Total ten clinically diagnosed Rheumatoid Arthritis patients were enrolled in the study. Purposive sampling technique was used to select each study subject from medicine wards of Rajshahi Medical College Hospital. Alpha-tocopherol, an anti-oxidant in plasma was measured as marker of anti-oxidant defense. The patients were then treated with oral MTX at a dose of 10 mg weekly and Indomethacin 150 mg in three divided doses daily for 2 months. After 2 months of continuous aforementioned treatment, alpha-tocopherol levels were estimated again. Moreover qualitative assessment of rheumatoid factor was done. For statistical analysis, paired t-test was done. Results: After two months of treatment with Methotrexate and Indomethacin, plasma alpha-tocopherol levels were significantly higher (P<0.05) in Rheumatoid Arthritis patients. However no significant change was observed in qualitative assessment of rheumatoid factors. Conclusion: From the findings of this study, it can be concluded that the endogenous alpha-tocopherol level increases even without any supplementation of alpha-tocopherol by combined treatment with MTX and Indomethacin in Rheumatoid Arthritis patients and thereby reduces oxidative stress. So alpha-tocopherol level is a better marker for early assessment of prognosis of Rheumatoid arthritis than Rheumatoid factor test. Mediscope 2021;8(2): 80-86

Immuno-biological Assessments of Temporomandibular Joint Disease in Patients with Immune-mediated Rheumatic Conditions. A cross sectional study of 273 cases

2018 ◽  
Vol 68 (12) ◽  
pp. 2987-2991
Author(s):  
Cristina Iordache ◽  
Bogdan Vascu ◽  
Eugen Ancuta ◽  
Rodica Chirieac ◽  
Cristina Pomirleanu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Temporomandibular Joint ◽  
Final Analysis ◽  
Cross Sectional Study ◽  
Joint Disease ◽  
Sectional Study ◽  
Cross Sectional ◽  
Immune Parameters ◽  
Immune Mediated

Temporomandibular joint (TMJ) is commonly involved in various immune-mediated rheumatic disorders accounting for significant disability and impaired quality of life. The aim of our study was to assess inflammatory and immune parameters in patients with TMJ arthritis related to rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) and to identify potential relation with severity and dysfunction of TMJ pathology. We performed a cross-sectional study in a cohort of 433 consecutive RA, 32 JIA, 258 AS, and 103 PsA. Only patients presenting with clinically significant TMJ involvement (273) related to their rheumatic condition were included in the final analysis. TMJ involvement is traditionally described in chronic inflammatory rheumatic disorders, particularly in patients with higher levels of inflammation as detected in rheumatoid arthritis and psoriatic arthritis. Disease activity and severity, as well as biological and positive serological assessments (rheumatoid factor, anti-cyclic citrullinated peptide, IL-1) remain significant determinants of the severity of TMJ arthritis.

Sign in / Sign up

Export Citation Format

Share Document