The liver is an important organ of the body, which has a vital role in metabolic functions. The non-steroidal anti-inflammatory drug (NSAID), diclofenac causes hepato-renal toxicity and gastric ulcers. NSAIDs are noted to be an agent for the toxicity of body organs. This review has elaborated various scientific perspectives of the toxicity caused by diclofenac and its mechanistic action in affecting the vital organ. This review suggests natural products are better remedies than current clinical drugs against the toxicity caused by NSAIDs. Natural products are known for their minimal side effects, low cost and availability. On the other hand, synthetic drugs pose the danger of adverse effects if used frequently or over a long period. Copyright © 2016 John Wiley & Sons, Ltd.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/jat.3391 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Assessing and alleviating pain in animals involved in research is critically important. However, the effective implementation of pain management depends on the knowledge and attitudes of the personnel involved. Following a Federation of European Laboratory Animal Science Associations 'Pain in Mice' working group initiative, a questionnaire to survey current practices concerning analgesic use in laboratory mice was distributed to several professional groups in the field of laboratory animal science.
View Article and Find Full Text PDFRisks of anti- therapy and long-term therapy with antisecretory drugs.
World J Gastroenterol
January 2025
Department of Therapy, North Caucasus State Academy, Cherkessk 369000, Russia.
() infection has a protective effect on gastroesophageal reflux disease (GERD). Both of these diseases have a very high incidence and prevalence. As a result, GERD often recurs after anti- therapy.
View Article and Find Full Text PDFExploring the anti-inflammatory potential of vitamin D in cardiometabolic diseases.
Metabol Open
March 2025
Department of Life and Consumer Sciences, College of Agriculture and Environmental Sciences, University of South Africa, Calabash Building, Office no: 02-047 Florida Campus, 1710, South Africa.
The prevalence of cardiometabolic diseases is rising, and this is fuelled by inflammation, which tends to be worse in individuals with vitamin D (VD) deficiency. While non-steroidal anti-inflammatory interventions are available, they present with coagulation events. Hence, alternative therapy in the form of VD supplements is gaining research interest.
View Article and Find Full Text PDFIbuprofen reduces inflammation, necroptosis and protects photoreceptors from light-induced retinal degeneration.
J Neuroinflammation
January 2025
Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Background: The retinal degenerative diseases retinitis pigmentosa (RP) and atrophic age- related macular degeneration (AMD) are characterized by vision loss from photoreceptor (PR) degeneration. Unfortunately, current treatments for these diseases are limited at best. Genetic and other preclinical evidence suggest a relationship between retinal degeneration and inflammation.
View Article and Find Full Text PDFFinerenone: Will It Be a Game-changer?
Card Fail Rev
December 2024
Department of Nephrology and Renal Transplant Medicine, Max Super Speciality Hospital Saket, New Delhi, India.
Heart failure (HF) is a major contributor to hospitalisations and accounts for 7% of cardiovascular-related deaths, with patients who have chronic kidney disease and type 2 diabetes at heightened risk. Existing treatment guidelines inadequately address these comorbidities. Steroidal mineralocorticoid receptor antagonists (MRAs) are commonly used in HF with reduced ejection fraction but pose risks, such as hyperkalaemia and acute kidney injury.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!