An Insight about Diclofenac induced hepato-renal toxicity: A Review Article | ||||
| Zagazig University Medical Journal | ||||
| Articles in Press, Accepted Manuscript, Available Online from 06 April 2024 | ||||
| Document Type: Review Articles | ||||
| DOI: 10.21608/zumj.2024.277963.3265 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Esraa Mohamed Naguib Khalil  1; Nabila Hassan Fahmy EL-baroudy2; Laila Ahmed Mahgoub1; Mahitab Mohamed Nageeb1
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| 1Clinical Pharmacology Department, Faculty of Medicine, Zagazig university | ||||
| 2Clinical pharmacology department faculty of medicine zagazig university | ||||
| Abstract | ||||
| Background: Diclofenac is a medication that has received FDA approval for the treatment and management of acute and chronic pain brought on by inflammatory disorders, particularly those that affect the musculoskeletal system. Although diclofenac (DIC) has many beneficial therapeutic uses, it also carries the potential of serious adverse effects, such as kidney damage, liver damage, gastrointestinal problems, and cardiovascular hazards. We aimed to present an Insight about Diclofenac induced hepato-renal toxicity. Conclusion: Diclofenac is the NSAID most frequently implicated in hepatocellular and renal injury development. Diclofenac sodium damages hepatic and renal tissues by generating malondialdehyde (MDA) and reducing glutathione (GSH) in hepatic tissues. This oxidative stress leads to the secretion of cytochrome c, which in turn activates the caspase cascade and causes hepatocytes to undergo apoptosis. Diclofenac's main harmful mechanism involves mitochondrial oxidative stress and ROS generation. Lysosomal dysfunction and impaired autophagy flux are brought on by intracellular ROS, which prevents the efficient destruction of damaged mitochondria to stop the creation of more ROS. Hepatotoxicity and cellular oxidative stress are made worse by the vicious loop of mitochondrial damage and impaired autophagy. | ||||
| Keywords | ||||
| Diclofenac; Hepatotoxicity; Renal Toxicity | ||||
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