ArticleBiological trace element research2026
Boswellic Acid and Carnosine Ameliorate Vanadyl-Sulfate-Induced Renal Damage via Regulating Nrf2/HO-1 and PI3K/AKT Pathways.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephrotoxicity is a condition caused by the negative effects of several chemotherapy treatments on the kidneys. Our target was to determine how boswellic and carnosic acids protected rats against vanadyl sulfate (VOS)-induced nephrotoxicity. A total of 30 male Wistar albino rats were used in the investigation. They were divided into sex groups (five rats in each group) as follows: Rats in the control group were given carboxymethyl cellulose (CMC) at a concentration of 0.5%. VOS group was administered a weekly intraperitoneal injection of VOS 50 mg/kg for six consecutive weeks. For 6 weeks in a row, rats in the boswellic acid group were given injections of BA every day at a dose of 100 mg/kg orally. Group receiving carnosic acid received 100 mg/kg of CA orally daily for 6 consecutive weeks. For 6 weeks, rats in the boswellic acid plus VOS group were given 50 mg/kg of VOS intraperitoneally (i.p.) once a week and 100 mg/kg of BA orally daily. For 6 weeks, the carnosic acid plus VOS group received 50 mg/kg of VOS intraperitoneally once a week and 100 mg/kg of CA orally daily. In contrast to the control group, our results demonstrated that the injection of vanadyl sulfate to the VOS group contributed a significant increase in creatinine and blood urea as well as disordered kidney oxidative antioxidant interaction. The injection of vanadyl sulfate to the VOS group produced an increase in renal MDA concentration and a decrease in renal SOD activity, GSH content, GR, and CAT activities in comparison to the control group. When compared to the control group, our study on renal mRNA expression revealed that administering vanadyl sulfate to the VOS group increases renal iNOS, PI3K, and AKT mRNA expressions and modulates the mRNA expression of renal Nrf2 and HO-1. According to the current investigation, treating rats with BA or CA can reduce their nephrotoxicity from VOS; when the defective kidney oxidative antioxidant redox levels were returned to normal, the fibrosis in the Van-treated animals decreased. These findings are consistent with interactions between the Pi3k/Akt and Nrf2/Ho-1 pathways, as one of the human body's most vital organs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.