摘要
目的观察化浊祛湿方对脂代谢紊乱大鼠模型血脂水平的影响及对miR-27bmRNA及其下游有关脂代谢靶基因表达的影响,分析其调节血脂代谢的可能机制。方法54只SD大鼠适应性喂养3 d后,随机选出10只作为空白组,其余大鼠采用高脂饲料喂养建立脂代谢紊乱动物模型。根据血脂水平及油红O染色结果判定脂代谢紊乱模型是否成功,将造模成功大鼠分为模型组(8只)、辛伐他汀组(8只)、低剂量组(8只)、中剂量组(9只)、高剂量组(9只)。辛伐他汀组给予辛伐他汀片混悬液(按照大鼠的等效剂量为人日剂量的7倍计算)灌胃,低、中、高剂量组给予化浊祛湿方灌胃,中剂量为人的等效剂量(按照大鼠的等效剂量为人日剂量的7倍计算),低剂量为人等效剂量的1/2剂量,高剂量为人等效剂量的2倍剂量。药物干预12周后,检测血脂水平,肝脏组织进行实时定量PCR检测miR-27b、胆固醇调节元件结合蛋白1(SREBP 1)、乙酰辅酶A羧化酶(ACC)、过氧化物酶体增殖物激活受体α(PPARα)、激素敏感性甘油三酯脂肪酶(HSL)基因表达。结果药物干预12周后,与模型组比较,化浊祛湿方低、中、高剂量组、辛伐他汀组甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)水平下降(P<0.05)。大鼠肝脏组织目的基因表达:化浊祛湿方低剂量组与模型组miR-27b比较差异有统计学意义(P<0.05);化浊祛湿方各剂量组与模型组SREBP1、ACC表达比较差异无统计学意义(P>0.05);化浊祛湿方各剂量组与模型组PPARα、HSL表达比较差异有统计学意义(P<0.05)。结论化浊祛湿方可以有效地调节脂代谢紊乱大鼠的血脂水平,其调节机制可能是与化浊祛湿方抑制miR-27b表达,调节下游靶基因,增加PPARα及HSL表达,调节肝组织脂肪代谢,促进脂质分解,从而发挥调节脂代谢的作用有关。
Objective To observe the effect of Huazhuo Qushi Decoction on blood lipid levels in a rat model of lipid metabolism disorder and its effect on miR-27 bmRNA and its target gene expression,and to analyze its possible mechanism of regulating blood lipid metabolism.Methods After 54 SD rats were adaptively fed for 3 days,10 rats were randomly selected as the blank group,and the remaining rats were fed with high-fat diet to establish a lipid metabolism disorder animal model.According to the blood lipid level and the results of oil red O staining,the lipid metabolism disorder model was judged to be successful.The rat model group(8 rats),the simvastatin group(8 rats),the low-dose group(8 rats),and the medium-dose fed with high-fat diet Group(9 animals),high-dose group(9 animals).The simvastatin group was given the simvastatin tablet suspension(calculated according to the equivalent dose of rats which is 7 times the human daily dose)by gavage,the low,medium and high-dose groups were given the Huazhuo Qushi Decoction by gavage,and the middle dose was for humans.The equivalent dose(calculated according to the equivalent dose in rats is 7 times the human daily dose),the low dose is 1/2 the human equivalent dose,and the high dose is 2 times the human equivalent dose.After 12 weeks of drug intervention,blood lipid levels were detected,and liver tissues were subjected to real-time quantitative PCR to detect miR-27 b,cholesterol regulatory element binding protein 1(SREBP 1),acetyl-coenzyme A carboxylase(ACC),and peroxisome proliferator activation Receptorα(PPARα),hormone-sensitive triglyceride lipase(HSL)gene expression.Results After 12 weeks of drug intervention,compared with the model group,the low,medium and high dose groups of Huazhuo Qushi Decoction,the triglyceride(TG),total cholesterol(TC),and low density lipoprotein(LDL)of the simvastatin group)The level decreased(P<0.05).The expression of target gene in rat liver tissue,the difference of miR-27 b between the low-dose group of Huazhuo Qushi Decoction and the model group was statistically significant(P<0.05);the expression of SREBP1 and ACC was compared between each dose group of Huazhuo Qushi Decoction and the model group The difference was not statistically significant(P>0.05);there was a statistically significant difference in the expression of PPARαand HSL between each dose group of Huazhuo Qushi Decoction and the model group(P<0.05).Conclusion Huazhuo Qushi Decoction can effectively regulate the blood lipid level of rats with lipid metabolism disorders.The regulation mechanism may be the same as that of Huazhuo Qushi Decoction in inhibiting the expression of miR-27 b,regulating downstream target genes,and increasing the expression of PPARαand HSL.Fat metabolism in liver tissue promotes lipid decomposition and plays a role in regulating lipid metabolism.
作者
肖璐
隋歌川
冯玲
XIAO Lu;SUI Ge-chuan;FENG Ling(Guang’anmen Hospital,China Academy of Chinese Medical Sciences,Beijing 100053;Beijing First Hospital of Integrated Traditional Chinese and Western Medicine,Beijing 100021)
出处
《世界中西医结合杂志》
2021年第4期648-652,共5页
World Journal of Integrated Traditional and Western Medicine
基金
国家自然基金面上项目(81774128)
国家自然基金面上项目(81470184)。
关键词
化浊祛湿方
脂代谢
过氧化物酶体增殖物激活受体Α
Huazhuo Qushi Decoction
Lipid Metabolism
Peroxisome Proliferator Activated Receptorα
