Novel protective effect of diosmin against cisplatin-induced prostate and seminal vesicle damage: Role of oxidative stress and apoptosis

Abou-Elghait, Amal T.; Elgamal, Dalia A.; el‐Rady, Nessren M. Abd; Hosny, Ahmed; El-Samie, El Zahraa Abd Allah Abd; Ali, Fares E.M.

doi:10.1016/j.tice.2022.101961

Cited by 2 publications

(1 citation statement)

References 66 publications

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“…Diosmin also reduces the release of pro-inflammatory enzymes such as myeloperoxidase and cytokines, notably tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the striatum, prefrontal cortex, and hippocampus in LPS exacerbated ketamine-induced experimental psychosis [20]. Additionally, through its antioxidant and antiapoptotic properties, diosmin attenuates numerous reproductive organ damage caused by cisplatin via inhibition of caspase-3 and Bax expressions with increased levels of Bcl-2, CD44 and Ki67 in the prostate and seminal vesicles [21]. Hence, this study investigated the potential protective benefits of diosmin against DOX-induced reproductive impairment in male rats.…”

Section: Introductionmentioning

confidence: 99%

Diosmin protects the testicles from doxorubicin-induced damage by increasing steroidogenesis and suppressing oxido-inflammation and apoptotic mediators

Oyovwi

2024

Int J Biochem Mol Biol

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Background: Cancer chemotherapy with doxorubicin (DOX) has been linked to serious testicular damage and spermatotoxicity due to the induction of oxidative stress, inflammation, and apoptosis. Thus, the current study was carried out to assess the potential ameliorative impact of diosmin, an antioxidant drug, against DOX-mediated spermatoxicity and testicular injury in rats. Material and Methods: In the experimental protocol, rats were grouped into 4: Group 1 received vehicle and saline for 8 weeks while group 2 received diosmin and saline concomitantly for 8 weeks. Group 3 was given 3 mg/kg intraperitoneal DOX once every 7 days for 8 weeks. Group 4 was given 40 mg/ kg of diosmin orally for 56 days followed by DOX diosmin administration after one hour. After 56 days of treatment, sperm quality, hormonal testing, biochemical parameters, and histological alterations in the testes were evaluated. Results: DOX-induced reduce spermatogenic function, testicular 3-and 17β-Hydroxysteroid dehydrogenases, and serum follicle stimulating hormone, luteinizing hormone, and testosterone. It also enhanced inflammation, testicular oxidative damage, and apoptosis. The histopathologic examinations corroborated the biochemical results obtained. Significantly, diosmin treatment reduced DOX-induced injury, as evidenced by restored testicular architecture, increased steroidogenesis, preservation of spermatogenesis, suppression of oxide-inflammatory response, and apoptosis. Conclusion: It was found that through diosmin antioxidant, anti-apoptotic, and anti-oxido-inflammatory it presents a possible therapeutic alternative for protecting testicular tissue against DOX's harmful effects.

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Section: Introductionmentioning

confidence: 99%

Diosmin protects the testicles from doxorubicin-induced damage by increasing steroidogenesis and suppressing oxido-inflammation and apoptotic mediators

Oyovwi

2024

Int J Biochem Mol Biol

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Complanatuside A Inhibits Seminal Vesicle Cell Apoptosis by Activating SerpinB1a in Type 2 Diabetic Mice

Ni,

Liu,

You

et al. 2024

Andrologia

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Type 2 diabetes mellitus (T2DM) can trigger cell apoptosis of seminal vesicles (SVs) and impair seminal secretory functions. Complanatuside A (CA) is known for its anti‐inflammatory and antioxidant effects, as well as its ability to repair cellular damage. This study aimed to explore the potential molecular mechanisms through which CA mitigates cell apoptosis in the SVs of type 2 diabetic mice. A streptozotocin‐induced type 2 diabetic mice model was utilized, and a 1‐month intervention using CA (70 mg/kg) was administered. We monitored body weight, blood glucose levels, SV volume, and concentration of SV fluid. Hematoxylin and eosin staining was used to assess tissue damage. RNA sequencing was applied to identify differential gene expression, and the expression of target genes (ARG2, PBK, SerpinB1a, E2F2) was verified by qRT‐PCR. Changes in the apoptosis level of SV tissues in mice were detected with TUNEL staining. Compared to the control group, mice with T2DM exhibited decreased SV volume and SV fluid content, which was improved with CA treatment. Elevated expression of SerpinB1a and reduced apoptosis were observed in the T2DM‐CA group compared to T2DM mice. In summary, CA can inhibit cell apoptosis in the SVs, there by improving tissue damage in type 2 diabetic mice. SerpinB1a may be involved in this process. This study provides a new theoretical foundation for the treatment of seminal vesicle secretory dysfunction in type 2 diabetes mellitus.

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Novel protective effect of diosmin against cisplatin-induced prostate and seminal vesicle damage: Role of oxidative stress and apoptosis

Cited by 2 publications

References 66 publications

Diosmin protects the testicles from doxorubicin-induced damage by increasing steroidogenesis and suppressing oxido-inflammation and apoptotic mediators

Diosmin protects the testicles from doxorubicin-induced damage by increasing steroidogenesis and suppressing oxido-inflammation and apoptotic mediators

Complanatuside A Inhibits Seminal Vesicle Cell Apoptosis by Activating SerpinB1a in Type 2 Diabetic Mice

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