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Hesperidin attenuates cisplatin-induced acute renal injury by decreasing oxidative stress, inflammation and DNA damage.
Phytomedicine. 2013 Mar 15; 20(5):453-60.P

Abstract

Nephrotoxicity is an important complication in cancer patients undergoing cisplatin therapy. Oxidative stress, inflammation and apoptosis/necrosis are the major patho-mechanisms of cisplatin induced nephrotoxicity. In the present study, hesperidin, a naturally-occurring bioflavonoid has been demonstrated to have protective effect on cisplatin-induced renal injury in rats. Cisplatin intoxication resulted in structural and functional renal impairment which was revealed by massive histopathological changes and elevated blood urea nitrogen and serum creatinine levels, respectively. Renal injury was associated with oxidative stress/lipid peroxidation as evident by increased reactive oxygen species (ROS) and malondialdehyde (MDA) formation with decreased levels of antioxidants such as reduced glutathione, vitamin C, catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione-S-transferase. Cisplatin administration also triggered inflammatory response in rat kidneys by inducing pro-inflammatory cytokine, TNF-α, with the increased expression of myeloperoxidase (MPO). Furthermore, cisplatin increased the activity of caspase-3 and DNA damage with decreased tissue nitric oxide levels. Hesperidin treatment significantly attenuated the cisplatin-induced oxidative stress/lipid peroxidation, inflammation (infiltration of leukocytes and pro-inflammatory cytokine), apoptosis/necrosis (caspase-3 activity with DNA damage) as well as increased expression of nitric oxide in the kidney and improved renal function. Thus, our results suggest that hesperidin co-administration may serve as a novel and promising preventive strategy against cisplatin-induced nephrotoxicity.

Authors+Show Affiliations

Pharmacology Division, Indian Institute of Chemical Technology, Hyderabad, India.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23353054

Citation

Sahu, Bidya Dhar, et al. "Hesperidin Attenuates Cisplatin-induced Acute Renal Injury By Decreasing Oxidative Stress, Inflammation and DNA Damage." Phytomedicine : International Journal of Phytotherapy and Phytopharmacology, vol. 20, no. 5, 2013, pp. 453-60.
Sahu BD, Kuncha M, Sindhura GJ, et al. Hesperidin attenuates cisplatin-induced acute renal injury by decreasing oxidative stress, inflammation and DNA damage. Phytomedicine. 2013;20(5):453-60.
Sahu, B. D., Kuncha, M., Sindhura, G. J., & Sistla, R. (2013). Hesperidin attenuates cisplatin-induced acute renal injury by decreasing oxidative stress, inflammation and DNA damage. Phytomedicine : International Journal of Phytotherapy and Phytopharmacology, 20(5), 453-60. https://doi.org/10.1016/j.phymed.2012.12.001
Sahu BD, et al. Hesperidin Attenuates Cisplatin-induced Acute Renal Injury By Decreasing Oxidative Stress, Inflammation and DNA Damage. Phytomedicine. 2013 Mar 15;20(5):453-60. PubMed PMID: 23353054.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hesperidin attenuates cisplatin-induced acute renal injury by decreasing oxidative stress, inflammation and DNA damage. AU - Sahu,Bidya Dhar, AU - Kuncha,Madhusudana, AU - Sindhura,G Jeevana, AU - Sistla,Ramakrishna, Y1 - 2013/01/23/ PY - 2012/08/13/received PY - 2012/11/15/revised PY - 2012/12/15/accepted PY - 2013/1/29/entrez PY - 2013/1/29/pubmed PY - 2013/9/14/medline SP - 453 EP - 60 JF - Phytomedicine : international journal of phytotherapy and phytopharmacology JO - Phytomedicine VL - 20 IS - 5 N2 - Nephrotoxicity is an important complication in cancer patients undergoing cisplatin therapy. Oxidative stress, inflammation and apoptosis/necrosis are the major patho-mechanisms of cisplatin induced nephrotoxicity. In the present study, hesperidin, a naturally-occurring bioflavonoid has been demonstrated to have protective effect on cisplatin-induced renal injury in rats. Cisplatin intoxication resulted in structural and functional renal impairment which was revealed by massive histopathological changes and elevated blood urea nitrogen and serum creatinine levels, respectively. Renal injury was associated with oxidative stress/lipid peroxidation as evident by increased reactive oxygen species (ROS) and malondialdehyde (MDA) formation with decreased levels of antioxidants such as reduced glutathione, vitamin C, catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione-S-transferase. Cisplatin administration also triggered inflammatory response in rat kidneys by inducing pro-inflammatory cytokine, TNF-α, with the increased expression of myeloperoxidase (MPO). Furthermore, cisplatin increased the activity of caspase-3 and DNA damage with decreased tissue nitric oxide levels. Hesperidin treatment significantly attenuated the cisplatin-induced oxidative stress/lipid peroxidation, inflammation (infiltration of leukocytes and pro-inflammatory cytokine), apoptosis/necrosis (caspase-3 activity with DNA damage) as well as increased expression of nitric oxide in the kidney and improved renal function. Thus, our results suggest that hesperidin co-administration may serve as a novel and promising preventive strategy against cisplatin-induced nephrotoxicity. SN - 1618-095X UR - https://www.unboundmedicine.com/medline/citation/23353054/Hesperidin_attenuates_cisplatin_induced_acute_renal_injury_by_decreasing_oxidative_stress_inflammation_and_DNA_damage_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0944-7113(12)00508-9 DB - PRIME DP - Unbound Medicine ER -