<p>Bisphenol A (BPA) is an endocrine-disrupting chemical known to cause testicular toxicity through oxidative stress and apoptosis. Panax ginseng (PG) is a natural product with anti-inflammatory effects. This study aimed to evaluate the protective effect of PG against BPA-induced testicular damage in rats. Thirty-two Wistar Albino rats aged 10–12 weeks were divided into four groups: Control, PG, BPA, and BPA + PG. BPA (50 mg/kg/day) and PG (100 mg/kg/day) were orally administered for 6 weeks. BPA significantly increased serum total oxidant status and decreased antioxidant status (<i>p</i> &lt; 0.001, <i>p</i> &lt; 0.001). Also, the levels of superoxide dismutase (an antioxidant enzyme) (<i>p</i> = 0.0005) and androgen receptor-mRNA (an androgen signaling marker) decreased (<i>p</i> = 0.014). However, caspase 3 (an apoptosis marker) (<i>p</i> = 0.0067), 8-hydroxy-2’-deoxyguanosine (a marker of oxidative DNA damage) (<i>p</i> &lt; 0.001), and tumor necrosis factor-α (a proinflammatory cytokine) (<i>p</i> &lt; 0.001) levels increased in testicular tissues. Rats treated with PG showed improvements in all oxidative and inflammatory markers and significantly restored androgen receptor expression. Histopathological examination revealed degeneration in seminiferous tubules and reduced spermatozoa in the BPA group, while the BPA + PG group showed marked improvement. These findings suggest that PG may alleviate oxidative stress-related testicular damage at both molecular and histological levels and may offer insights for future clinical studies.</p>

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Protective effects of panax ginseng against bisphenol a-induced testicular toxicity in rats

  • Dogancan Dorucu,
  • Goksel Sener,
  • Seren Ede Pazarbasi,
  • Burcin Irem Abas,
  • Yasemin Cesur,
  • Ozge Cevik,
  • Feriha Ercan,
  • Tarik Emre Sener,
  • Kamil Cam

摘要

Bisphenol A (BPA) is an endocrine-disrupting chemical known to cause testicular toxicity through oxidative stress and apoptosis. Panax ginseng (PG) is a natural product with anti-inflammatory effects. This study aimed to evaluate the protective effect of PG against BPA-induced testicular damage in rats. Thirty-two Wistar Albino rats aged 10–12 weeks were divided into four groups: Control, PG, BPA, and BPA + PG. BPA (50 mg/kg/day) and PG (100 mg/kg/day) were orally administered for 6 weeks. BPA significantly increased serum total oxidant status and decreased antioxidant status (p < 0.001, p < 0.001). Also, the levels of superoxide dismutase (an antioxidant enzyme) (p = 0.0005) and androgen receptor-mRNA (an androgen signaling marker) decreased (p = 0.014). However, caspase 3 (an apoptosis marker) (p = 0.0067), 8-hydroxy-2’-deoxyguanosine (a marker of oxidative DNA damage) (p < 0.001), and tumor necrosis factor-α (a proinflammatory cytokine) (p < 0.001) levels increased in testicular tissues. Rats treated with PG showed improvements in all oxidative and inflammatory markers and significantly restored androgen receptor expression. Histopathological examination revealed degeneration in seminiferous tubules and reduced spermatozoa in the BPA group, while the BPA + PG group showed marked improvement. These findings suggest that PG may alleviate oxidative stress-related testicular damage at both molecular and histological levels and may offer insights for future clinical studies.