Chodari Leila, Mohammadi Mustafa, Mohaddes Gisou, Alipour Mohammad Reza, Ghorbanzade Vajiheh, Dariushnejad Hassan, Mohammadi Shima
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Arq Bras Cardiol. 2016 Dec;107(6):532-541. doi: 10.5935/abc.20160174. Epub 2016 Nov 10.
Impaired angiogenesis in cardiac tissue is a major complication of diabetes. Protein kinase B (AKT) and extracellular signal regulated kinase (ERK) signaling pathways play important role during capillary-like network formation in angiogenesis process.
To determine the effects of testosterone and voluntary exercise on levels of vascularity, phosphorylated Akt (P- AKT) and phosphorylated ERK (P-ERK) in heart tissue of diabetic and castrated diabetic rats.
Type I diabetes was induced by i.p injection of 50 mg/kg of streptozotocin in animals. After 42 days of treatment with testosterone (2mg/kg/day) or voluntary exercise alone or in combination, heart tissue samples were collected and used for histological evaluation and determination of P-AKT and P-ERK levels by ELISA method.
Our results showed that either testosterone or exercise increased capillarity, P-AKT, and P-ERK levels in the heart of diabetic rats. Treatment of diabetic rats with testosterone and exercise had a synergistic effect on capillarity, P-AKT, and P-ERK levels in heart. Furthermore, in the castrated diabetes group, capillarity, P-AKT, and P-ERK levels significantly decreased in the heart, whereas either testosterone treatment or exercise training reversed these effects. Also, simultaneous treatment of castrated diabetic rats with testosterone and exercise had an additive effect on P-AKT and P-ERK levels.
Our findings suggest that testosterone and exercise alone or together can increase angiogenesis in the heart of diabetic and castrated diabetic rats. The proangiogenesis effects of testosterone and exercise are associated with the enhanced activation of AKT and ERK1/2 in heart tissue.
心脏组织中血管生成受损是糖尿病的主要并发症。蛋白激酶B（AKT）和细胞外信号调节激酶（ERK）信号通路在血管生成过程中的毛细血管样网络形成中起重要作用。
确定睾酮和自愿运动对糖尿病及去势糖尿病大鼠心脏组织中血管化水平、磷酸化Akt（P-AKT）和磷酸化ERK（P-ERK）的影响。
通过腹腔注射50mg/kg链脲佐菌素诱导动物患I型糖尿病。在用睾酮（2mg/kg/天）或单独或联合自愿运动治疗42天后，收集心脏组织样本，用于组织学评估，并通过ELISA法测定P-AKT和P-ERK水平。
我们的结果表明，睾酮或运动均可增加糖尿病大鼠心脏中的毛细血管密度、P-AKT和P-ERK水平。用睾酮和运动治疗糖尿病大鼠对心脏中的毛细血管密度、P-AKT和P-ERK水平具有协同作用。此外，在去势糖尿病组中，心脏中的毛细血管密度、P-AKT和P-ERK水平显著降低，而睾酮治疗或运动训练均可逆转这些影响。而且，同时用睾酮和运动治疗去势糖尿病大鼠对P-AKT和P-ERK水平具有相加作用。
我们的研究结果表明，单独或联合使用睾酮和运动均可增加糖尿病及去势糖尿病大鼠心脏中的血管生成。睾酮和运动的促血管生成作用与心脏组织中AKT和ERK1/2的激活增强有关。
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