Hesperidin (HD), a citrus bioflavonoid possesses a variety of biological activities including antioxidant, anti-inflammatory, anti-apoptotic and anti-carcinogenic properties. In the present study, we investigated the effect of HD treatment on N,N'-dimethylhydrazine (DMH) induced oxidative stress, inflammation, apoptosis and goblet cell disintegration in the colon of Wistar rats. Administration of HD was done at two doses (100 and 200 mg/kg body weight) orally to rats daily for 14 days followed by a single subcutaneous injection of DMH (40 mg/kg body weight) on the 14th day and next day animals were sacrificed. The protective potential of HD against colon toxicity was measured through membrane oxidation, antioxidant status, inflammatory and apoptotic markers expression, and histological changes. Results demonstrated that HD inhibited DMH mediated oxidative damage by diminishing the level of peroxidation of lipids and increasing the activity of superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, glutathione-s-transferase, and glutathione reductase. Moreover, HD attenuated inflammatory (NF-кB, IL-6, and COX-2) and apoptotic (p38-MAPK, p53, and caspase-3) markers expression. HD also attenuated the DMH induced goblet cell disintegration and restored histoarchitecture of the colon. The results of the present study demonstrate that HD efficiently protects against DMH induced colon toxicity by modulating oxidative stress, inflammation, and apoptosis.

中文翻译：

---

橙皮苷对 N,N'-二甲基肼诱导的 Wistar 大鼠结肠氧化应激、炎症和凋亡反应的保护作用


橙皮苷 (HD) 是一种柑橘类生物类黄酮，具有多种生物活性，包括抗氧化、抗炎、抗凋亡和抗癌特性。在本研究中，我们研究了 HD 治疗对 N,N'-二甲基肼 (DMH) 诱导的 Wistar 大鼠结肠氧化应激、炎症、细胞凋亡和杯状细胞崩解的影响。连续 14 天，每天给大鼠口服两次剂量的 HD（100 和 200 mg/kg 体重），然后在第 14 天皮下注射一次 DMH（40 mg/kg 体重），第二天对动物进行皮下注射。牺牲了。通过膜氧化、抗氧化状态、炎症和凋亡标记物表达以及组织学变化来测量 HD 对结肠毒性的保护潜力。结果表明，HD 通过降低脂质过氧化水平并增加超氧化物歧化酶、过氧化氢酶、还原型谷胱甘肽、谷胱甘肽过氧化物酶、谷胱甘肽-s-转移酶和谷胱甘肽还原酶的活性来抑制 DMH 介导的氧化损伤。此外，HD 还可减弱炎症（NF-кB、IL-6 和 COX-2）和细胞凋亡（p38-MAPK、p53 和 caspase-3）标志物的表达。 HD 还减弱了 DMH 诱导的杯状细胞崩解并恢复了结肠的组织结构。本研究的结果表明，HD 通过调节氧化应激、炎症和细胞凋亡，有效防止 DMH 诱导的结肠毒性。