ArticleVeterinary sciences2026
Evaluating the Antioxidant Potential of Coumestrol in the Treatment of Tripterygium Glycoside-Induced Oligospermia in Rats and Its Potential Mechanisms.
Article in Veterinary sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Prenatal road traffic noise impairs early testicular development in Sprague-Dawley offspring: pharmacological rescue by melatonin and edaravone; developmental preservation by environmental enrichment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Tripterygium glycoside (TG) is known to disrupt the oxidative balance in bio-systems, inducing oxidative stress-mediated toxic effects on testicular tissue. This study aimed to explore the therapeutic potential of coumestrol (COU) against these adverse effects. Sixty-four male Sprague-Dawley rats were randomized into control and Tripterygium glycoside (TG) groups for four weeks. Following initial intervention, eight rats per group were sacrificed to verify the establishment of the oligospermia model and hormonal dysfunction. The remaining rats were subdivided into five therapeutic subgroups, TG, TG + L-carnitine, and three COU dosage groups (low, medium, and high) to evaluate potential protective effects. The present study comprehensively analyzed its impacts on testicular histomorphology, circulating testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, and redox balance status, as well as a suite of serum biochemical and physiological biomarkers. Our results revealed that TG induced oligospermia in rats, causing significant testicular oxidative stress characterized by excessive accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), alongside depleted superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC). Conversely, COU treatment effectively mitigated these impairments by significantly downregulating ROS and MDA levels while restoring SOD activity and T-AOC.
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Registered trials
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