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1. 深圳市中医院筋伤科
2. 深圳市中医院推拿科
3. 佛山市中医院针灸科
4. 广东省中医院传统疗法科
纸质出版日期:2018
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李知行, 张海华, 蓝丹纯, 等. 电针对高脂诱导胰岛素抵抗大鼠肝脏固醇调节元件结合蛋白-1c、脂肪酸合成酶的影响[J]. 针刺研究, 2018,43(1):8-13.
LI Zhi-xing, ZHANG Hai-hua, LAN Dan-chun, et al. Effect of Eletroacupuncture Intervention on Insulin Resistance,Lipid Metabolic Disorder and Expression of Hepatic SREBP-1c and Fatty Acid Synthase Proteins in Rats with Hyperlipidemia[J]. Acupuncture research, 2018, 43(1): 8-13.
李知行, 张海华, 蓝丹纯, 等. 电针对高脂诱导胰岛素抵抗大鼠肝脏固醇调节元件结合蛋白-1c、脂肪酸合成酶的影响[J]. 针刺研究, 2018,43(1):8-13. DOI: 10.13702/j.1000-0607.170517.
LI Zhi-xing, ZHANG Hai-hua, LAN Dan-chun, et al. Effect of Eletroacupuncture Intervention on Insulin Resistance,Lipid Metabolic Disorder and Expression of Hepatic SREBP-1c and Fatty Acid Synthase Proteins in Rats with Hyperlipidemia[J]. Acupuncture research, 2018, 43(1): 8-13. DOI: 10.13702/j.1000-0607.170517.
目的:观察电针对胰岛素抵抗(IR)大鼠肝组织固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合成酶(FAS)的影响
探讨电针治疗IR的作用机制。方法:将40只雄性SD大鼠随机选取8只作为空白组
其余通过高脂饮食诱导IR模型
选取24只造模成功的大鼠按随机区组原则分为模型组(8只)、西药组(8只)和电针组(8只)。西药组以吡格列酮(10mg/kg)灌胃
电针组取双侧"丰隆""三阴交"穴电针治疗
1次/日
连续2周。观察各组大鼠葡萄糖输注率(GIR)、空腹血糖(FBG)、血清胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)、游离脂肪酸(FFA)、甘油三酯(TG)、胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)
蛋白免疫印迹法检测肝组织SREBP-1c、FAS蛋白的表达。结果:与空白组比较
模型组大鼠GIR显著降低(P<0.01)
HOMA-IR显著升高(P<0.01)
FBG、FINS、FFA、TG、TC、LDL含量显著升高(P<0.01)
HDL含量显著降低(P<0.01)
SREBP-1c、FAS蛋白表达水平显著升高(P<0.01)。与模型组比较
电针组、西药组大鼠GIR显著升高(P<0.01)
HOMA-IR显著降低(P<0.01)
FBG、FINS、FFA、TG、TC、LDL含量显著降低(P<0.05
P<0.01)
HDL含量显著升高(P<0.01)
SREBP-1c、FAS蛋白表达水平显著降低(P<0.01)。结论:电针可明显改善IR大鼠的脂质代谢紊乱
其作用机制可能与电针降低肝组织SREBP-1c、FAS的表达
由此下调脂肪酸合成相关酶的活性
使肝组织内合成TG、TC减少
改善肝组织IR有关。
Objective To observe the effect of electroacupuncture(EA)of"Fenglong"(ST 40)and"Sanyinjiao"(SP6)on lipid metabolic disorder
insulin resistance(IR)and expression of sterol regulatory element blinding protein-1(SREBP-1)c and fatty acid synthase(FAS)proteins in the liver tissue in hyperlipidemia rats with IR
so as to reveal its mechanisms underlying improvement of IR.Methods Forty male SD rats were randomly divided into blank control
model
medication and EA groups(n=8 in each group).The IR model was established by feeding the rat with high-fat diet.Rats of the medication group were treated by intragastric administration of pioglitazone(10 mL/kg).For rats of the EA group
EA(2 Hz/100 Hz
1 mA)was applied to bilateral ST 40 and SP 6
once daily for 14 days.The insulin sensitivity index(ISI)was assessed by calculating 60-120 min glucose infusion rate(GIR 60-120)with euglycemic hyperinsulinemic clamp in reference to Kraegen's and colleagues' methods.Fasting blood samples(10 mL)were collected and analyzed for fasting blood glucose(FBG)using enzyme method
serum fasting insulin(FINS)using ELISA
free fatty acid(FFA)using spectrophotometry
and total triglyceride(TG)and total cholesterol(TC)employing glycerine phosphate oxidase peroxidase(GPO-PAP)assay
low density lipoprotein(LDL)
high density lipoprotein(HDL)levels using combined filiter paper activity and lipase activity methods
respectively.The IR level was assessed by calculating homeostatic model assessment of insulin resistance(HOMA-IR)using the formula(FBG×FINS)/22.5.The expression levels of SREBP-1 cand FAS proteins in the liver tissue were detected by Western blot.Results Following modeling
the GIR60-120 and serum HDL were significantly decreased(P<0.01)
and the HOMA-IR
serum FBG
FINS
FFA
TG
TC and LDL
and the expression levels of hepatic SREBP-1 cand FAS proteins were significantly increased in comparison with the blank control group(P<0.01).After the intervention
the decreased GIR 60-120 and serum HDL levels were considerably up-regulated(P<0.01)
and the increased FBG
FINS
FFA
TG
TC and LDL
and hepatic SREBP-1 cand FAS protein levels were notably down-regulated in both EA and medication groups relevant to the model group(P<0.05
P<0.01).No significant differences were found between the EA and medication groups in all the indexes mentioned above(P>0.05).Conclusion EA intervention is able to improve the disorder of lipid metabolism of IR rats
which may be associated with its effects in reducing the expression of SREBP-1 cand FAS proteins and in lowering the synthesis of fatty acid.
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