Nephrotoxicity becomes a provoked problem as the kidneys are the target of many chemotherapies. For this reason, we aimed to study the protective effect of Galaxaura elongata extract (GE) against the vanadyl sulfate (Van) induced nephrotoxicity in rats. Forty Wistar albino rats (male) were divided into four groups (n = 10) as follows: control group: rats received 0.5% carboxymethyl cellulose (CMC). Galaxa group: rats received GE at a dose (100 mg/kg orally) daily for 6 weeks. Van group: rats injected with Van at a dose (50 mg/kg i.p.) once weekly for 6 successive weeks. Galaxa + Van group: rats received GE at a dose (100 mg/kg orally) daily for 6 weeks concurrently with Van at a dose (50 mg/kg i.p.) for 6 weeks. Our results showed that Van significantly raised urea and creatinine serum levels as compared to the control group as well as disordered renal oxidative/antioxidant redox. Administration of GE with Van alleviated the adverse impact of Van over the kidney tissues. Furthermore, GE administration in Galaxa + Van group downregulates angiotensin-converting enzyme (ACE1) mRNA expression, angiotensin II (Ang II) concentration, transforming growth factor β (TGF-β) mRNA expression and protein concentration and Nuclear factor κB (NF-κB) mRNA expression as compared to Van group. Also, GE administration caused a noticeable upregulation of Nrf2 and heme oxygenase-1 (HO-1) expressions with a consequent decrease of DNA fragmentation % compared to Van group. The results of the current study show that simultaneous treatment with GE can alleviate nephrotoxicity caused by Van in diabetic rats. The GE treatment of the Van treated animals restored altered renal oxidative/antioxidant redox values towards normal and lessened fibrosis. These results are consistent with these effects being caused by interactions with the TGF-B/Smads and Nrf2/NF-κB signaling pathways.

中文翻译：

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Galaxaura elongata Extract (GE) 通过调节 TGF-β/Smads 和 Nrf2/NF-κB 通路来调节硫酸氧钒诱导的肾损伤。

由于肾脏是许多化学疗法的目标，因此肾毒性成为一个棘手的问题。出于这个原因，我们旨在研究长春花提取物 (GE) 对硫酸氧钒 (Van) 诱导的大鼠肾毒性的保护作用。将四十只 Wistar 白化大鼠（雄性）分为四组（n = 10），如下所示： 对照组：大鼠接受 0.5% 羧甲基纤维素（CMC）。Galaxa 组：大鼠每天接受剂量（100 mg/kg 口服）的 GE，持续 6 周。Van组：大鼠每周一次以剂量（50mg/kg ip）注射Van，连续6周。Galaxa + Van 组：大鼠每天接受剂量（100 mg/kg 口服）的 GE，持续 6 周，同时接受剂量（50 mg/kg ip）的 Van，持续 6 周。我们的研究结果表明，与对照组相比，Van 显着提高了尿素和肌酐血清水平，以及肾脏氧化/抗氧化氧化还原紊乱。GE与Van一起给药减轻了Van对肾组织的不利影响。此外，Galaxa + Van 组中的 GE 给药下调血管紧张素转换酶 (ACE1) mRNA 表达、血管紧张素 II (Ang II) 浓度、转化生长因子 β (TGF-β) mRNA 表达和蛋白质浓度以及核因子 κB (NF-κB) ) 与 Van 组相比的 mRNA 表达。此外，与 Van 组相比，GE 给药导致 Nrf2 和血红素加氧酶-1 (HO-1) 表达显着上调，从而导致 DNA 片段化百分比降低。目前的研究结果表明，与 GE 的同时治疗可以减轻糖尿病大鼠由 Van 引起的肾毒性。Van 治疗动物的 GE 治疗将改变的肾氧化/抗氧化氧化还原值恢复到正常和减少的纤维化。这些结果与由与 TGF-B/Smads 和 Nrf2/NF-κB 信号通路相互作用引起的这些效应一致。