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茉莉酸甲酯通过调节炎症和凋亡过程减少睾酮诱导的大鼠良性前列腺增生。

Methyl jasmonate reduces testosterone-induced benign prostatic hyperplasia through regulation of inflammatory and apoptotic processes in rats.

机构信息

Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, Nigeria.

Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, Nigeria.

出版信息

Biomed Pharmacother. 2017 Nov;95:1493-1503. doi: 10.1016/j.biopha.2017.08.106. Epub 2017 Sep 21.

DOI:10.1016/j.biopha.2017.08.106
PMID:28946212
Abstract

BACKGROUND

Phytotherapy is becoming a treatment option in management of diseases including benign prostatic hyperplasia (BPH). We have shown previously that methyl jasmonate (MeJA) ameliorated BPH, however the underlying mechanism of action remains unknown. This study was designed to investigate in mechanistic terms the protective role of MeJA in BPH.

METHODS

BPH was induced by daily injections of testosterone propionate (TP) (3mg/kg) for 28 days.

RESULTS

The weight and organo-somatic weight of prostate in BPH rats were 6.8 and 5.1 times higher than castrated-control group, respectively. Inflammatory markers; prostatic myeloperoxidase and total nitric oxide were significantly increased in BPH group. The activity of aniline hydroxylase (Phase I drug metabolizing enzyme) was significantly increased in BPH rats by 22%. In BPH group, immuno-histochemistry revealed strong expression of prostatic inducible nitric oxide synthase, cyclooxygenase-2 and Bcl, while mild expression of p53 and Bax were seen. Serum triglyceride and total cholesterol were significantly increased, while HDL-c was decreased in BPH. Interestingly, MeJA and finasteride (singly or combination) attenuated inflammatory indices and induced apoptotic parameters in BPH rats.

CONCLUSION

MeJA protects against TP-induced BPH via mechanisms that involve anti-inflammation, induction of apoptosis and inhibition of phase I drug metabolizing enzyme.

摘要

背景

植物疗法在包括良性前列腺增生(BPH)在内的疾病的治疗中成为一种治疗选择。我们之前已经表明,茉莉酸甲酯(MeJA)可改善 BPH,但作用机制尚不清楚。本研究旨在从机制上研究 MeJA 在 BPH 中的保护作用。

方法

通过每天注射丙酸睾酮(TP)(3mg/kg)28 天诱导 BPH。

结果

BPH 大鼠的体重和前列腺器官体重分别比去势对照组高 6.8 和 5.1 倍。BPH 组前列腺髓过氧化物酶和总一氧化氮等炎症标志物显著增加。BPH 大鼠的苯胺羟化酶(I 相药物代谢酶)活性增加了 22%。在 BPH 组中,免疫组织化学显示前列腺诱导型一氧化氮合酶、环氧化酶-2 和 Bcl 的表达强烈,而 p53 和 Bax 的表达较弱。BPH 患者的血清甘油三酯和总胆固醇明显升高,而高密度脂蛋白胆固醇降低。有趣的是,MeJA 和非那雄胺(单独或联合)可减轻 BPH 大鼠的炎症指标并诱导其细胞凋亡。

结论

MeJA 通过抗炎、诱导细胞凋亡和抑制 I 相药物代谢酶来预防 TP 诱导的 BPH。

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