ArticlePlants (Basel, Switzerland)2024
Chokeberry Products and By-Products as the Potential Pharmaceuticals for Kidney Protection-An Experimental Study in Rats.
Article in Plants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Bioactivity ofPlants (Basel, Switzerland) · 2026Article
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The study aimed to investigate the protective effects of chokeberry fruit products and by-products against cisplatin-induced acute nephrotoxicity in rats. Potential mechanisms involving oxidative stress and inflammatory responses were examined through biochemical and histopathological analyses of kidney tissue. Chokeberry waste, along with the whole fruit extract and juice, was evaluated as a potential raw material for pharmaceutical use. The chemical composition of chokeberry juice and extracts was analyzed using spectrophotometry and HPLC. Rats were treated with chokeberry preparations via intragastric tube for ten days, with a single intraperitoneal dose of cisplatin (8 mg/kg BW) administered on the third day. Post-sacrifice, plasma samples were analyzed for biochemical nephrotoxicity markers, oxidative stress, and inflammatory markers. Kidneys were removed for histopathological and biochemical analysis. Cisplatin-induced acute nephrotoxicity was confirmed by elevated plasma creatinine and blood urea nitrogen levels. Additionally, lipid peroxidation was significantly elevated, while reduced glutathione and catalase activity were significantly reduced. Pro-inflammatory mediators IL-1
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