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纸质出版日期:2016
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贾亚敏, 武俊紫, 胡跃高, 等. 富硒灵芝多糖调节SCD1,PPAR改善非酒精性脂肪肝病大鼠症状[J]. 中国实验方剂学杂志, 2016,22(3):102-106.
JIA Ya-min, WU Jun-zi, HU Yue-gao, et al. Se-enriched Polysaccharides Improve Nonalcoholic Fatty Liver Disease in Rats by Regulating SCD1 and PPAR[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(3): 102-106.
贾亚敏, 武俊紫, 胡跃高, 等. 富硒灵芝多糖调节SCD1,PPAR改善非酒精性脂肪肝病大鼠症状[J]. 中国实验方剂学杂志, 2016,22(3):102-106. DOI: 10.13422/j.cnki.syfjx.2016030102.
JIA Ya-min, WU Jun-zi, HU Yue-gao, et al. Se-enriched Polysaccharides Improve Nonalcoholic Fatty Liver Disease in Rats by Regulating SCD1 and PPAR[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(3): 102-106. DOI: 10.13422/j.cnki.syfjx.2016030102.
目的:探讨富硒灵芝多糖对非酒精性脂肪肝病(NAFLD)大鼠血脂、炎性因子、硬脂酰辅酶A去饱和酶(SCD1)和过氧化物酶体增殖物激活受体α(PPARα)的影响。方法:120只SD大鼠随机分为正常组
高脂饮食组(模型组)
多烯磷脂酰胆碱(50 mg·kg-1)组和富硒灵芝多糖低、中、高剂量(0.3
0.6
1.2 g·kg-1
ig)组
高脂高糖饮食12周复制NAFLD模型
相应治疗4和8周后处死大鼠各半
测定血清中高密度脂蛋白胆固醇(HDL-C)
低密度脂蛋白胆固醇(LDL-C)
白细胞介素-1α(IL-1α)
白细胞介素-1β(IL-1β)
肿瘤坏死因子-α(TNF-α)
肝脏匀浆中SCD1和PPARα含量。结果:处理4周后
与正常组相比
模型组肝脏有明显脂肪空泡
且伴有炎症反应;与模型组相比
富硒灵芝3个治疗组脂肪颗粒明显减少。处理8周后
与正常组相比
模型组HDL-C
LDL-C
IL-1α
IL-1β和TNF-α明显升高
与模型组相比
富硒灵芝多糖3个组的HDL-C
LDL-C
IL-1α
IL-1β和TNF-α明显降低(P<0.05)
治疗8周后进一步降低
与多烯磷脂酰胆碱组无显著差异。处理4周后
与正常组相比
模型组肝脏SCD1和PPARα mRNA和蛋白表达降低
与模型组相比
富硒灵芝多糖3个组肝脏SCD1和PPARα mRNA和蛋白表达明显升高
多烯磷脂酰胆碱处理对肝脏SCD1和PPARα mRNA和蛋白表达改善优于富硒灵芝多糖治疗组。结论:富硒灵芝多糖可改善NAFLD大鼠肝脏SCD1和PPARα表达
效果虽弱于多烯磷脂酰胆碱
但也可较好的调节血脂和炎症。
Objective: To investigate the effect of Se-enriched Ganoderma lucidum polysaccharides on blood lipids
inflammatory factors
stearoyl coenzyme1 (SCD1) and peroxisome proliferator-activated receptor α (PPARα) expression in rats with nonalcoholic fatty liver disease (NAFLD). Method: One hundred and twenty SD rats were randomly divided into normal group
high-fat diet group (model group)
polyene phosphatidylcholine(50 mg·kg-1) group
Se-enriched G. lucidum polysaccharides low
medium and high dose groups (0.3
0.6
1.2 g·kg-1
ig). Rats were given high-fat and high-sucrose diet for 12 weeks to establish NAFLD models. After treatment for 4 weeks and 8 weeks
the rats were sacrificed half and half to detect high-density lipoprotein-C (HDL-C)
low-density lipoprotein-C (LDL-C)
interleukin-1α (IL-1α)
interleukin-1β (IL-1β)
tumor necrosis factor-α (TNF-α) in serum
as well as SCD1 and PPARα levels in liver homogenates. Result: Compared with the normal group
fat vacuoles were obvious and associated with inflammation after 4 weeks treatment in model group. Compared with the model group
Se-enriched G. lucidum polysaccharides treatment groups significantly decreased fat particles. Compared with the normal group
HDL-C
LDL-C
IL-1α
IL-1β and TNF-α levels were significantly increased in the model group after 8 weeks of treatment
Compared with the model group
HDL-C
LDL-C
IL-1α
IL-1β and TNF-α levels were significantly decreased in three Se-enriched G. lucidum polysaccharides treatment groups (P<0.05)
and they were further decreased after 8 weeks of treatment
but with no significant difference from the polyene phosphatidylcholine group. Compared with the normal group
SCD1 and PPARα mRNA and protein expressions in liver tissues were significantly decreased in model group after 4 weeks treatment. Compared with the model group
SCD1 and PPARα mRNA and protein expressions in liver tissues were significantly increased in three Se-enriched G. lucidum polysaccharides treatment groups
but the effect of polyene phosphatidylcholine was better than Se-enriched G. lucidum polysaccharides on the improvement of SCD1 and PPARα mRNA and protein expressions. Conclusion: Se-enriched G. lucidum polysaccharides could improve SCD1 and PPARα expressions in liver tissues of NAFLD rats
and could regulate blood lipids
and inflammation although its effect was inferior to polyene phosphatidylcholine.
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