ABSTRACT
Objective::To determine whether the main components of Glycyrrhizae Radix et Rhizoma can improve insulin resistance by regulating glycogen synthesis, glycolysis pathway and fatty acid synthesis in myoblasts of L6 rat myoblasts. Method::Insulin resistance (IR) model of L6 rat myoblasts was established through incubation with 0.05 mmol·L-1 palmitic acid (PA) for 9 hours. Normal group, model group, glycyrrhizic acid (GA, 25 μmol·L-1) group, 18β-glycyrrhetinic acid (18β-GA, 25 μmol·L-1) group, isoliquiritigenin (ILG, 25 μmol·L-1) group and isoliquiritin (ILQ, 25 μmol·L-1) group were set up, glucose content in supernatant of cell culture medium was detected by glucose kit, myoblasts glycogen content was determined by glycogen detection kit, protein expression levels of Sterol regulatory element binding protein-1c(SREBP-1c), fatty acid synthetase (FAS) and glycogen synthase kinase3β(GSK3β) were detected by Western blot, and the mRNA expressions of key enzymes in glycolysis were detected by quantitative real-time fluorescence polymerase chain reaction(Real-time PCR). Result::Compared with those in the normal group, the glucose consumption rate was significantly down-regulated in model group (P<0.01), the glycogen content was decreased (P<0.05), the protein expressions of Sterol regulatory element binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) were decreased (P<0.05, P<0.01), the mRNA expressions of fructose phosphate kinase 1 (PFK1), pyruvate kinase (PK) and hexokinase (HK) were down-regulated (P<0.05), and the protein expression of glycogen synthase kinase 3 (GSK3β) protein was increased (P<0.05). Compared with model group, GA, 18β-GA and ILG could significantly increase glycogen content in myoblasts of IR-L6 rats (P<0.05, P<0.01). GA, 18β-GA and ILQ could significantly increase the expression of SREBP-1c (P<0.05, P<0.01), and GA, 18β-GA, ILG and ILQ could significantly increase the expression of FAS (P<0.05, P<0.01), the mRNA expressions of PFK1, PK and HK (P<0.05, P<0.01), and down-regulate the protein expression of GSK3β (P<0.05). Conclusion::The main components of licorice improve the insulin resistance by promoting glycolysis and glycogen synthesis and regulating fatty acid synthesis.
ABSTRACT
Objective: To explore the effect and mechanism of genistein on oleic acid-induced lipid accumulation in HepG2 cells. Method: Lipid accumulation model in HepG2 cells was induced by different concentrations of oleic acid for 24 h, and 12.5, 25, 50 μmol·L-1genistein and oleic acid acted on cells for 24 h. Cell viability was determined by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Double staining with Nile red and DAPI was used to observe the intracellular lipid droplets. Intracellular triglyceride (TG) content was determined by kit. The protein expression levels of triglyceride lipase(ATGL),hormone-sensitive fatty acid(HSL),phosphorylation HSL(p-HSL),silent information regulator 1(STRT1),peroxisome proliferator-activated receptor α(PPARα),carnitine palmityl transferase 1(CPT-1) in oleic acid-induced HepG2 cells were detected by Western blot. Result: 0.5 mmol·L-1 oleic acid and 12.5, 25, 50 μmol·L-1 genistein had no significant effect on cell viability after treated cells for 24 h. Compared with normal group, the TG content and lipid droplets in oleic acid-induced HepG2 cells was significantly increased (PPPPα, and CPT-1 compared with model group (PPConclusion: Genistein can significantly improve the lipid accumulation in oleic acid-induced HepG2 cells, and its mechanism may be related to up-regulating the protein expression levels of ATGL, p-HSL/HSL, SIRT1, PPARα, CPT-1, and thus promoting lipid hydrolysis and oxidative metabolism.
ABSTRACT
The bitter taste is one of the important properties among five flavors of Chinese materia medica (CMM), characterized by downbearing and discharging, drying dampness, and consolidating Yin. In common CMM, bitter-taste CMM accounts for a large proportion, indicating the importance of it. Through the efficacy of clearing away heat and dampness, reducing fire and removing toxin, bitter-taste CMM has achieved good results in treating diabetes in clinical application, proving their definite therapeutic effect on regulating glucose and lipid metabolism (main features of diabetes). At present, there are many reports about the chemical constituents and pharmacological effects of CMM on diabetes, but there are few reviews on the chemistry and biology of bitter-taste CMM. This study summarized the properties and compatibility characteristics of bitter-taste CMM for treating diabetes, and mainly analyzed the chemistry and biology basis of bitter-taste CMM with function of regulating glycolipid metabolism, laying foundation for further researches on properties theory of CMM.