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花色苷对去势动物模型前列腺的作用:花色苷补充可部分预防前列腺细胞快速凋亡。

The effect of anthocyanin on the prostate in an andropause animal model: rapid prostatic cell death by apoptosis is partially prevented by anthocyanin supplementation.

机构信息

Department of Urology, The Catholic University of Korea College of Medicine, Seoul, Korea.

Health Promotion Center, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, Korea.

出版信息

World J Mens Health. 2013 Dec;31(3):239-46. doi: 10.5534/wjmh.2013.31.3.239. Epub 2013 Dec 24.

Abstract

PURPOSE

To evaluate the anti-apoptotic effect of the antioxidant reaction of anthocyanin on the prostate in an andropause animal model.

MATERIALS AND METHODS

Sprague-Dawley rats were divided into three groups (n=12 in each): control (Group I), andropause (Group II), andropause treated with anthocyanin (Group III). For induction of andropause, Group II and III underwent bilateral orchiectomy. Group III was treated with daily oral anthocyanin (160 mg/kg) for 8 weeks. After 8 weeks, the rats were sacrificed and their blood and prostates were examined pathohistologically and evaluated for oxidative stress and apoptosis. Oxidative stress was assessed by the activity of superoxide dismutase (SOD) and apoptosis in the prostate was identified by terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling assay.

RESULTS

Group II showed markedly increased activity of SOD in serum over that observed in Group I, whereas the rats in Group III showed reduced oxidative stress compared to Group II. Despite no significant differences in prostate weight between Group II and III (p=0.078), the apoptotic index was significantly greater in Group II than Group I, and was significantly lesser in Group III than Group II.

CONCLUSIONS

We suggest that the oxidative stress caused by low testosterone may be another inducer of apoptosis, and this apoptosis may partly contribute to the overall apoptosis of the prostate in the andropause animal model. Therefore, anthocyanin supplementation may contribute to preventing excessively rapid cell death by apoptosis in the prostate in an animal model of andropause.

摘要

目的

评估花色苷抗氧化反应对去势动物模型前列腺的抗凋亡作用。

材料与方法

将 Sprague-Dawley 大鼠分为 3 组(每组 12 只):对照组(I 组)、去势组(II 组)和去势加花色苷组(III 组)。为了诱导去势,II 组和 III 组进行双侧睾丸切除术。III 组每天口服给予花色苷(160mg/kg)8 周。8 周后处死大鼠,对其血液和前列腺进行病理组织学检查,并评估氧化应激和细胞凋亡。通过超氧化物歧化酶(SOD)活性评估氧化应激,通过末端脱氧核苷酸转移酶介导的 dUTP-地高辛切口末端标记法鉴定前列腺中的细胞凋亡。

结果

与 I 组相比,II 组大鼠血清中 SOD 活性明显升高,而 III 组大鼠的氧化应激水平较 II 组降低。尽管 II 组和 III 组的前列腺重量无显著差异(p=0.078),但 II 组的细胞凋亡指数明显高于 I 组,而 III 组明显低于 II 组。

结论

我们认为,低睾酮引起的氧化应激可能是另一种诱导细胞凋亡的因素,这种凋亡可能部分导致去势动物模型中前列腺的整体凋亡。因此,花色苷补充可能有助于预防去势动物模型中前列腺细胞凋亡过度导致的快速细胞死亡。

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