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淫羊藿苷II和二甲双胍对伴有勃起功能障碍的2型糖尿病大鼠阴茎勃起功能、糖代谢、活性氧、超氧化物歧化酶及线粒体自噬的影响。

Effect of icariside II and metformin on penile erectile function, glucose metabolism, reaction oxygen species, superoxide dismutase, and mitochondrial autophagy in type 2 diabetic rats with erectile dysfunction.

作者信息

Zhang Jian, Li Shu, Li Shuang, Zhang Shiqing, Wang Yonghui, Jin Shipeng, Zhao Chunli, Yang Wenzeng, Liu Yuexin, Fang Dong, Li Xuesong, Xin Zhongcheng

机构信息

Department of Urology, Beijing Geriatric Hospital, Beijing 100000, China.

Emergency Department, Beijing Luhe Hospital, Beijing 100000, China.

出版信息

Transl Androl Urol. 2020 Apr;9(2):355-366. doi: 10.21037/tau.2020.02.07.

DOI:10.21037/tau.2020.02.07
PMID:32420141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7214985/
Abstract

BACKGROUND

Icariside II (ICAII) is a flavonoid isolated from herb Epimedium that has been shown to improve erectile function in rats. However, ICAII's underlying mechanism remains unclear.

METHODS

Type 2 diabetes mellitus erectile dysfunction (T2DMED) rats were induced by single intraperitoneal injection of 25 mg/kg streptozotocin (STZ) and fed a high-fat, high-sugar, and high-calorie diet for 8 weeks. In the control and T2DMED groups, rats were administered with normal saline; in the metformin (MET) group, rats were administered with MET at 0.2 g/kg/day; and in the ICAII + MET group, rats were administered with ICA II at 10 mg/kg/day and MET for 0.2 g/kg/day. The deposition of advanced glycation end products (AGEs), expression of receptor for AGEs (RAGEs), reactive oxygen species (ROS), and superoxide dismutase (SOD) activity, and corpus cavernosum smooth muscle cells (CCSMCs) mitochondrial autophagy were measured. We also evaluated the expression of LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K.

RESULTS

ICAII and MET can improve erectile function, and decrease the levels of fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and AGEs in rats with T2DMED. Furthermore, ICAII and MET can decrease excessive CCSMC mitochondrial autophagy and the level of RAGE and oxidant stress in rats with T2DMED. ICAII and MET may enhance signaling via the PI3K-AKT-mTOR pathway in order to reduce the excessive mitochondrial autophagy of CCSMCs.

CONCLUSIONS

ICAII may effectively improve penile erectile function via decreasing excessive CCSMCs mitochondrial autophagy, RAGE, and oxidant stress. Furthermore, ICAII may enhance signaling via the PI3K-AKT-mTOR pathway in order to reduce excessive CCSMC mitochondrial autophagy.

摘要

背景

淫羊藿苷II(ICAII)是从淫羊藿中分离出的一种黄酮类化合物,已被证明可改善大鼠的勃起功能。然而,ICAII的潜在机制仍不清楚。

方法

通过单次腹腔注射25mg/kg链脲佐菌素(STZ)诱导2型糖尿病性勃起功能障碍(T2DMED)大鼠,并给予高脂、高糖和高热量饮食8周。在对照组和T2DMED组中,大鼠给予生理盐水;在二甲双胍(MET)组中,大鼠给予MET,剂量为0.2g/kg/天;在ICAII + MET组中,大鼠给予ICA II,剂量为10mg/kg/天和MET,剂量为0.2g/kg/天。测量晚期糖基化终产物(AGEs)的沉积、AGEs受体(RAGEs)的表达、活性氧(ROS)和超氧化物歧化酶(SOD)活性,以及海绵体平滑肌细胞(CCSMCs)的线粒体自噬。我们还评估了LC3-II/I、Beclin-1、P70S6K、PI3K/Akt、mTOR、磷酸化Akt、磷酸化mTOR和磷酸化P70S6K的表达。

结果

ICAII和MET可改善勃起功能,并降低T2DMED大鼠的空腹血糖(FPG)、糖化血红蛋白(HbA1c)和AGEs水平。此外,ICAII和MET可减少T2DMED大鼠过度的CCSMCs线粒体自噬以及RAGE和氧化应激水平。ICAII和MET可能通过PI3K-Akt-mTOR途径增强信号传导,以减少CCSMCs过度的线粒体自噬。

结论

ICAII可能通过减少CCSMCs过度的线粒体自噬、RAGE和氧化应激来有效改善阴茎勃起功能。此外,ICAII可能通过PI3K-Akt-mTOR途径增强信号传导,以减少CCSMCs过度的线粒体自噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/7b5d113fde64/tau-09-02-355-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/e02abd57a949/tau-09-02-355-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/ea0e44e6e8be/tau-09-02-355-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/af0f4e2c8f09/tau-09-02-355-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/5795c655b656/tau-09-02-355-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/e925f0f195ba/tau-09-02-355-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/1a93f97de0d6/tau-09-02-355-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/c4a99811d28f/tau-09-02-355-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/f62f384d03cb/tau-09-02-355-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/7b5d113fde64/tau-09-02-355-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/e02abd57a949/tau-09-02-355-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/ea0e44e6e8be/tau-09-02-355-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/af0f4e2c8f09/tau-09-02-355-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/5795c655b656/tau-09-02-355-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/e925f0f195ba/tau-09-02-355-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/1a93f97de0d6/tau-09-02-355-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/c4a99811d28f/tau-09-02-355-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/f62f384d03cb/tau-09-02-355-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3916/7214985/7b5d113fde64/tau-09-02-355-f9.jpg

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