Biochemistry Department, Faculty of Sciences, Beni-Suef University, Beni-Suef, 62511, Egypt.
Department of Medical Histology and Cell Biology, Faculty of Medicine, Beni-Suef University, Beni-Suef, 62511, Egypt.
Biol Trace Elem Res. 2022 Jul;200(7):3187-3204. doi: 10.1007/s12011-021-02913-w. Epub 2021 Sep 17.
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.
肾毒性成为一个引发的问题，因为肾脏是许多化疗药物的靶点。因此，我们旨在研究 Galaxaura elongata 提取物（GE）对硫酸氧钒（Van）诱导的大鼠肾毒性的保护作用。将 40 只 Wistar 白化大鼠（雄性）分为四组（n = 10）如下：对照组：大鼠给予 0.5%羧甲基纤维素（CMC）。Galaxa 组：大鼠给予 GE 剂量（100mg/kg 口服），每日一次，连续 6 周。Van 组：大鼠每周一次注射 Van 剂量（50mg/kg ip），连续 6 周。Galaxa+Van 组：大鼠给予 GE 剂量（100mg/kg 口服），每日一次，连续 6 周，同时给予 Van 剂量（50mg/kg ip），连续 6 周。我们的结果表明，与对照组相比，Van 显著升高了血清尿素和肌酐水平，并导致肾脏氧化/抗氧化还原失衡。Van 给药同时给予 GE 可减轻 Van 对肾脏组织的不良影响。此外，与 Van 组相比，Galaxa+Van 组中给予 GE 下调了血管紧张素转换酶（ACE1）mRNA 表达、血管紧张素 II（Ang II）浓度、转化生长因子-β（TGF-β）mRNA 表达和蛋白浓度以及核因子 κB（NF-κB）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）表达明显上调，同时 DNA 片段化%降低。本研究结果表明，同时给予 GE 可减轻糖尿病大鼠 Van 引起的肾毒性。Van 处理动物的 GE 治疗恢复了改变的肾氧化/抗氧化还原值，减轻了纤维化。这些结果与 TGF-B/Smads 和 Nrf2/NF-κB 信号通路的相互作用引起这些作用的结果一致。
