Anti-hyperlipidemic effect of rice bran polysaccharide and its potential mechanism in high-fat diet mice

Abstract

Hyperlipidemia occurs very often in modern society along with a high calorie intake and is regarded as one of the greatest risk factors for the prevalence of cardiac vascular disease (CVD). In this study, we investigated the anti-hyperlipidemic effect of the rice bran polysaccharides (RBP) and its mechanism in a high fat diet animal model. 60 ICR mice were randomly divided into 3 groups, which included Control, HFD (high fat diet) and HFD + RBP, and each group included 20 mice. The control group was fed with a standard diet while the other two groups were fed with HFD. In addition, the HFD + RBP group was fed with 500 mg kg of rice bran polysaccharides by intragastric administration while the other two groups were intragastrically administered with water. The results showed that RBP treatment for 10 weeks obviously decreased the body weight, liver weight and adipose tissues of mice; and it decreased the levels of total cholesterol (TC), triglycerides (TG) and low density lipoprotein-cholesterol (LDL-c) in the plasma. H&E staining of the liver tissues showed that RBP treatment decreased the size of fat droplets compared with the HFD group. Microarray analysis revealed that RBP treatment results in 80 genes being up-regulated while 72 genes were down-regulated in the tissues of liver. IPA software analysis suggested that NF-κB may play a vital role in the lipid-lowering effect of RBP. Real-time quantitative PCR confirmed that the mRNA levels of PPAR-α, PPAR-γ, PPAR-δ, SREBP-1C, FASN, ACC, SIRT and CD36, which are related to lipid metabolism, were significantly regulated by RBP supplementation compared to HFD. The western blot analysis further confirmed these altered expressions after RBP treatment. Taken together, these results suggest that the oral administration of RBP exerts lipid-lowering in high fat diet mice via regulating the lipid metabolism-related gene expression.

Evaluation of Physicochemical and DPPH� Cleaning Activity of Ultrasonic Assisted Extraction of Polysaccharide from Leonurus japonicus

“…In the cosmetics industry, it is currently being used as facial masks or ointments and also in food products, accompanied with other components to treat skin disease as well as help in activation of blood circulation [3]. Presently, the replacement of synthetic antioxidant with naturally occurring antioxidant is increasing due to the side effects associated with synthetic antioxidant such as increased risk of cancer [4][5][6][7][8][9][10][11][12][13][14][15].…”

Cigarette Smoke Extract Modulates Functions of Peroxisome Proliferator-Activated Receptors

“…Since the effects of cigarette smoking on LDL-C levels has not reached to the crucial conclusions, [2][3][4][5][6][18][19][20][21] in the current study, as mentioned above, we tested the hypothesis that whether CSE affects the target genes associated with metabolic pathway of LDL-C. Even though our epidemiological observation made us quite clear, there has been several reports depicting that smoking habit elevated LDL-C in epidemiology investigations.…”

“…Even though our epidemiological observation made us quite clear, there has been several reports depicting that smoking habit elevated LDL-C in epidemiology investigations. [18][19][20][21] Thus, by using quantitative RT-PCR, we examined whether CSE affects the expression of genes (such as PPARα, PPARβ/δ, PPARγ, ATP-binding cassette, subfamily A transporter 1(ABCA1), PGC1a, PGC1b, SREBP1a, SREBP1c, SREBP2, Fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), sirtuin (SIRT), CD36, FOXO1, STAT5B, Liver X receptor (LXR) α, LXRβ, Farnesoid X receptor (FXR), vitamin D receptor, hydroxymethylglutaryl-CoA (HMG-CoA) reductase, and uncoupling protein (UCPs)), associated with LDL-C metabolism in HepG2 cells 22) (data not shown except Fig. 6).…”

Scutellarin, a modulator of mTOR, attenuates hepatic insulin resistance by regulating hepatocyte lipid metabolism via SREBP‐1c suppression

“…These data indicated that Scu decreased lipid accumulation occurred by reducing the level of TG in PA‐treated HepG2 cells. Moreover, Fasn regulates the synthesis and degradation of TG, ACC is the rate‐limiting enzyme for fatty acid synthesis, and CD36 is a fatty acid transporter that promotes lipid uptake by the cells (Nie et al, ). PA incubation increased the mRNA expression levels of Fasn, ACC, and CD36.…”