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1.
China Journal of Chinese Materia Medica ; (24): 1109-1112, 2017.
Article in Chinese | WPRIM | ID: wpr-350218

ABSTRACT

Nonalcoholic fatty liver disease(NAFLD) is a kind of metabolic liver injury, which is closely associated with insulin resistance and genetic susceptibility. Traditional Chinese herbs used in the treatment of nonalcoholic fatty liver disease are widely investigated in recent years. A series of recent studies show that the effects of the active components in traditional Chinese herbs on NAFLD are associated with activating AMPK signaling pathway, improving insulin resistance, modulating the activity and expression of peroxisome proliferator-activated receptor γ, antioxidant and anti-inflammatory activities and regulating intestinal flora. In this review, the potential therapeutic targets of the active components from traditional Chinese herbs for NAFLD would be summarized to provide a new thought for further research and clinical treatment of nonalcoholic fatty liver disease.

2.
Chinese journal of integrative medicine ; (12): 116-123, 2016.
Article in English | WPRIM | ID: wpr-287127

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of Shouwu Jiangqi Decoction (SJD) on polycystic ovary syndrome (PCOS) with insulin resistance (IR) in rats and to explore the underlining molecular mechanisms.</p><p><b>METHODS</b>A total of 51 female Sprague-Dawley rats were randomly divided into 6 groups: control group (n=7), model group (n=8), SJD high-dose group (n=9), SJD medium-dose group (n=9), SJD low-dose group (n=9) and DMBG group (n=9). Radioimmunoassay was used to measure serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone concentrations and qRT-PCR and western blot were used to examine the expression levels of mRNA and protein respectively of insulin receptor substrate 1 (IRS-1) and phosphatidylinositide 3-kinases (PI3K) p85α in different groups.</p><p><b>RESULTS</b>FSH level significantly decreased in the model group compared with the normal control (P<0.01), and high-dose SJD and DMBG can significantly increase FSH level (P<0.01). LH level showed a mild increase without statistic significance in the model group compared with the control and different dosages of SJD had no significance effect on LH level, while DMBG can significantly decrease LH level (P<0.01). Testosterone level significantly increased in the model group compared with the control group (P<0.01), and high-dose SJD and DMBG can significantly decrease testosterone level (P<0.01). The expression of IRS-1 as well as PI3Kp85α were significantly decreased in the model group compared with the normal control group at both mRNA (P<0.001) and protein (P<0.01) level, and both high-dose SJD and DMBG can enhance IRS-1 and PI3K expression (P<0.05).</p><p><b>CONCLUSIONS</b>SJD has potent therapeutic effects on PCOS with IR in rats. The therapeutic effects of SJD on IR and ovulatory dysfunction are probably achieved through correcting the defective insulin signaling transduction.</p>


Subject(s)
Animals , Female , Blood Glucose , Metabolism , Drugs, Chinese Herbal , Therapeutic Uses , Fasting , Blood , Follicle Stimulating Hormone , Blood , Insulin , Blood , Insulin Receptor Substrate Proteins , Metabolism , Insulin Resistance , Liver , Pathology , Luteinizing Hormone , Blood , Ovary , Pathology , Phosphatidylinositol 3-Kinases , Metabolism , Polycystic Ovary Syndrome , Blood , Drug Therapy , Rats, Sprague-Dawley , Testosterone , Blood
3.
China Journal of Chinese Materia Medica ; (24): 4448-4452, 2014.
Article in Chinese | WPRIM | ID: wpr-341838

ABSTRACT

Previous studies have shown that ginsenoside Rb1 (Rb1), one of active components in ginseng, can activate insulin signaling pathway and promote translocation of glucose transporters (GLUTs) to increase glucose uptake in adipocytes. However, the effect of Rb1 on the expressions of GLUTs remains unknown. In this study, the effects of Rb1 on GLUT1 and GLUT4 were observed in 3T3-L1 adipocytes and epididymal adipose tissue of db/db obese diabetic mice. Male db/db mice were treated with Rb1 by intraperitoneal injection at the dosage of 20 mg x kg(-1) for 14 d. Rb1 reduced HOMA-IR significantly (P < 0.05, n = 5), and FBG and FINS sowed declining trend after treatment with Rb1. Rb1 recovered the expressions of GLUT1 and GLUT4 and phosphorylation of AKT in adipose tissue of db/db mice. In vitro, glucose consumption in 3T3-L1 adipocytes treated with 10 micromol x L(-1) Rb1 for 24 h was elevated (P < 0.05, n=3), and mRNA of GLUT1 and GLUT4 were up-regulated (P < 0.05, n=3) and proteins of GLUT1 and GLUT4 were also increased. AKT was activated in adipocytes treated with Rb1 for 3 h. It can be concluded that ginsenoside Rb1 can up-regulate the expression of GLUTs in adipose tissue, in addition to activate insulin signalling pathway, which may partially account for its insulin sensitizing activity and regulating effect of glucose metabolism.


Subject(s)
Animals , Male , Mice , 3T3 Cells , Adipocytes , Cell Line , Diabetes Mellitus, Experimental , Metabolism , Ginsenosides , Pharmacology , Glucose , Metabolism , Glucose Transport Proteins, Facilitative , Metabolism , Mice, Inbred C57BL , Mice, Inbred NOD , Up-Regulation
4.
China Journal of Chinese Materia Medica ; (24): 4119-4123, 2013.
Article in Chinese | WPRIM | ID: wpr-287627

ABSTRACT

Ginsenoside Rb1 is an active component in ginseng. Previous in vitro experiments showed that ginsenoside Rb1, could inhibit lipolysis and promote glucose transporter in adipocytes. This study focused on the effect of ginsenoside Rb1 in insulin resistance and ectopic fat deposit in obese mice induced by high fat diet and its molecular mechanism. Obese male C57/L mice induced by high fat diet were randomly divided into the diet-induced obesity group (DIO group), the ginsenoside Rb1 group (Rb1 group) and the rosiglitazone group (Rog group), and continuously fed with high fat diet. In addition, male C57/L mice fed with normal diet were selected as the normal group (NC group). Mice in Rb1 group and Rog groups were intraperitoneally injected with ginsenoside Rb1 and rosiglitazone with the dosage of 20 mg x kg(-1) and 10 mg x kg(-1), respectively. NC and DIO groups were intraperitoneally injected with the same amount of saline. Two weeks later, the intraperitoneal glucose tolerance test (IPGTT) was performed. Three days later, the mice were killed, and their serum samples were collected to detect insulin and free fatty acid (FFA). Their livers were weighed to examine the triglyceride content, and a pathological detection was performed. Epididymal adipose tissues were weighed, and PDE3B, HSL and perilipin were detected by Western blotting. The results showed that the treatment with ginsenoside Rb1 for two weeks could improve the glucose tolerance of obese mice. Except for 0-120 min, the areas under the glucose tolerance curve (0-30 min, 0-60 min and 0-90 min) in the Rb1 group were less than that in the DIO group (P < 0.05, n = 5), with a much lower HOMA-IR (P < 0.05, n = 5). The fat level of obese mice was significantly reduced by Rbl (P < 0.05, n = 5), and so were liver weight/weight (P < 0.05, n = 8). The increased serum FFA of obese mice declined after the treatment of Rb1 (P < 0.05, n = 8). Rb1 could partially recover the expression of perilipin in adipose tissues, but without obvious change in the expressions of PDE3B and HSL and the phosphorylated activation. The above findings indicated that ginsenoside Rb1 could reduce the release of FFA and alleviate the ectopic deposit of triglyceride by up-regulating the expression of perilipin in adipose tissue, which may be one of its mechanisms for improving the insulin resistance and abnormal glucose metabolism of organisms.


Subject(s)
Animals , Male , Mice , Adipose Tissue , Pathology , Body Weight , Diet, High-Fat , Dose-Response Relationship, Drug , Fatty Acids, Nonesterified , Blood , Gene Expression Regulation , Ginsenosides , Pharmacology , Glucose Tolerance Test , Insulin , Blood , Insulin Resistance , Liver , Metabolism , Mice, Inbred C57BL , Obesity , Blood , Metabolism , Pathology , Organ Size , Triglycerides , Metabolism
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