Morinda citrifolia protective effects on paclitaxel-induced testis parenchyma toxicity: An experimental study

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Sidika Genc , Betul Cicek , Yesim Yeni , Mehmet Kuzucu , Ahmet Hacimuftuoglu , Ismail Bolat , Serkan Yildirim , Himasadat Zaker , Athanasios Zachariou , Nikolaos Sofikitis , Charalampos Mamoulakis , Aristidis Tsatsakis , Ali Taghizadehghalehjoughi
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引用次数: 0

Abstract

The current study aimed to investigate the sensitivity of male testis parenchyma cells to chemotherapy agents and the protective effects and mechanisms of Morinda citrifolia (Noni) administration against structural and functional changes before and after chemotherapy (Paclitaxel (PTX)). For this purpose, rats were randomly assigned into four groups (Control = G1, PTX 5 mg/kg = G2; PTX + Noni 10 mg/kg = G3, PTX + Noni 20 mg/kg = G4). PTX was injected intraperitoneally for 4 consecutive weeks, at a dose of 5 mg/kg to all groups except the control group. Then noni was administrated in 10 (G3) and 20 (G4) mg/kg groups orally (gavage) for 14 days. Biochemical analyses, Real-Time Polymerase Chain Reaction (PCR), and immunohistochemical analyses were performed. According to our results, Total Oxidative Stress (TOS) and Malondialdehyde (MDA) were significantly increased in the PTX group (P < 0.01). Superoxide Dismutase (SOD) enzyme activity and Total Antioxidant Capacity (TAC) levels were decreased (P < 0.01). The changes in the rats treated with PTX + Noni 20 mg/kg were noteworthy. The increased levels of IL1-β (Interleukin 1 beta) and TNFα (tumor necrosis factor-alpha) with PTX were down-regulated after treatment with PTX + Noni 20 mg/kg (P < 0.01) (9 % and 5 % respectively). In addition, Noni restored the testicular histopathological structure by reducing caspase-3 expression and significantly (61 %) suppressed oxidative DNA damage and apoptosis (by regulating the Bax (bcl-2-like protein 4)/Bcl-2 (B-cell lymphoma gene-2) ratio). In conclusion, Noni reduced cellular apoptosis and drastically changed Caspase 8 and Bax/Bcl-2 levels. Furthermore, it considerably decreases oxidative damage and can be used in testicular degeneration.

海巴戟对紫杉醇诱导的睾丸实质毒性的保护作用:一项实验研究。
本研究旨在探讨雄性睾丸实质细胞对化疗药物的敏感性,以及在化疗(紫杉醇(PTX))前后服用诺丽(诺丽)对结构和功能变化的保护作用和机制。为此,大鼠被随机分为四组(对照组= G1;PTX 5毫克/千克= G2;PTX + 诺丽10毫克/千克= G3;PTX + 诺丽20毫克/千克= G4)。除对照组外,其他各组均连续 4 周腹腔注射 PTX,剂量为 5 毫克/千克。然后按 10(G3)和 20(G4)毫克/千克的剂量给各组口服诺丽果(灌胃)14 天。研究人员进行了生化分析、实时聚合酶链反应(PCR)和免疫组化分析。结果显示,PTX 组的总氧化应激(TOS)和丙二醛(MDA)显著增加(P<0.05)。
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来源期刊
Reproductive toxicology
Reproductive toxicology 生物-毒理学
CiteScore
6.50
自引率
3.00%
发文量
131
审稿时长
45 days
期刊介绍: Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.
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