大豆异黄酮减轻大鼠非酒精性脂肪肝病变的作用研究
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摘要
目的研究大豆异黄酮(SIF)对高脂诱导的大鼠非酒精性脂肪性肝病(NAFLD)病变的影响及可能机制。方法2017年3月选取雄性SD大鼠24只,建立大鼠NAFLD模型,采用随机数字表法将大鼠分为健康对照组(7只)、健康给药组(5只)、模型组(7只)和模型给药组(5只)。采用苏木精-伊红染色观察大鼠肝脏病理改变,生化方法检测大鼠肝脏抗氧化因子变化,实时定量-聚合酶链反应检测大鼠肝脏炎性细胞因子单核细胞趋化蛋白(MCP-1) mRNA转录量,免疫组织化学法检测大鼠肝脏MCP-1蛋白表达量。结果成功建立大鼠NAFLD模型; SIF能减轻模型大鼠肝脏的病理改变,显著增加大鼠肝脏超氧化物歧化酶、还原型谷胱甘肽的活力,降低丙二醛含量,明显抑制MCP-1 mRNA的转录,降低肝脏MCP-1蛋白的表达,差异均有统计学意义(P <0. 05)。结论 SIF可能通过增强肝脏抗氧化能力、抑制炎症相关基因表达,从而减轻高脂诱导的NAFLD大鼠肝脏的脂肪性改变。
Objective To investigate the effect of soybean isoflavone( SIF) on rat non-alcoholic fatty liver disease( NAFLD) induced by high fat diet and its possible mechanism. Methods Twenty-four SD male rats were selected for establishing the rat NAFLD model in March 2017 and divided into the healthy control group( 7 cases),healthy medication group( 5 cases) and model medication group( 5 cases) by adopting to the random number table method. The pathological changes of rat liver were observed with the HE staining,the changes of antioxidant factors in rat liver were determined by using the biochemical method,the transcriptional quantity of inflammatory cytokine monocyte chemotactic protein-1( MCP-1) mRNA in rat liver was detected by using the real time PCR,and the expression level of MCP-1 protein in rat liver was detected by using the immunohistochemical method. Results The rat NAFLD model was successfully established.SIF could reduce the pathological changes of model rat liver,significantly increased the activity of superoxide dismutase and glutathione,decreased the level of methylene dioxyamphetamine,significantly inhibited the transcription of MCP-1 mRNA and reduced the expression of MCP-1 protein in rat liver,and the differences were statistically significant( P < 0. 05). Conclusion SIF can alleviate the fatty changes in the liver of high fat diet induced rat NAFLD by enhancing the liver antioxidant capacity and inhibiting the expression of inflammation related genes.
Objective To investigate the effect of soybean isoflavone( SIF) on rat non-alcoholic fatty liver disease( NAFLD) induced by high fat diet and its possible mechanism. Methods Twenty-four SD male rats were selected for establishing the rat NAFLD model in March 2017 and divided into the healthy control group( 7 cases),healthy medication group( 5 cases) and model medication group( 5 cases) by adopting to the random number table method. The pathological changes of rat liver were observed with the HE staining,the changes of antioxidant factors in rat liver were determined by using the biochemical method,the transcriptional quantity of inflammatory cytokine monocyte chemotactic protein-1( MCP-1) mRNA in rat liver was detected by using the real time PCR,and the expression level of MCP-1 protein in rat liver was detected by using the immunohistochemical method. Results The rat NAFLD model was successfully established.SIF could reduce the pathological changes of model rat liver,significantly increased the activity of superoxide dismutase and glutathione,decreased the level of methylene dioxyamphetamine,significantly inhibited the transcription of MCP-1 mRNA and reduced the expression of MCP-1 protein in rat liver,and the differences were statistically significant( P < 0. 05). Conclusion SIF can alleviate the fatty changes in the liver of high fat diet induced rat NAFLD by enhancing the liver antioxidant capacity and inhibiting the expression of inflammation related genes.
引文
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[9]罗洁,秦旭,韦余,等.大豆异黄酮对动脉粥样硬化大鼠炎症分子相关基因表达的影响[J].江苏大学学报(医学版),2014,24(2):99-104.
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[12]张超贤,郭李柯,秦咏梅,等. MCP-1基因-2518A/G与GPx-1基因Pro198Leu多态性的交互作用与非酒精性脂肪性肝病的关系[J].中山大学学报(医学科学版),2015,36(5):739-744.
[13]旷历琼,王晓敏.非酒精性单纯性脂肪肝患者血清甘丙肽水平及其与炎性脂肪因子相关性[J].国际消化病杂志,2013,33(6):422-425.
[14] HAUKELAND JW,DAMAS JK,KONOPSKI Z,et al. Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2[J]. J Hepatol,2006,44(6):1167-1174.
[15]刘英娇,王拱辰.单核细胞趋化蛋白-1与慢性肝病及并其发症的相关性[J].中国肝脏病杂志,2017,9(4):31-37.
[2]华雨薇,李春阳,王帆,等.大豆皂苷和异黄酮对小鼠血脂的调节作用[J].安徽农业科学,2015(21):3-4.
[3]张云波,那晓琳,赵新宇,等.大豆异黄酮及羧甲基纤维素钠对去卵巢大鼠体重、血脂的影响[J].中国老年学杂志,2009,29(17):2195-2197.
[4]纪桂元,蒋卓勤,张贵锋.大豆异黄酮降血脂作用研究进展[J].中国公共卫生,2011,27(2):253-254.
[5]崔春吉,延光海,李良昌,等.大豆异黄酮对实验性大鼠脂肪肝的治疗作用[J].延边大学医学学报,2009,32(3):163-165.
[6]蒋兴亮,张均,刘素兰,等.非酒精性脂肪肝患者氧化应激和抗氧化酶状态[J].四川医学,2009,30(12):1958-1960.
[7] GRECO D,KOTRONEN A,WESTERBACKA J,et al. Gene expression in human NAFLD[J]. Am J Physiol Gastrointest Liver Physiol,2008,294(5):G1281-1287.
[8]张艳,卢洁,周莹群,等.非酒精性脂肪性肝病与氧化应激[J].世界临床药物,2013,34(8):459-463.
[9]罗洁,秦旭,韦余,等.大豆异黄酮对动脉粥样硬化大鼠炎症分子相关基因表达的影响[J].江苏大学学报(医学版),2014,24(2):99-104.
[10]鲍荣辉,刘先哲.单核细胞趋化蛋白受体的研究进展[J].生命科学,2006,18(5):477-480.
[11]沈红艳,邓演超,王庆美,等. MCP-1在慢性乙型肝炎合并非酒精性脂肪性肝病肝组织中的表达[J].细胞与分子免疫学杂志,2012,28(9):975-978.
[12]张超贤,郭李柯,秦咏梅,等. MCP-1基因-2518A/G与GPx-1基因Pro198Leu多态性的交互作用与非酒精性脂肪性肝病的关系[J].中山大学学报(医学科学版),2015,36(5):739-744.
[13]旷历琼,王晓敏.非酒精性单纯性脂肪肝患者血清甘丙肽水平及其与炎性脂肪因子相关性[J].国际消化病杂志,2013,33(6):422-425.
[14] HAUKELAND JW,DAMAS JK,KONOPSKI Z,et al. Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2[J]. J Hepatol,2006,44(6):1167-1174.
[15]刘英娇,王拱辰.单核细胞趋化蛋白-1与慢性肝病及并其发症的相关性[J].中国肝脏病杂志,2017,9(4):31-37.