[Effects of pure total flavonoids from Citrus changshan-huyou on blood lipid metabolism in hyperlipidemic rats].

To observe and investigate the effects and mechanisms of the pure total flavonoids from Citrus changshan-huyou(PTFC) on blood lipid metabolism in hyperlipidemic rats. SD rats were fed with high fat diet for 4 weeks to induce hyperlipidemic rats model, meanwhile three dosages (50, 100, 200 mg•kg ⁻¹•d ⁻¹) of PTFC were administrated intragastrically for 4 weeks respectively.After 2 weeks of modeling, their tail blood was taken and serum TC, TG, and HDL-C levels were detected by biochemical method and their body weight was measured. After 4 weeks of modeling, their body weight was measured and liver weight was measured, then the levels of TC, TG, HDL-C, LDL-C, ALT, AST, MDA and SOD in serum were detected to calculate lipid comprehensive index(LDL-C/HDL-C and LDL-C/TC ratios) and atherogenic index(AI); in addition, MDA and SOD levels were detected by biochemical method. The hitopathological changes of the liver tissues were observed by HE staining; the protein expression levels of PPAR-α, Lpl, and Lipc were detected by ELISA; and the mRNA expression levels of PPAR-α in the liver tissue were detected by Real-time PCR. The results showed that gavage administration of the PTFC significantly decreased the body weight, liver weight, liver index, serum ALT and AST activities, the levels of serum TC, TG, LDL-C, LDL-C/HDL-C, AI and increased serum HDL and LDL/TC level. Moreover, the PTFC significantly enhanced SOD activity and decreased the concentration of MDA in serum and liver tissue. Further mechanism investigation indicated that PTFC inhibited serum lipid accumulation by increasing the expressions PPAR-α, Lpl, Lipc protein and PPAR-α mRNA of the liver tissues. PTFC could actively regulate blood lipid metabolism by ameliorating hepatic function, improving the body's antioxidant capacity, lowering levels of oxidative stress, as well as positively regulating the expression levels of PPAR-α, Lpl, Lipc protein and PPAR-α mRNA of the liver tissues in rats.

Yang PL ，Jiang JP ，Li QQ ，Wu XM ，Chen ZY ... -  《-》

Hypolipidemic effect of pure total flavonoids from peel of Citrus (PTFC) on hamsters of hyperlipidemia and its potential mechanism.

Citrus is a group of popular fruit that includes oranges, lemons, limes and grapefruit but research of its peel on hyperlipidemia and its mechanism is rare reported. We examined the effect of pure total flavonoids from peel of Citrus (PTFC), an extract from the peel of Citrus Changshan-huyou which is a popular fruit in China, on hamsters with hyperlipoidemia induced by high-fat diet (HFD). We found that PTFC significantly reduced levels of serum cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-c) and improved levels of alanine transaminase (ALT), aspartate transaminase (AST) and Alkaline phosphatase (ALP) which associated with liver function in golden hamsters. Liver pathological results confirmed that the liver pathological section of golden hamster treated with PTFC was significantly improved compared with that of HFD group. The content of main cholesterol metabolic enzymes Cholesterol 7a-hydroxylase (CYP7A1) in liver was obviously recovered with PTFC treatment. Further studies shown that PTFC attenuated oxidative stress and free radical damage through superoxide dismutase (SOD) and malonyldialdehyde (MDA) tests and inflammatory injury by levels of Tumor Necrosis Factor-alpha (TNF-α) and interleukin-6 (IL-6) both in serum and hepatocyte of golden hamsters. Moreover, PTFC increased levels of RNA and protein expression of Peroxisome proliferator-activated receptor-α (PPAR-α) and PPAR-γ in liver, fat and skeletal muscle of hyperlipidemia golden hamster, significantly. Our results suggested that PTFC could play a hypolipidemic role through improvement of liver function by antioxidant and anti-inflammatory effects in hyperlipoidemia hamsters, its mechanism of action may through activating of PPARα and PPARγ.

Ling Y ，Shi Z ，Yang X ，Cai Z ，Wang L ，Wu X ，Ye A ，Jiang J ... -  《-》

[Effect of pure total flavonoids from citrus on hepatic SIRT1/PGC-1alpha pathway in mice with NASH].

Chen ZY ，Li JS ，Jiang JP ，Yan MX ，He BH ... -  《-》

[Lipid-lowering effect and mechanism of Danhong Injection on hyperlipidemia rats based on lipid metabolism disorder].

DU HX ，Zhou HF ，He Y ，Wan HT ，Yang JH ... -  《-》

Daming capsule, a hypolipidaemic drug, lowers blood lipids by activating the AMPK signalling pathway.

Hyperlipidaemia is a major risk factor for cardiovascular and cerebrovascular diseases. Daming capsule (DMC), a medicine for lowering blood lipids, is marketed in China; however, its mechanism is unclear. The present study aimed to investigate the mechanism by which DMC reduces blood lipids. A rat model of hyperlipidaemia was established by feeding rats a high-fat diet (HFD), and the serum lipid levels were detected with an automatic biochemical analyser. DMC (162 mg/kg) and atorvastatin calcium (10 mg/kg) were orally administered to the hyperlipidaemic rats for 4 weeks. HFD feeding markedly induced increases in the levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c); however, DMC treatment significantly decreased the levels of TC, TG, and LDL-c in rats serum. Meanwhile, the hepatic TC and TG levels, liver weight/body weight ratio, and body weight were significantly lower in the DMC-treated rats than in the HFD rats. Moreover, DMC significantly alleviated hepatomegaly, hepatic lipid deposition, and hepatic steatosis. The protein expression level of phospho-adenosine monophosphate-activated protein kinase (p-AMPK) (Thr172) in HFD rat livers was lower than that in normal rat livers, whereas it increased in the liver of the DMC-treated rats; however, the protein expression level of total-AMPK in the liver was not different among the groups. The AMPK-activating effect of DMC was blocked by Compound C (a specific AMPK inhibitor) in HepG2 cells. Additionally, DMC considerably increased peroxisome proliferator-activated receptor-alpha (PPARα) protein expression and lipoprotein lipase (LPL) transcription and concentration in the liver. This effect of DMC was also inhibited by Compound C in HepG2 cells. DMC also promoted LDL receptor (LDLR) protein expression by activating AMPK. We further found that DMC reduced the levels of TC and TG in oleic acid-treated HepG2 cells, and it restored the expression levels of p-AMPK, PPARα, LPL, and LDLR compared to the decreased levels observed in oleic acid-treated HepG2 cells. DMC lowered lipids in serum and the liver by activating AMPK. On the one hand, the activation of AMPK enhanced PPARα expression and LPL transcription to lead to the hydrolysis of TG; on the other hand, it increased LDLR protein expression to promote lipid metabolism.

Bian Y ，Li X ，Li X ，Ju J ，Liang H ，Hu X ，Dong L ，Wang N ，Li J ，Zhang Y ，Yang B ... -  《-》