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蜂胶可减轻遭受镉毒性的雌性白化大鼠垂体和生殖系统的组织病理学改变。

Propolis mitigates histopathological alterations in the pituitary gland and reproductive system of female albino rats subjected to cadmium toxicity.

作者信息

Albishtue Abdulla A, Mohsin Al-Mahmmodi Aqeel, Almamoori Hasan A, Alahmer Mustafa Ali

机构信息

Department of Anatomy and Histology, Faculty of Veterinary Medicine, University of Kufa, Najaf, Iraq.

Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Kufa, Najaf, Iraq.

出版信息

Vet World. 2025 Jun;18(6):1466-1478. doi: 10.14202/vetworld.2025.1466-1478. Epub 2025 Jun 10.

DOI:10.14202/vetworld.2025.1466-1478
PMID:40689186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12273156/
Abstract

BACKGROUND AND AIM

Cadmium (Cd) is a pervasive environmental toxin that disrupts endocrine function and induces oxidative damage in reproductive organs. Propolis (PRO), a resinous substance produced by bees, has garnered attention for its antioxidant and estrogenic properties. This study investigated the protective potential of PRO on the pituitary-ovarian-uterine axis in female rats subjected to Cd-induced toxicity.

MATERIALS AND METHODS

Thirty adult female albino rats were randomized into five groups (n = 6/group): Control (C), Cd-only (T0), and Cd plus PRO at 150, 300, and 500 mg/kg body weight (BW) (T1-T3, respectively). Cadmium chloride was administered orally at 5 mg/kg for 4 weeks. PRO was co-administered daily through gavage. At the proestrus stage, animals were euthanized for tissue collection. Vaginal cytology was used to confirm estrous stage. Histopathological examination of the ovary, uterus, and pituitary gland was performed using H&E staining. Serum estradiol (E2) and superoxide dismutase (SOD) activity were assessed to evaluate hormonal and oxidative responses. Morphometric measurements were statistically analyzed through one-way analysis of variance with Tukey's test.

RESULTS

Cd exposure (T0) led to prolonged estrous cycles, ovarian atresia, uterine degeneration, and significant disruption of pituitary architecture, accompanied by reduced E2 and SOD levels (p < 0.05). PRO administration dose-dependently ameliorated these alterations. The highest PRO dose (T3) restored the histological architecture of all target organs to near-normal levels, significantly increased ovarian and uterine weight ratios, and elevated both E2 and SOD activity. Histomorphometric analysis confirmed increased follicle survival, thickened ovarian surface epithelium, and elevated interstitial cell counts. Pituitary endocrine cell counts and uterine gland numbers were also significantly higher in PRO-treated groups, particularly T3.

CONCLUSION

PRO supplementation at 500 mg/kg BW significantly attenuates Cd-induced reproductive and endocrine toxicity in female rats by restoring histological integrity and enhancing antioxidant and estrogenic responses. These findings suggest PRO as a promising candidate for mitigating heavy metal-induced reproductive dysfunction.

摘要

背景与目的

镉(Cd)是一种普遍存在的环境毒素,会扰乱内分泌功能并在生殖器官中引发氧化损伤。蜂胶(PRO)是蜜蜂产生的一种树脂状物质,因其抗氧化和雌激素特性而受到关注。本研究调查了蜂胶对遭受镉诱导毒性的雌性大鼠垂体-卵巢-子宫轴的保护潜力。

材料与方法

将30只成年雌性白化大鼠随机分为五组(每组n = 6):对照组(C)、仅镉处理组(T0)以及镉加150、300和500毫克/千克体重(BW)的蜂胶处理组(分别为T1 - T3)。以5毫克/千克的剂量口服氯化镉,持续4周。蜂胶通过灌胃每日共同给药。在动情前期阶段,对动物实施安乐死以收集组织。使用阴道细胞学检查确认发情阶段。使用苏木精-伊红(H&E)染色对卵巢、子宫和垂体进行组织病理学检查。评估血清雌二醇(E2)和超氧化物歧化酶(SOD)活性以评估激素和氧化反应。通过单因素方差分析和Tukey检验对形态学测量结果进行统计分析。

结果

镉暴露(T0)导致发情周期延长、卵巢闭锁、子宫退化以及垂体结构显著破坏,同时伴有E2和SOD水平降低(p < 0.05)。蜂胶给药呈剂量依赖性地改善了这些改变。最高剂量的蜂胶(T3)将所有靶器官的组织学结构恢复至接近正常水平,显著增加了卵巢和子宫重量比,并提高了E2和SOD活性。组织形态计量学分析证实卵泡存活率增加、卵巢表面上皮增厚以及间质细胞计数升高。在蜂胶处理组中,尤其是T3组,垂体内分泌细胞计数和子宫腺数量也显著更高。

结论

以500毫克/千克体重补充蜂胶可通过恢复组织学完整性并增强抗氧化和雌激素反应,显著减轻镉诱导的雌性大鼠生殖和内分泌毒性。这些发现表明蜂胶有望成为减轻重金属诱导的生殖功能障碍的候选物质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/857ae511903f/Vetworld-18-1466-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/84aa041fb397/Vetworld-18-1466-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/78552951159d/Vetworld-18-1466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/11da8d0e7566/Vetworld-18-1466-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/35e15c47d953/Vetworld-18-1466-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/09de2c94a621/Vetworld-18-1466-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/a978e7ead329/Vetworld-18-1466-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/857ae511903f/Vetworld-18-1466-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/84aa041fb397/Vetworld-18-1466-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/74af291b9db9/Vetworld-18-1466-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/78552951159d/Vetworld-18-1466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/11da8d0e7566/Vetworld-18-1466-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/35e15c47d953/Vetworld-18-1466-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/09de2c94a621/Vetworld-18-1466-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/a978e7ead329/Vetworld-18-1466-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0902/12273156/857ae511903f/Vetworld-18-1466-g008.jpg

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