ArticleBiological trace element research2022
Galaxaura elongata Extract (GE) Modulates Vanadyl Sulfate-Induced Renal Damage via Regulating TGF-β/Smads and Nrf2/NF-κB Pathways.
Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Boswellic Acid and Carnosine Ameliorate Vanadyl-Sulfate-Induced Renal Damage via Regulating Nrf2/HO-1 and PI3K/AKT Pathways.Biological trace element research · 2026Article
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation.International journal of molecular sciences · 2023Review
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4 authors at 1 institution in 1 country.
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Abstract
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.
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