Ellagic acid and rosmarinic acid attenuate doxorubicin-induced testicular injury in rats

Georgy, Gehan S.; Maher, Omar W.

doi:10.1002/jbt.21937

Cited by 27 publications

(12 citation statements)

References 42 publications

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“…In the group in which CR was co‐administered with MTX, the reduction in TNF‐α and IL‐1β levels suggests that CR has anti‐inflammatory properties. Previous studies have also reported increased TNF‐α and IL‐1β levels after different treatments (Georgy & Maher, ; Sherif, Abdel‐Aziz, & Sarhan, ).…”

Section: Discussionmentioning

confidence: 76%

Effect of chrysin on methotrexate-induced testicular damage in rats

et al. 2018

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This study was conducted on 28 male Wistar albino rats to determine the effects of chrysin on methotrexate‐induced damage to testicular tissue. Rats were grouped into four groups of seven rats reach: Group 1 (n = 7) was the control group to which no drugs were administered; this group was only provided with food and water. Group 2 (n = 7) was administered 20 mg/kg of methotrexate once intraperitoneally. Group 3 (n = 7) was administered 50 mg/kg of chrysin for 7 days orally. Group 4 (n = 7) was administered 20 mg/kg of methotrexate once intraperitoneally, followed by oral administration of 50 mg/kg of chrysin for 7 days. At the end of the experiment, rats were anaesthetised, rat testes were removed, and spermatozoon was obtained from the cauda epididymis. It was determined that sperm count and motility, glutathione peroxidase, superoxide dismutase and catalase activities decreased in the methotrexate group, whereas malondialdehyde, tumour necrosis factor‐α, interleukin‐1β and nuclear kappa factor B expression levels increased. Furthermore, damage to tubulus seminiferus structures and affusion in germ cells was identified. In the methotrexate + chrysin administered group, sperm count improved, biochemical enzyme levels increased, and structural improvements were observed in testicular tubules. These findings demonstrated that chrysin plays a protective role in testicular damage in rats.

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Section: Discussionmentioning

confidence: 76%

Effect of chrysin on methotrexate-induced testicular damage in rats

et al. 2018

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“…Reduction of this increase in TNF-alpha and IL-1 Beta levels by administration of hesperidin in addition to MTX suggests that hesperidin has anti-inflammatory effects. It was reported in a previous study that MTX led to an increase in TNF-alpha level [40] . It is consistent with this study that Cisplatin, Doxorubicin and Sodium nitrite increase TNF-alpha and IL-1 Beta levels among pro-inflammatory cytokines in testicular tissue [40][41][42].…”

Section: Discussionmentioning

confidence: 86%

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Belhan¹,

Özkaraca²,

Kandemir³

et al. 2017

Kafkas Univ Vet Fak Derg

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Citation of This ArticleBelhan S, Özkaraca M, Kandemir FM, Gülyüz F, Yıldırım S, Ömür AD, Yener Z: Effectiveness of hesperidin on methotrexate-induced testicular toxicity in rats. Kafkas Univ Vet Fak Derg, 23 (5): 789-796, 2017789-796, . DOI: 10.9775/kvfd.2017 AbstractThe aim of this study was to investigate the effect of hesperidin on male reproductive system in rats to which methotrexate (MTX) was administered. In the study, 28 male Wistar albino rats at the age of 8 weeks and had 250-300 g of live weight were used. Four experimental groups were formed; Group 1 (n=7): The control group, only feed and water were given. Group 2 (n=7): MTX group, a single dose of 20 mg/ kg of i.p. MTX was administered. Group 3 (n=7): Hesperidin group, 200 mg/kg of hesperidin was administered by gavage for 7 days. Group 4: MTX + hesperidin group (n=7): Following administration of a single dose of 20 mg/kg i.p. MTX , 200 mg/kg of Hesperidin was administered by oral gavage for 7 days. At the end of the experiment, rats were decapitated and biochemical, histopathological and spermatological parameters were examined. It was observed that in the MTX group, sperm motility and density, the enzymes CAT, GPx and SOD and GSH level decreased, TNF-alpha and IL-1 Beta, as well as MDA, levels were increased, regular structure of spermatogenic cells was impaired, and seminiferous tubules became necrotic and degenerative. It was determined that spermatological parameters improved and, necrotic and degenerative changes diminished by the administration of MTX+hesperidin. These outcomes indicated that hesperidin had a protective effect on destructive effects of MTX in rat testiclesv. Keywords: Male rat, Hesperidin, Methotrexate, Sperm, Reproductive system Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi ÖzetBu çalışmanın amacı, metoraksat (MTX) uygulanan ratlarda hesperidinin erkek üreme sistemi üzerindeki etkisini araştırmaktı. Çalışmada 8 haftalık yaşta, 250-300 g canlı ağırlığa sahip 28 erkek Wistar albino cinsi rat kullanıldı. Dört deney grubu oluşturuldu; Grup 1 (n=7): kontrol grubu, sadece yem ve su verildi. Grup 2 (n=7): MTX grubu, 20 mg/kg MTX i.p. tek doz uygulandı. Grup 3 (n=7): Hesperidin grubu, 200 mg/kg hesperidin 7 gün süre ile ağızdan sonda yardımıyla verildi. Grup 4 (n=7): MTX + hesperidin grubu, 20 mg/kg MTX i.p tek doz uygulamasını takiben 200 mg/kg hesperidin 7 gün süre ile ağızdan sonda yardımıyla verildi. Deney sonunda ratlar dekapite edilerek biyokimyasal, histopatolojik ve spermatolojik parametreler incelendi. MTX grubunda sperm motilitesi ve yoğunluğunun, CAT, GPx ve SOD enzimlerinin ve GSH düzeyinin düştüğü, TNF-alpha ve IL-1 Beta ile MDA düzeyinin arttığı, spermatojenik hücrelerin düzenli yapısının bozulduğu, seminifer tubullerin nekrotik ve dejeneratif bir hal aldığı gözlendi. MTX + hesperidin uygulaması ile spermatolojik parametrelerin düzeldiği, nekrotik ve dejeneratif değişikliklerin azaldığı tespit edildi. Bu sonuçlar hesperidinin rat testislerinde MTX tarafından oluşan yıkıcı etkiler üze...

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“…Many studies have reported that ADR could trigger impairment in testicular function in male rats [3, 8]. ADR can significantly increase oxidative stress and lipid peroxidation of testicular tissue, cause alteration in testicular histology, decrease sperm parameters, and increase apoptosis in rats [1, 2, 17]. Furthermore, ADR can significantly alter gonadotropin (LH, FSH) and testosterone levels known to be prime regulators of germ cell development [3, 4, 18, 19].…”

Section: Discussionmentioning

confidence: 99%

“…Adriamycin (ADR), an anthracycline-group antibiotic, is one of the most commonly used antineoplastic agents against a wide range of tumors such as hematological malignancy, ovarian cancer, breast cancer, and testicular cancer [1]. It inhibits DNA replication by intercalating into DNA strands and stabilizing topoisomerase II-DNA complex formation [2].…”

Section: Introductionmentioning

confidence: 99%

“…ADR-induced testicular toxicity is caused by a combination of different pathophysiological events including oxidative stress, lipid peroxidation, mitochondrial dysfunction, increase tumor necrosis factor-α (TNF-α), and cellular apoptosis [3, 8]. Based on this concept, numerous studies in animals have tested various antioxidants and anti-apoptotic agents in an attempt to limit ADR-induced testicular damage [1, 2, 9–11].…”

Section: Introductionmentioning

confidence: 99%

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Cross-talk between ER stress and mitochondrial pathway mediated adriamycin-induced testicular toxicity and DA-9401 modulate adriamycin-induced apoptosis in Sprague–Dawley rats

et al. 2019

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Background DA-9401 was prepared as a mixture of Chinese medicinal herb extracts from roots of Morinda officinalis How (Rubiaceae), outer scales of Allium cepa L. (Liliceae) and seeds of Cuscuta chinensis Lamark (Convolvulaceae). The present study was designed to investigate the possible protective role of DA-9401 in adriamycin (ADR)-induced testicular toxicity associated with oxidative stress, endoplasmic reticulum (ER) stress, and apoptosis. Methods Fifty healthy 8-week-old male Sprague–Dawley rats were equally divided into five groups. The first CTR group was treated with normal saline 2 ml/day by gavage. The second was treated with DA-100 (DA-9401 100 mg/kg/day). The third (ADR) group received ADR (2 mg/kg/once a week) intraperitoneally, while the combination of ADR and DA-9401 was given to the fourth ADR + DA-100 (100 mg/kg/day p.o) group and fifth ADR + DA-200 (200 mg/kg/day p.o) group. At the end of the 8-week treatment period, body weight, reproductive organ weights, fertility rate, pups per female were recorded, and serum were assayed for hormone concentrations. Tissues were subjected to semen analysis, histopathological changes, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), oxidative stress markers and expression levels of endoplasmic reticulum (ER) stress markers, apoptosis markers, tight junction protein markers, steroidogenic acute regulatory protein (StAR), cation channel of sperm (CatSper) and glycogen synthase kinase-3 (GSK-3) by western blot. Results DA-9401 administration to ADR-treated rats significantly decreased serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels, interleukin-6, TNF-α, MDA level, ROS/RNS level, ER stress response protein levels, tunnel positive cells, cleaved caspase-3, and Bax/Bcl2 ratio. Moreover, pretreatment with DA-9401 significantly increased body weight, reproductive organ weights, fertility rate, pups per female, Johnsen’s score, spermatogenic cell density, sperm count and sperm motility, serum testosterone concentration, testicular superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), tight junction protein markers, star protein level, CatSper, and GSK-3 level. Conclusions ADR treatment can markedly impair testicular function and induce testicular cell death presumably by causing significant changes in oxidative stress, ER stress, and mitochondrial pathway. DA-9401 exerts beneficial effects against oxidative stress, ER stress, and mitochondria-mediated cell death pathway in testis tissue by up-regulating expression levels of tight junction protein markers, steroidogenic acute regulatory protein, GSK-3 alpha, and cation channels of sperm. Electronic supplementary material The online version of this article (10.1186/s12935-019-0805-2) contains supplementary material, which is available to authorized users.

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Ellagic acid and rosmarinic acid attenuate doxorubicin-induced testicular injury in rats

Cited by 27 publications

References 42 publications

Effect of chrysin on methotrexate-induced testicular damage in rats

Effect of chrysin on methotrexate-induced testicular damage in rats

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Cross-talk between ER stress and mitochondrial pathway mediated adriamycin-induced testicular toxicity and DA-9401 modulate adriamycin-induced apoptosis in Sprague–Dawley rats

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