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<p>7,12-Dimethylbenz[a]anthracene (DMBA) induces reactive oxygen species (ROS) formation, oxidative stress, and apoptosis in target tissues. Royal jelly (RJ) is rich in flavonoids, phenolic acids, and peptides. This study evaluated whether RJ can mitigate DMBA-induced oxidative, apoptotic, and histopathological changes in the rat mammary gland and skin. Female Wistar rats were divided into four groups, including the Control (no treatment), RJ (300&#xa0;mg/kg/week, orally), DMBA (single dose 80&#xa0;mg/kg, IP), and DMBA + RJ (same doses). After 8 weeks, mammary gland and skin specimens were collected. Oxidative stress markers were quantified in tissue homogenates. Apoptotic gene and protein expression were measured by qRT-PCR and Western blot, respectively. Ki67 expression was assessed by immunohistochemistry. Additionally, histopathological evaluation (H&amp;E stain) was conducted. DMBA significantly increased MDA, reduced GPx, SOD, and TAC. Pro-apoptotic markers were upregulated, while Bcl2 was downregulated. Histopathology revealed vacuolar degeneration, necrosis, mitotic figures, and corpora amylacea in the mammary gland, and epidermal hyperplasia, mitotic figures, follicular hyperplasia, and focal necrosis in skin. RJ co-treatment restored GPx and SOD levels to almost those of the control group, reduced MDA, decreased p53 and <i>Bax</i> to near-control levels, and increased Bcl2 to the approximate level of the control group. Moreover, RJ treatment normalized the mammary gland histologically, while skin showed attenuated necrosis and decreased epidermal hyperplasia and mitotic index. RJ effectively countered DMBA-induced oxidative stress and apoptosis in the rat mammary gland while preserving tissue integrity. In skin, RJ mitigated oxidative damage and reduced proliferation. These outcomes suggest RJ’s potential as an adjuvant antioxidant in glandular disorders, while showing the anticarcinogenic potential.</p>

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Royal jelly attenuates DMBA induced preneoplastic lesions in rat mammary gland and Skin

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月6日

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  • Alireza Salehi,
  • Fatemeh Yaghoobi,
  • Seyed Mohammad Hosseini,
  • Seyedeh-Sara Hashemi

摘要

7,12-Dimethylbenz[a]anthracene (DMBA) induces reactive oxygen species (ROS) formation, oxidative stress, and apoptosis in target tissues. Royal jelly (RJ) is rich in flavonoids, phenolic acids, and peptides. This study evaluated whether RJ can mitigate DMBA-induced oxidative, apoptotic, and histopathological changes in the rat mammary gland and skin. Female Wistar rats were divided into four groups, including the Control (no treatment), RJ (300 mg/kg/week, orally), DMBA (single dose 80 mg/kg, IP), and DMBA + RJ (same doses). After 8 weeks, mammary gland and skin specimens were collected. Oxidative stress markers were quantified in tissue homogenates. Apoptotic gene and protein expression were measured by qRT-PCR and Western blot, respectively. Ki67 expression was assessed by immunohistochemistry. Additionally, histopathological evaluation (H&E stain) was conducted. DMBA significantly increased MDA, reduced GPx, SOD, and TAC. Pro-apoptotic markers were upregulated, while Bcl2 was downregulated. Histopathology revealed vacuolar degeneration, necrosis, mitotic figures, and corpora amylacea in the mammary gland, and epidermal hyperplasia, mitotic figures, follicular hyperplasia, and focal necrosis in skin. RJ co-treatment restored GPx and SOD levels to almost those of the control group, reduced MDA, decreased p53 and Bax to near-control levels, and increased Bcl2 to the approximate level of the control group. Moreover, RJ treatment normalized the mammary gland histologically, while skin showed attenuated necrosis and decreased epidermal hyperplasia and mitotic index. RJ effectively countered DMBA-induced oxidative stress and apoptosis in the rat mammary gland while preserving tissue integrity. In skin, RJ mitigated oxidative damage and reduced proliferation. These outcomes suggest RJ’s potential as an adjuvant antioxidant in glandular disorders, while showing the anticarcinogenic potential.