Bijani Soroush, Naserzadeh Parvaneh, Hosseini Mir-Jamal
Zanjan Applied Pharmacology Research Center, Health and Metabolic Diseases Research Institute, Zanjan University of Medical Sciences, Zanjan, Iran.
Department of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.
Heliyon. 2024 Sep 24;10(19):e38289. doi: 10.1016/j.heliyon.2024.e38289. eCollection 2024 Oct 15.
The heat exposure and white noise can induce damage on reproductive organs. The main objective of this study is to observe, if betanin administration could ameliorate oxidative stress, apoptosis and inflammation in testis of rodents following noise and scrotal hyperthermia exposure. Wistar rats were divided into 6 groups; control, betanin, noise, hyperthermia and two treatment groups. Scrotal hyperthermia model was performed by heat exposure of rat testicular (43 °C) for 15 min and 3 times per weeks for 14 days. Noise induction model was done following exposure of rats with 100-dB noise level for 14 days and 8 h daily similar to real exposure condition in human. Betanin was administrated at the sub-effective dose (15 mg/kg) by gavage route for 4 weeks (5 times a week) to male rats. The animals were euthanized and testis were dissected and stored at -80 °C. Then, the oxidative stress biomarkers (MDA and GSH), apoptosis (cytochrome & Annexin V), and inflammatory cytokines (TNF-α & IL-6) were measured by the real time polymerase chain reaction (RT-PCR) of testis collected samples. The data output demonstrates the impact of noise and hyperthermia in testicular toxicity induction by mitigating oxidative damage, apoptosis and inflammatory mediators. Following treatment with 15 mg/kg per day of betanin, lipid peroxidation and GSH content have been modulated, and TNF-α and IL-6 gene expression has been declined. Our results revealed that in Wistar rats, betanin displays protective effects against noise and scrotal hyperthermia-induced acute testicular toxicity through the inhibition of oxidative stress, apoptosis, and inflammation.
热暴露和白噪声可对生殖器官造成损害。本研究的主要目的是观察给予甜菜红素是否能改善噪声和阴囊高温暴露后啮齿动物睾丸中的氧化应激、细胞凋亡和炎症。将Wistar大鼠分为6组：对照组、甜菜红素组、噪声组、高温组和两个治疗组。通过将大鼠睾丸暴露于43°C的热环境中15分钟，每周3次，共14天来建立阴囊高温模型。按照与人类实际暴露情况相似的条件，让大鼠每天暴露于100分贝的噪声水平下8小时，持续14天，以此建立噪声诱导模型。通过灌胃途径以亚有效剂量（15毫克/千克）给雄性大鼠施用甜菜红素，持续4周（每周5次）。对动物实施安乐死后，解剖睾丸并储存在-80°C。然后，通过对收集的睾丸样本进行实时聚合酶链反应（RT-PCR）来测量氧化应激生物标志物（丙二醛和谷胱甘肽）、细胞凋亡（细胞色素和膜联蛋白V）以及炎性细胞因子（肿瘤坏死因子-α和白细胞介素-6）。数据输出表明，噪声和高温通过减轻氧化损伤、细胞凋亡和炎性介质对睾丸毒性诱导产生影响。在用每天15毫克/千克的甜菜红素治疗后，脂质过氧化和谷胱甘肽含量得到调节，肿瘤坏死因子-α和白细胞介素-6基因表达下降。我们的结果显示，在Wistar大鼠中，甜菜红素通过抑制氧化应激、细胞凋亡和炎症，对噪声和阴囊高温诱导的急性睾丸毒性具有保护作用。
