Mandarin peel ethanolic extract attenuates diclofenac sodium induced hepatorenal toxicity in rats by mitigating oxidative stress and inflammation.
Yavuz Osman BirdaneHülya AtikOrkun AtikRecep AslanPublished in: Drug and chemical toxicology (2022)
Nonsteroidal anti-inflammatory drugs (NSAIDs) constitute approximately one-third of the global pharmaceutical market and are the first drugs of choice when treating fever and pain. Furthermore, among NSAIDs, the use of diclofenac sodium (DS) is preferred as it is a strong inhibitor of cyclooxygenase enzyme. However, despite its strong efficacy, DS is known for its potential to cause hepatorenal damage. Currently, to mitigate the adverse effects of certain drugs, medically effective agricultural products are often preferred as they are inexpensive, effective and safe. One such agricultural product-mandarin-is noteworthy for its high phenolic contents. The purpose of the present study was to assess the efficacy of mandarin peel ethanolic extract (MPEE) in protecting against hepatorenal damage induced by DS. Four groups (six/group) of adult male albino rats received oral administration of physiological saline (control group), DS (10 mg/kg body weight), MPEE (200 mg/kg body weight), and DS + MPEE for 7 days. Rats in the DS group showed increased serum levels of ALT, AST, ALP, BUN, CRE, and UA. Furthermore, the hepatic and renal tissue levels of MDA, TNF-α and IL-1β increased, whereas those of GSH, SOD, GP-x and IL-10 decreased ( p < 0.05). Investigation of MPEE in terms of its effects on biochemical, oxidative and inflammatory parameters, it exerted protective and healing effects. Therefore, MPEE can be used to ameliorate DS-induced hepatorenal damage.
Keyphrases
- oxidative stress
- body weight
- diabetic rats
- anti inflammatory drugs
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- risk assessment
- heavy metals
- drug induced
- emergency department
- climate change
- spinal cord injury
- cell death
- spinal cord
- decision making
- breast cancer cells
- pi k akt
- fluorescent probe
- nitric oxide synthase