Hesperetin may alleviate the development of doxorubicin-induced pulmonary toxicity by decreasing oxidative stress and apoptosis in male rats
Yükleniyor...
Tarih
2021
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Elsevier
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Doxorubicin (DOX) is one of the most widely used chemotherapeutic agents. However, it causes pulmonary toxicity which decreases its clinical use in human cancer therapy. The present study was undertaken to obtain an insight into the potential protective effect of hesperetin (HES) against doxorubicin-induced pulmonary toxicity in rats. The animals were divided into 4 groups with 7 rats per group. The experimental treatments were as follows: Control, DOX, DOX + HES, and HES groups. DOX was administered at the dosage of 15 mg/kg i.p for a single dose. HES was administered at the dosage of 50 mg/kg by oral gavage every other day. After 28 days, biochemical parameters, oxidative stress status, histopathological changes, apoptosis-related genes and apoptotic index (AI) were examined of lung tissue. Histopathological changes, Poly [ADP-ribose] polymerase 1 (PARP-1), Caspase-3 (Casp3), Cytochrome c (Cytc), apoptosis-related genes, and AI significantly increased in the DOX group relative to the control group. Malondialdehyde (MDA) significantly increased, while superoxide dismutase (SOD) and glutathione peroxidase (GPx) decreased in the DOX group relative to the control group. However, histopathological findings, MDA, AI, and PAPR1, Casp3 protein expression, mRNA expression of Cytc significantly decreased, while SOD, GPx increased in the DOX + HES group relative to the DOX group. These results attested HES might be a potential agent for the treatment of DOX-induced pulmonary toxicity.
Açıklama
Anahtar Kelimeler
Apoptosis; Doxorubicin; Hesperetin; Oxidative stress; Poly [ADP-ribose] polymerase 1; Pulmonary toxicity.
Kaynak
Tissue and Cell
WoS Q Değeri
Q2
Scopus Q Değeri
N/A
Cilt
73
Sayı
Künye
Erdem Guzel, E., & Kaya Tektemur, N. (2021). Hesperetin may alleviate the development of doxorubicin-induced pulmonary toxicity by decreasing oxidative stress and apoptosis in male rats. In Tissue and Cell (Vol. 73, p. 101667). Elsevier BV. https://doi.org/10.1016/j.tice.2021.101667
Bağlantı
https://doi.org/10.1016/j.tice.2021.101667
https://pubmed.ncbi.nlm.nih.gov/34653889/#affiliation-1
https://hdl.handle.net/20.500.12514/2890
https://www.scopus.com/record/display.uri?eid=2-s2.0-85116937423&origin=SingleRecordEmailAlert&dgcid=raven_sc_affil_en_us_email&txGid=e591d92435b6818862c80b1529a849ce
https://www.webofscience.com/wos/woscc/full-record/WOS:000744263100001?AlertId=d383397b-4355-449e-9419-70f9e0e77c15&SID=E1579H1bfcewtgOvZ82
https://pubmed.ncbi.nlm.nih.gov/34653889/#affiliation-1
https://hdl.handle.net/20.500.12514/2890
https://www.scopus.com/record/display.uri?eid=2-s2.0-85116937423&origin=SingleRecordEmailAlert&dgcid=raven_sc_affil_en_us_email&txGid=e591d92435b6818862c80b1529a849ce
https://www.webofscience.com/wos/woscc/full-record/WOS:000744263100001?AlertId=d383397b-4355-449e-9419-70f9e0e77c15&SID=E1579H1bfcewtgOvZ82