Yousefinejad Abbas, Siassi Fereydoon, Mirshafiey Abbas, Eshraghian Mohammad-Reza, Koohdani Fariba, Javanbakht Mohammad Hassan, Sedaghat Reza, Ramezani Atena, Zarei Mahnaz, Djalali Mahmoud
Dept. of Nutrition, School of Public Health, Bushehr University of Medical Sciences, Bushehr, Iran.
Dept. of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
Iran J Public Health. 2015 Oct;44(10):1339-47.
Nephrotic syndrome is a disorder that leads to hyperlipidemia. L-carnitine and genistein can effect on lipid metabolism and the syndrome. In the present study, we have delved into the separate and the twin-effects of L-carnitine and genistein on the gene expressions of HMG-COA reductase and LDL receptor in experimental nephrotic syndrome.
In this controlled experimental study, 50 male Sprague-Dawley rats were randomly divided into five groups: NC (normal-control), PC (patient-control), LC (L-carnitine), G (genistein), LCG (L-carnitine-genistein). Adriamycin was used for inducing nephrotic syndrome and the spot urine samples and urine protein-to-creatinine ratio were measured. Hepatocytic RNA was extracted and real-time PCR was used for HMG-COA Reductase and LDL receptor gene Expression measurement.
The final weight of the patients groups were lower than the NC group (P=0.001), and weight gain of the NC group was higher than the other groups (P<0.001). The proteinuria and urine protein-to-creatinine ratio showed significant differences between PC group and LC, G and LCG groups at week 7 (P<0.001). The expression of HMGCOA Reductase mRNA down regulated in LC, G and LCG groups in comparison with PC group (P<0.001). ΔCT of LDLr mRNA showed significant differences between the PC group and the other patient groups (P<0.001).
This study shows a significant decreasing (P<0.001) and non-significant increasing trend in HMG-COA Reductase and LDLr gene expression, respectively, and synergistic effect of L-carnitine and genistein on these genes in experimental nephrotic syndrome.
肾病综合征是一种导致高脂血症的病症。左旋肉碱和染料木黄酮可影响脂质代谢及该综合征。在本研究中,我们深入探究了左旋肉碱和染料木黄酮对实验性肾病综合征中HMG - COA还原酶和低密度脂蛋白受体基因表达的单独及协同作用。
在这项对照实验研究中,50只雄性斯普拉格 - 道利大鼠被随机分为五组:NC(正常对照)、PC(患病对照)、LC(左旋肉碱)、G(染料木黄酮)、LCG(左旋肉碱 - 染料木黄酮)。阿霉素用于诱导肾病综合征,并检测随机尿样和尿蛋白与肌酐比值。提取肝细胞RNA,采用实时定量PCR检测HMG - COA还原酶和低密度脂蛋白受体基因表达。
患病组的最终体重低于NC组(P = 0.001),且NC组的体重增加高于其他组(P < 0.001)。在第7周时,PC组与LC、G和LCG组之间的蛋白尿及尿蛋白与肌酐比值存在显著差异(P < 0.001)。与PC组相比,LC、G和LCG组中HMGCOA还原酶mRNA的表达下调(P < 0.001)。PC组与其他患病组之间的LDLr mRNA的ΔCT存在显著差异(P < 0.001)。
本研究表明,在实验性肾病综合征中,HMG - COA还原酶基因表达显著降低(P < 0.001),低密度脂蛋白受体基因表达有不显著的增加趋势,且左旋肉碱和染料木黄酮对这些基因有协同作用。