详细信息
姜黄素衍生物B06对2型糖尿病大鼠睾酮合成的影响 被引量:4
Effect of curcumin derivative B06 Bob on synthesis of testosterone from type 2 diabetic rats
文献类型:期刊文献
中文题名:姜黄素衍生物B06对2型糖尿病大鼠睾酮合成的影响
英文题名:Effect of curcumin derivative B06 Bob on synthesis of testosterone from type 2 diabetic rats
作者:林中民[1];王芳[1];张泉波[1];陈霖[1];陈三妹[2];陈国荣[1]
机构:[1]温州医科大学附属第一医院病理科;[2]绍兴文理学院医学院
年份:2016
卷号:32
期号:2
起止页码:352
中文期刊名:中国病理生理杂志
外文期刊名:Chinese Journal of Pathophysiology
收录:CSTPCD、、北大核心2014、CSCD2015_2016、北大核心、CSCD
基金:浙江省自然科学基金资助项目(No.LY12H26002);浙江省公益性技术应用研究计划项目(No.2011c23123)
语种:中文
中文关键词:糖尿病;姜黄素衍生物B06;Leydig细胞;睾酮;类固醇激素合成急性调节蛋白
外文关键词:Diabetes mellitus; Curcumin derivative B06; Leydig cells; Testosterone; Steroidogenic acute re- gulatory protein
中文摘要:目的:研究姜黄素衍生物B06对2型糖尿病大鼠睾酮合成的影响。方法:雄性SD大鼠35只,随机均分为正常对照组(C组)、高脂组(H组)、高脂治疗组(HT组)、糖尿病组(D组)和糖尿病治疗组(DT组),后4组高脂喂养4周后,D组及DT组用低剂量链脲佐菌素诱导糖尿病,HT组和DT组用0.2 mg·kg^(-1)·d^(-1)的B06灌胃8周。微量血糖仪测定大鼠血糖浓度;ELISA法测定血胰岛素水平,并计算胰岛素抵抗指数;光镜和电镜观察睾丸形态;放射免疫法测定血睾酮、雌二醇水平;免疫组化检测Leydig细胞的类固醇激素合成急性调节蛋白(StAR)表达;RT-PCR检测睾丸Leydig细胞StAR、胆固醇侧链裂解酶(P450scc)、细胞色素P450 17A1(P450c17)、细胞色素P450芳香化酶(P450arom)、3β-羟基类固醇脱氢酶(HSD)及17β-HSD的mRNA表达水平。结果:H组及D组血糖、胰岛素抵抗指数升高,血清睾酮水平降低,经B06治疗后好转;H组及D组睾丸曲细精管变形,生精细胞脱落,Leydig细胞内线粒体肿胀,内质网减少且扩张,胞核皱缩,染色质稀疏,经B06治疗后病变减轻;D组的StAR蛋白表达减弱,经B06治疗后表达增强;H组及D组Leydig细胞St AR、P450scc mRNA表达降低,经B06治疗后升高,P450c17、P450arom、3β-HSD及17β-HSD mRNA表达未见明显差异。结论:B06可缓解2型糖尿病大鼠睾丸病变,提高血清睾酮水平,这可能与B06改善机体代谢紊乱并上调Leydig细胞StAR及P450scc mRNA表达水平相关。
外文摘要:AIM: To investigate the effect of curcumin derivatives B06(B06) on the synthesis of testosterone from type 2 diabetic rats. METHODS: Male Sprague-Dawley rats were evenly divided into 5 groups randomly: normal control group ( C group), high fat group ( H group ), high fat treatment group ( HT group ), diabetes mellitus group ( D group) and diabetes treatment group ( DT group). The rats in the later 4 groups were fed with high fat diet, after 4 weeks of high fat diet feeding, the rats from D group and DT group were injected with low dose of streptozotocin intraperitoneally to induce diabetes mellitus, while the rats in HT group and DT group were garaged with B06 at the dose of 0.2 mg · kg^-1 d^-1 for 8 weeks. The blood glucose was detected by glucometer, blood insulin was assayed by ELISA and the insulin resist- ance index was calculated. The morphology of testes were observed by light and transmission electron microscopy. Serum testosterone and estradiol were measured by radioimmunoassay. The protein expression of steroidogenic acute regulatory pro- tein (STAR) was detected by immunohistochemistry. The mRNA expression of STAR, cholesterol side-chain cleavage en- zyme ( P450scc), cytochrome P450 17A1 ( P450c17 ), cytochrome P450 aromatizing enzyme ( P450arom), 313-hydroxyste- roid dehydrogenase (HSD) and 1713-HSD was detected by RT-PCR. RESULTS: The levels of blood glucose and insulin resistance index were increased in H group and D group, and serum testosterone was decreased, all of which were reversed after the treatment of B06. Testicular seminiferous tubule was distorted, spermatogenic cells were dropped in H group and D group. In addition, leydig ceils were found to have swelling mitochondria in H group and D group, endoplasmic reticu- lum was reduced, and there was karyopyknosis accompany with sparse chromatin, all of which were ameliorated by B06. The protein expression of StAR was decreased in D group. The mRNA expression of StAR and P450scc was decreased in H group and D group, all of which were increased in B06 treatment group. There was no significant difference in the mRNA expression of P450c17, P450arom, 313-HSD and 17[5-HSD. CONCLUSION: B06 may increase serum testosterone and relieve the damage of testes from type 2 diabetic rats. B06 improves metabolic disorder by up-regulating mRNA expression of StAR and P450scc.
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