Preventive Effects of Kaempferol on High-Fat Diet-Induced Obesity Complications in C57BL/6 Mice.

Kaempferol is a dietary flavanol that regulates cellular lipid and glucose metabolism. Its mechanism of action in preventing hepatic steatosis and obesity-related disorders has yet to be clarified. The purpose of this research was to examine kaempferol's antiobesity effects in high-fat diet- (HFD-) fed mice and to investigate its impact on their gut microbiota. Using a completely randomized design, 30 mice were equally assigned to a control group, receiving a low-fat diet, an HFD group, receiving a high-fat diet, and an HFD+kaempferol group, receiving a high-fat diet and kaempferol doses of 200 mg/kg in the diet. After eight weeks, the HFD mice displayed substantial body and liver weight gain and high blood glucose and serum cholesterol levels. However, treatment with kaempferol moderated body and liver weight gain and elevation of blood glucose and serum cholesterol and triglyceride levels. Examination of 16S ribosomal RNA showed that HFD mice exhibited decreased microbial diversity, but kaempferol treatment maintained it to nearly the same levels as those in the control group. In conclusion, kaempferol can protect against obesity and insulin resistance in mice on a high-fat diet, partly through regulating their gut microbiota and moderating the decrease in insulin resistance.

Starch isolated from different hulless barley cultivars differs in their chemical and structural characteristics.

This study aimed to isolate starch and evaluate its chemical and structural characteristics from six Chinese hulless barley (HB) cultivars. Starch isolated from naked barley displays A-type crystalline packing and a regular granular shape. We measured peak viscosity values ranging from 237 to 264 cP, trough viscosity values from 305 to 380 cP, breakdown values from 390 to 535 cP, final viscosities from 357 to 523 cP, setback values from 245 to 354 cP and 383 to 460 cP, peak times from 5.53 to 5.73 min, and pasting temperatures from 93.10 to 94.65°C by RVA. Transition temperatures (T 0, T p, and T c), gelatinization temperature ranges (ΔT r), and enthalpies of gelatinization (ΔH) were measured on a differential scanning calorimeter analyzer (DSC) and ranged from 57.81 to 61.25°C, 64.36 to 67.57°C, 82.03 to 84.70°C, and 21.52 to 26.89°C and 7.14 to 10.66 J/g, respectively. The varying chemical and structural characteristics of HB starch isolated from different cultivars suggested the potential for broader applications of the cereal.

Vitamin E conditionally inhibits atherosclerosis in ApoE knockout mice by anti-oxidation and regulation of vasculature gene expressions.

Lipid deposition in artery walls is implied in the pathogenesis of atherosclerosis and imbalance between uptake and efflux of cholesterol favors the deposition. We investigated the effect of vitamin E with the same dose and duration on the different stages of atherosclerosis in Apolipoprotein E knockout (ApoE KO) mice and explored the potential mechanisms. The results showed that the ApoE KO mouse spontaneously develops atherosclerosis in an age-dependent manner from 14 to 46 weeks on the regular chow. Vitamin E (100 mg/kg) supplementation to ApoE KO mice at 6, 14, and 22 weeks for 8 weeks significantly reduced the atherosclerotic lesion area by 41, 29 and 19% respectively compared to the age-matched control mice; however had no significant effect on the lesion when given at 30 and 38 weeks. In addition, vitamin E supplemented at the ages from 6 to 30 weeks decreased the contents of serum oxLDL and TBARS without affecting the TC and TAG contents in serum and liver. Furthermore, vitamin E supplemented at 6, 14 and 22 weeks down-regulated vasculature mRNA expressions of scavenger receptor CD36 and up-regulated mRNA expressions of PPARγ, LXRα and ABCA1 which are involved in reverse cholesterol transportation; however had no significant effects on these genes when given at 30 and 38 weeks. In conclusion, vitamin E with same dose and duration inhibits the early but not advanced atherosclerotic lesion in ApoE KO mice by anti-oxidation and regulation of mRNA expression of genes involved in cholesterol uptake and efflux, which favors the improvement of atherosclerosis.

Tanshinone IIA attenuates atherosclerosis in ApoE(-/-) mice through down-regulation of scavenger receptor expression.

This study is designed to investigate the protection of tanshinone IIA (TSIIA) against atherosclerosis in apolipoprotein E deficient (ApoE(-/-)) mice and to explore the mechanisms by focusing on the expressions of scavenger receptors, scavenger receptor-A (SR-A) and CD36. The in vivo study demonstrated that TSIIA (10-90mg/kg) inhibited the atherosclerotic lesions, down-regulated the CD68 protein expression in lesion and decreased the contents of cholesterol in aortas of ApoE(-/-) mice. In addition, TSIIA reduced the serum levels of oxidized LDL (oxLDL) and down-regulated the mRNA expression of CD36, SR-A and peroxisome proliferator-activated receptor gamma (PPARγ) in aortas. The in vitro study showed that TSIIA (0.1-10µM) decreased cholesterol level and DiI-oxLDL uptake in mouse peritoneal macrophages treated with oxLDL (50µg/ml). In addition, TSIIA down-regulated the mRNA and protein expression of CD36 but not that of SR-A in oxLDL treated macrophages. TSIIA also down-regulated the mRNA expression of PPARγ in oxLDL treated macrophages. Furthermore, TSIIA reduced the mRNA expression of CD36 in macrophages treated with PPARγ agonist 15d-PGJ(2) (2µM) or troglitazone (50µM), whereas both 15d-PGJ(2) (0.5-1.5µM) and troglitazone (5-20µM) dose-dependently abolished the down-regulation of CD36 expression by TSIIA in oxLDL treated macrophages. These results suggest that TSIIA attenuates the atherosclerotic lesion in ApoE(-/-) mice, which might be attributed to the properties of both anti-oxidation and down-regulation of scavenger receptors. Furthermore, antagonism of PPARγ might be involved in the down-regulation of CD36 by TSIIA.

Combined treatment with minocycline and prednisone attenuates experimental autoimmune encephalomyelitis in C57 BL/6 mice.

There has been enormous progress in the treatment of multiple sclerosis (MS) in recent years, but further improvement in therapy is still required because not all patients respond optimally to existing treatments. Increasing evidence has demonstrated that combination therapies produce a more favorable clinical outcome than monotherapy in MS treatment. Minocycline is effective in experimental autoimmune encephalomyelitis (EAE), and is a promising candidate for future MS medication. Glucocorticosteroids (GCS) belong to the most potent immunosuppressive drugs and are the mainstay for treatment of acute relapses in MS. In this study, we tested whether the combination of minocycline and prednisone (a synthetic GCS) at suboptimal doses could produce synergistic effects in EAE. Our findings showed that the combination of these two drugs functioned better than when they were individually administered in EAE mice, as evidenced by decreased clinical scores, reduced inflammation and demyelination, and improved magnetic resonance imaging outcomes. Further studies revealed that the combined treatment prevented the reduction of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA expression in cerebral cortex of EAE mice. In conclusion, our findings indicated that this combination therapy suppressed disease severity of EAE partially through blocking the downregulation of neurotrophic factor expression, suggesting that the combination of minocycline and prednisone could be a novel treatment in MS.

Tanshinone II A attenuates atherosclerotic calcification in rat model by inhibition of oxidative stress.

AIM: We have previously proved that oxidized low-density lipoprotein (oxLDL), a proatherogenic lipoprotein, plays a pivotal role in the development of atherosclerotic calcification (AC). The present study was performed to investigate whether tanshinone II A (TS II A), an anti-oxidant which has been shown to inhibit in vitro oxidation of LDL, has the effects to inhibit AC in rat model and by which, if any, mechanisms. METHODS: Rat AC model was induced by excessive vitamin D(2) (VD) and high cholesterol diet (HCD), which was proven to be successful histopathologically and biochemically. RESULTS: Administration of AC rats with TS II A (35, 70 mg/kg) dose-dependently attenuated the AC pathological changes, meanwhile reduced the vessel contents of lipid and calcium. However, TS II A had no effects on serum levels of lipids, calcium and 25-OH VD. Further studies revealed that TS II A decreased serum concentration of oxLDL, reduced the superoxide anion production and malondialdehyde (MDA) in vessel. In addition, TS II A increased vessel Cu/Zn SOD activity, upregulated vessel mRNA and protein expression of Cu/Zn SOD. CONCLUSION: The results suggested that TS II A significantly attenuated the AC in rat model, which might be attributed to its inhibition of oxLDL production independent of the serum levels of lipids, calcium and 25-OH VD, and that increasing of Cu/Zn SOD activity as well as mRNA and protein expression by TS II A might protect LDL against oxidation induced by superoxide anion in vessel.