Herbal Extract Diminishes Diclofenac-Induced Nephrotoxicity
DOI:
https://doi.org/10.21070/nabatia.v14i1.1694Keywords:
Artemisinin, Diclofenac, Hepatic toxicity, Renal toxicityAbstract
Nonsteroidal Anti-Inflammatory Medications (NSAIDs) are among the most frequently recommended painkillers, and their renal toxicity effects are predictable. Numerous studies have shown a link between the development of advanced-stage chronic kidney disease (CKD) and high doses of NSAID exposure and frequently prescribed medications that make up 5–10% of all prescriptions written in the US. Diclofenac (DFC) is widely used as an analgesic and anti-inflammatory agent. The use of medicinal plants is a new strategy to mitigate the adverse effects of other medications. Artemisinin has now led to the development of vital antimalarial medications for the increasingly prevalent therapy-resistant malaria strains. While Artemisinin was primarily used to treat malaria, numerous subsequent studies have confirmed that it has additional pharmacological functions, including antitumor, antiarrhythmic, and antifibrotic effects. This study aimed to examine the capacity of Artemisinin to reduce (DFC) and to stimulate hepatic and renal toxicity in a rat model.DFC was injected intramuscularly twice daily for seven days, and Artemisinin was administered by oral gavage for the same time. Hematological and biochemical profiles were analyzed. Tissue damage was assessed under microscopy and histopathological reporting. DFC administration produced renal and hepatic function test abnormalities and decreased hematocrit and hemoglobin values, but increased WBC and platelet counts. Histopathological examination revealed renal tubular injury, hepatocyte injury, and increased fibrosis in the DFC rat group. Artemisinin administration, in addition to DFC treatment, reduced hematological test irregularities and DFC, thereby causing renal functional damage, as evidenced by a marked increase in serum creatinine and uremia levels.
References
[1] Prigent, A. 2008 ‘Monitoring renal function and limitations of renal function tests’, in Seminars in nuclear medicine. Elsevier, pp. 32–46. PMID: 18096462 DOI: 10.1053/j.semnuclmed.2007.09.003
[2] Youde, J. 2012 Global health governance. Polity.
[3] Sureshbabu, A.,et al. 2015 ‘Oxidative stress and autophagy: crucial modulators of kidney injury’, Redox Biology, 4, pp. 208–214. PMID: 25613291 PMCID: PMC4803795 DOI: 10.1016/j.redox.2015.01.001van Swelm, R. P. L. et al. (2013) ‘Urinary proteomic profiling reveals diclofenac-induced renal injury and hepatic regeneration in mice’, Toxicology and applied pharmacology, 269(2), pp. 141–149. PMID: 23506792 DOI: 10.1016/j.taap.2013.03.005
[4] Green, G. A. 2001‘Understanding NSAIDs: from aspirin to COX-2’, Clinical cornerstone, 3(5), pp. 50–59. DOI: 10.1016/s1098-3597(01)90069-9
[5] Prince, S. E. 2018‘Diclofenac-induced renal toxicity in female Wistar albino rats is protected by the pre-treatment of aqueous leaves extract of Madhuca longifolia through suppression of inflammation, oxidative stress, and cytokine formation’, Biomedicine & Pharmacotherapy, 98, pp. 45–51. PMID: 29245065 DOI: 10.1016/j.biopha.2017.12.028
[6] Chen, D.-Q. et al. 2018 ‘Natural products for the prevention and treatment of kidney disease’, Phytomedicine, 50, pp. 50–60. doi: 10.1016/j.phymed.2018.09.182. Epub 2018 Sep 17. PMID: 30466992.
[7] Chang, Z. 2016 ‘The discovery of Qinghaosu (artemisinin) as an effective anti-malaria drug: a unique China story’, Science China Life Sciences, 59(1), pp. 81–88. https://doi.org/10.1007/s11427-015-4988-z
[8] Lalloo, D. G. et al. 2016 ‘UK malaria treatment guidelines 2016’, Journal of Infection, 72(6), pp. 635–649. DOI: 10.1016/j.jinf.2016.02.001 PMID: 26880088 PMCID: PMC7132403
[9] Li, Y. 2012‘Qinghaosu (artemisinin): chemistry and pharmacology’, Acta Pharmacologica Sinica, 33(9), pp. 1141–1146. doi: 10.1038/aps.2012.104
[10] An, J. et al. 2017 ‘Antimalarial drugs as immune modulators: new mechanisms for old drugs’, Annual review of medicine, 68, pp. 317–330. DOI: 10.1146/annurev-med-043015-123453
[11] Bancroft, J. D. and Layton, C. 2012 ‘The hematoxylins and eosin’, Bancroft’s theory and practice of histological techniques, pp. 173–186. https://doi.org/10.1016/B978-0-7020-4226-3.00010-X
[12] Shah, S. and Mehta, V. 2012 'Controversies and advances in nonsteroidal anti-inflammatory drug (NSAID) analgesia in chronic pain management, Postgraduate medical journal, 88(1036), pp. 73–78. PMID: 22052884 DOI: 10.1136/postgradmedj-2011-130291
[13] Ørnbjerg, L. M. et al. 2008 ‘What do patients in rheumatologic care know about the risks of NSAIDs?’, JCR: Journal of Clinical Rheumatology, 14(2), pp. 69–73. PMID: 18391673 DOI: 10.1097/RHU.0b013e31816b1e8e
[14] Galati, G. et al. 2002 ‘Idiosyncratic NSAID drug-induced oxidative stress’, Chemico-biological interactions, 142(1–2), pp. 25–41. DOI: 10.1016/s0009-2797(02)00052-2
[15] Hickey, E. J. et al. 2001 ‘Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death, Free Radical Biology and Medicine, 31(2), pp. 139–152. DOI: 10.1016/s0891-5849(01)00560-3
[16] Ng, L. E. et al. 2006 'Action of Diclofenac on kidney mitochondria and cells', Biochemical and biophysical research communications, 348(2), pp. 494–500. PMID: 16890207 DOI: 10.1016/j.bbrc.2006.07.089
[17] Shi, C. et al. 2015 'Anti-inflammatory and immunoregulatory functions of Artemisinin and its derivatives, Mediators of Inflammation, 2015. PMID: 25960615 PMCID: PMC4415672 DOI: 10.1155/2015/435713
[18] Adeyemi, W. J., and Olayaki, L. A. 2018‘Diclofenac–induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects’, Toxicology Reports, 5, pp. 90–95. doi: 10.1016/j.toxrep.2017.12.002
[19] Zorte, A. et al. 2019 ‘Effect of Oral Administration of Diclofenac Sodium on Coagulation Factors and Some Hematological Parameters in Wister Rats’, International Journal of Biochemistry Research & Review, pp. 1–7. DOI: 10.9734/ijbcrr/2019/v28i430154
Downloads
Published
How to Cite
Issue
Section
Categories
License
Copyright (c) 2026 Etab Abdul-Ameer AL-Ogla, Huda N. AL-baroody, Mohanad Yahya Al-Mhanna, Hadeel Khalaf Alboaklah

This work is licensed under a Creative Commons Attribution 4.0 International License.
Copyright Notice
Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution 4.0 International License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.


