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岩藻依聚糖改善大鼠睾酮诱导的良性前列腺增生(BPH)。

Fucoidan Ameliorates Testosterone-Induced Benign Prostatic Hyperplasia (BPH) in Rats.

作者信息

Shanmugasundaram Devanand, Dwan Corinna, Wimmer Barbara C, Srivastava Shalini

机构信息

Compliance and Operations (Toxicology), Vedic Lifesciences Private Limited, Mumbai, Maharashtra, India.

Marinova Proprietary Limited, Cambridge, Tasmania, Australia.

出版信息

Res Rep Urol. 2024 Oct 30;16:283-297. doi: 10.2147/RRU.S478740. eCollection 2024.

DOI:10.2147/RRU.S478740
PMID:39498260
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11532999/
Abstract

PURPOSE

Benign prostatic hyperplasia (BPH) is a major urological health issue for men globally. Fucoidan, a sulfated polysaccharide, displays diverse bioactivities such as anti-inflammatory, anti-tumor, antioxidant, and immunoregulatory effects. This 28-day study examined the effects of fucoidan on testosterone-induced BPH in rats.

METHODS

Forty-eight Sprague Dawley (SD) rats were randomly divided into six groups; G1- vehicle control, G2- testosterone alone BPH control group (3 mg/kg), G3- finasteride (10 mg/kg) + testosterone, G4- fucoidan (40 mg/kg) + testosterone, G5- fucoidan (400 mg/kg) + testosterone, and G6- fucoidan alone (400 mg/kg). The animals were observed for clinical signs, body weight, feed consumption, prostate weight, prostate index, and biochemical markers such as tumor necrosis factor-alpha (TNF-α), interleukin- 1β (IL-1β), prostate-specific antigen (PSA) and messenger ribonucleic acid (mRNA) expression of BCL-2-associated X protein (BAX) and B-cell lymphoma-2 (BCL-2) in serum. Testosterone and dihydrotestosterone (DHT) levels were evaluated in both serum and prostate.

RESULTS

Fucoidan significantly prevented an increase in prostate weight and prostate index induced by testosterone. DHT levels in the prostate of the intervention groups were significantly lower than in the BPH control group (p <0.05); however, no significant difference was observed in serum levels. Similarly, a significant reduction was observed in serum and prostate testosterone levels in the intervention groups compared to the BPH control group (p <0.05). Biochemical analyses showed PSA levels were significantly lower in the fucoidan groups compared to the BPH control group (p<0.05). Although not statistically significant, fucoidan groups showed a trend of reducing IL-1β and TNF-α levels. Fucoidan demonstrated pro-apoptotic potential in its ability to decrease BCL-2 and increase BAX. Histopathological evidence revealed fewer microscopic lesions in the fucoidan groups compared to the BPH control group.

CONCLUSION

The results suggest fucoidan can reduce testosterone-induced BPH symptoms in SD rats.

摘要

目的

良性前列腺增生(BPH)是全球男性面临的主要泌尿系统健康问题。岩藻依聚糖是一种硫酸化多糖,具有多种生物活性,如抗炎、抗肿瘤、抗氧化和免疫调节作用。这项为期28天的研究考察了岩藻依聚糖对睾酮诱导的大鼠良性前列腺增生的影响。

方法

将48只Sprague Dawley(SD)大鼠随机分为六组;G1-溶剂对照组,G2-仅睾酮诱导的BPH对照组(3 mg/kg),G3-非那雄胺(10 mg/kg)+睾酮组,G4-岩藻依聚糖(40 mg/kg)+睾酮组,G5-岩藻依聚糖(400 mg/kg)+睾酮组,以及G6-仅岩藻依聚糖组(400 mg/kg)。观察动物的临床体征、体重、饲料消耗量、前列腺重量、前列腺指数,以及血清中的生化标志物,如肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、前列腺特异性抗原(PSA),以及BCL-2相关X蛋白(BAX)和B细胞淋巴瘤-2(BCL-2)的信使核糖核酸(mRNA)表达。评估血清和前列腺中的睾酮和双氢睾酮(DHT)水平。

结果

岩藻依聚糖显著抑制了睾酮诱导的前列腺重量和前列腺指数增加。干预组前列腺中的DHT水平显著低于BPH对照组(p<0.05);然而,血清水平未观察到显著差异。同样,与BPH对照组相比,干预组血清和前列腺中的睾酮水平显著降低(p<0.05)。生化分析表明,岩藻依聚糖组的PSA水平显著低于BPH对照组(p<0.05)。尽管无统计学意义,但岩藻依聚糖组显示出降低IL-1β和TNF-α水平的趋势。岩藻依聚糖在降低BCL-2和增加BAX方面具有促凋亡潜力。组织病理学证据显示,与BPH对照组相比,岩藻依聚糖组的微观病变较少。

结论

结果表明岩藻依聚糖可减轻睾酮诱导的SD大鼠良性前列腺增生症状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2b635263af9a/RRU-16-283-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/69f6c447e4f3/RRU-16-283-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/cc3860792186/RRU-16-283-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/e4ce223dd47d/RRU-16-283-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2638df1cfbff/RRU-16-283-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/eacdb141bf46/RRU-16-283-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/366a4834324b/RRU-16-283-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2d9d2ac41837/RRU-16-283-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/befe557b6fc0/RRU-16-283-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2b635263af9a/RRU-16-283-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/69f6c447e4f3/RRU-16-283-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/cc3860792186/RRU-16-283-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/e4ce223dd47d/RRU-16-283-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2638df1cfbff/RRU-16-283-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/eacdb141bf46/RRU-16-283-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/366a4834324b/RRU-16-283-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2d9d2ac41837/RRU-16-283-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/befe557b6fc0/RRU-16-283-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3514/11532999/2b635263af9a/RRU-16-283-g0009.jpg

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