The Ameliorative Potential of Dexmedetomidine and Benincasa Cerifera Extract in Renal Ischemia/Reperfusion Injury in A Streptozotocin-Induced Diabetic Model

Renal ischemia/reperfusion injury (IRI) represents the main reason for acute kidney injury (AKI). Dexmedetomidine (Dex) and Benincasa cerifera (BC) have wide benefits due to their anti-inflammatory and antioxidant properties. This study aims to illustrate the protective effects of BC and Dex on renal IRI in a diabetic model. Sixty adult male albino rats (Wistar strain), weighing 250–300 g, were included in the study. The rats were divided into four groups, as follows: sham group: (non-diabetic); diabetes mellitus (DM) + IRI group: streptozotocin (STZ)-induced diabetic rats exposed to renal IRI on day 30 after diagnosis of diabetes; DM + IRI + BC group: STZ-induced diabetic rats treated with BC (500 mg/kg) for 30 days after diagnosis of diabetes, then exposed to renal IRI; and DM + IRI + Dex group: STZ-induced diabetic rats treated with Dex (100 µg/kg intraperitoneally) 5 min before induction of ischemia on day 30 after diagnosis of diabetes, then exposed to renal IRI. Biochemical parameters, histopathological examination, and immunohistochemical markers were evaluated. A significant improvement in the biochemical, histopathological, and immunohistochemical parameters were observed in the DM + IRI + BC group, while the DM + IRI + Dex group showed improvements in renal IRI and dyslipidemia. The present study demonstrated that oxidative stress plays a chief role in renal IRI in the STZ-induced diabetic model. Treatment with BC achieved excellent ameliorative effects, while treatment with DEX improved renal IRI.

肾缺血再灌注损伤（Renal ischemia/reperfusion injury, IRI）是急性肾损伤（acute kidney injury, AKI）的主要诱因。右美托咪定（Dexmedetomidine, Dex）与Benincasa cerifera (BC)因具备抗炎与抗氧化特性，具备多重有益作用。本研究旨在阐明BC与Dex对糖尿病模型中肾IRI的保护作用。本研究纳入60只体重250~300 g的成年雄性白化Wistar大鼠，将其分为4组：假手术组（非糖尿病模型）；糖尿病（diabetes mellitus, DM）+IRI组：链脲佐菌素（streptozotocin, STZ）诱导的糖尿病大鼠于糖尿病确诊后第30天接受肾IRI造模；DM+IRI+BC组：链脲佐菌素诱导的糖尿病大鼠于确诊糖尿病后连续30天予以BC（500 mg/kg）干预，随后于确诊后第30天接受肾IRI造模；DM+IRI+Dex组：链脲佐菌素诱导的糖尿病大鼠于糖尿病确诊后第30天、缺血造模前5分钟腹腔内注射Dex（100 μg/kg），随后接受肾IRI造模。本研究对生化指标、组织病理学检查及免疫组化标志物进行了检测评估。结果显示，DM+IRI+BC组的生化、病理及免疫组化指标均得到显著改善；而DM+IRI+Dex组则在肾IRI损伤与血脂异常方面呈现改善效果。本研究证实，氧化应激在链脲佐菌素诱导的糖尿病模型肾IRI中发挥关键作用。其中，BC治疗可取得优异的改善效果，而Dex治疗则可有效改善肾IRI损伤。