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ORAL PRESENTATION / SÖZLÜ SUNUM
Puerarin Nanoparticles in Liver and Kidney Toxicity:
Comparison with Free Form in Diclofenac Model
Zeliha KESKİN ALKAÇ 1,* Fatih Ahmet KORKAK Semra DURAK
3
2
İrem Solmaz AYHAN Pervin KARABULUT Canan HASÇİÇEK
6
5
4
¹Fırat University, Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Elazıg, TÜRKIYE
2 Fırat University, Faculty of Veterinary Medicine, Department of Pharmacology and
Toxicology, Elazıg, TÜRKIYE
3 Fırat University, Faculty of Pharmacy, Department of Pharmaceutical Technology, Elazıg, TÜRKIYE
4 Fırat University, Faculty of Pharmacy, Elazıg, TÜRKIYE
5 Fethi Sekin City Hospital, Medical Pathology, Elazıg, TÜRKIYE
6 Ankara University, Faculty of Pharmacy, Department of Pharmaceutical Technology,
Ankara, TÜRKIYE
*Correspound Author: zkeskin@firat.edu.tr
Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to control pain, fever, and
inflammation. NSAIDs affect prostaglandin synthesis by inhibiting the COX enzyme. Therefore,
despite their broad therapeutic effect, long-term and incorrect use of NSAIDs may lead to undesirable
effects in living beings. Diclofenac, an important member of the NSAID group, is widely distributed in
the body and has been reported to cause serious side effects in organs such as the liver and kidney,
as well as the stomach, intestines, heart and lungs. Puerarin, an isoflavonoid isolated from the roots
of the Pueraria lobata plant, has been intensively investigated in recent years for its various
biochemical and physiological effects, including anti-diabetic, antioxidant, and anti-inflammatory
effects. Puerarin is a substance with very poor oral bioavailability due to its low solubility. This
situation limits its clinical use even though it is a good compound. Therefore, in this study, it was
aimed to improve the oral bioavailability of Puerarin by loading it into polycapralactone nanoparticles
to overcome the limitations of low stability and poor bioavailability and to evaluate its efficacy against
Diclofenac-induced liver and kidney toxicity.
Thirty-two male Sprague-Dawley rats were used in the study. Rats were divided into 1: Control,
2: Diclofenac, 3: Diclofenac+Puerarin and 4: Diclofenac+Puerarin nanoparticle groups, with 8
animals in each group, and drug application was performed for seven days. On the eighth day, all rats
were decapitated and blood, liver and kidney tissues were collected.
A significant increase was observed in the body weights, liver and kidney organ weights,
aspartate aminotransferase, alanine aminotransferase, urea and creatinine values, as well as
malondialdehyde levels, which are biomarkers of oxidative stress, and pro-inflammatory cytokines,
which are indicators of inflammation, of rats administered diclofenac. There was also a significant
decrease in antioxidant defense systems such as reduced glutathione and superoxide dismutase.
Histopathologically, there was mononuclear cell infiltration and hyperemic vascularization in the
interstitium of the kidney tissue; focal hepatocyte degeneration, central vein dilatation, and
mononuclear cell infiltration were present in the liver. However, the application of Puerarin as a
preventive measure reduced the toxic effects of Diclofenac on the liver and kidney tissues. Application
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