The impact of flavonoids-rich Ziziphus jujuba Mill. Extract on Staphylococcus aureus biofilm formation.

BACKGROUND: To evaluate the in vitro antibacterial effect of flavonoids-rich Ziziphus jujuba Mill. extract (FZM) against the formation of bacterial biofilms (BBFs) in Staphylococcus aureus. RESULTS: FZM can effectively inhibit the formation of S. aureus biofilms in vitro. Morphological observation showed a decrease in both biofilm adhesion and thickness. Results of confocal laser scanning microscopy used to detect the thickness of the BBFs showed that FZM treatment reduced the thickness of the BBFs. Furthermore, after the Image-Pro Plus v.6.0 analysis of the fluorescence intensity, FZM treatment reduced the thickness of the BBFs as well as the proportion of green fluorescence. Scanning electron microscopy showed that FZM can disrupt the channels available for substance exchange in the biofilm, thus exposing the bacterial cells and damaging its three-dimensional structures. CONCLUSION: FZM can inhibit biofilm formation, improve the bacterial pH environment, and eliminate the hydrophobic effect of reactive oxygen species and flavonoids.

Ellagic acid promotes browning of white adipose tissues in high-fat diet-induced obesity in rats through suppressing white adipocyte maintaining genes.

Promoting brown adipose tissue (BAT) formation and function reduces obesity. Ellagic Acid (EA), located abundantly in plant extracts and fruits, has been shown to modulate formation and differentiation of adipocytes, although its role in the process of browning of white adipose tissue (WAT) has not been elucidated. In this study, fifty-six five-week old SD rats were randomly assigned to receive normal diet (ND, 10% lipids) or high-fat diet (HFD, 60% lipid) with or without various dosages of EA for 24 weeks. Our results showed that high fat diet intake triggered overweight, glucose intolerance and white adipocyte hypertrophy, the effects of which were mitigated by EA treatment. Meanwhile, EA supplementation reduced serum resistin levels, improved hepatic steatosis and serum lipid profile in DIO (high fat diet induced obesity) rats. Moreover, EA supplementation significantly decreased mRNA expression of Zfp423 and Aldh1a1, the key determinants of WAT plasticity. EA also increased mRNA expression of brown adipocyte markers including UCP1, PRDM16, Cidea, PGC1α, Ppar-α; beige markers including CD137and TMEM26; mitochondrial biogenesis markers including TFAM in inguinal WAT (iWAT) when compared to their counterparts. EA treatment significantly improved mitochondrial function, as measured by citrate synthase activity. More importantly, EA markedly elevated the expression of UCP1 in iWAT, which is a specific protein of brown adipocyte. In conclusion, our results provided evidence that EA improved obesity-induced dyslipidemia and hepatic steatosis in DIO rats via browning of iWAT through suppressing white adipocyte maintaining genes and promoting expression of key thermogenic genes. These findings suggest that EA could be a promising therapeutic avenue to treat metabolic diseases.

Astragaloside IV ameliorates renal fibrosis via the inhibition of mitogen-activated protein kinases and antiapoptosis in vivo and in vitro.

Apoptosis of renal tubular cells plays a crucial role in renal fibrosis. Astragaloside IV (AS-IV), a compound extracted from Radix Astragali, has been shown to inhibit renal tubular cell apoptosis induced by high glucose, but its role in preventing chronic renal fibrosis as well as the underlying molecular mechanisms involved still remain obscure. In this study, human kidney tubular epithelial cells induced by transforming growth factor-ß1 (TGF-ß1) were used to investigate the protective role of AS-IV in antifibrosis. As an in vivo model, mice subjected to unilateral ureteral obstruction (UUO) were administered AS-IV (20 mg/kg) by intraperitoneal injection for 7 days. AS-IV significantly alleviated renal mass loss and reduced the expression of α-smooth muscle actin, fibronectin, and collagen IV both in vitro and in vivo, suggesting that this compound functions in the inhibition of renal tubulointerstitial fibrosis. Furthermore, transferase-mediated dUTP nick-end labeling assay results both in vivo and in vitro showed that AS-IV significantly attenuated both UUO and TGF-ß1-induced cell apoptosis and prevented renal tubular epithelial cell injury in a dose-dependent manner. Western blotting results also revealed that the antiapoptotic effect of AS-IV was reflected in the inhibition of caspase-3 activation, which might be mediated primarily by the downregulation of mitogen-activated protein kinase effectors phospho-p38 and phospho-c-Jun N-terminal kinase. These data infer that AS-IV effectively attenuates the progression of renal fibrosis after UUO injury and may have a promising clinical role as a potential antifibrosis treatment in patients with chronic kidney disease.

Ellagic Acid Reduces Adipogenesis through Inhibition of Differentiation-Prevention of the Induction of Rb Phosphorylation in 3T3-L1 Adipocytes.

Ellagic acid (EA) present in many fruits and nuts serves as antiproliferation, anti-inflammatory, and antitumorigenic properties. However, the effect of EA on preadipocytes adipogenesis and its mechanism(s) have not been elucidated. The present study was designed to examine the effect of EA on adipogenesis in 3T3-L1 preadipocytes and underlying mechanism(s) of action involved. Data show that EA administration decreased the accumulation of lipid droplets. The inhibition was diminished when the addition of EA was delayed to days 2-4 of differentiation. Clonal expansion was reduced in the presence of EA. FACS analysis showed that EA blocked the cell cycle at the G1/S transition. EdU incorporation also confirmed that EA refrained cell from entering S phase. Our data also revealed that the differentiation-induced protein expression of Cyclin A and phosphorylation of the retinoblastoma protein (Rb) were impaired by EA. Differentiation-dependent expression and DNA-binding ability of C/EBP α were also inhibited by EA. Alterations in cell cycle-associated proteins may be important with respect to the antiadipogenic action of EA. In conclusion, EA is capable of inhibiting adipogenesis in 3T3-L1 adipocytes possibly through reduction of Cyclin A protein expression and Rb phosphorylation. With the blocking of G1/S phase transition, EA suppresses terminal differentiation and lipid accumulation in 3T3-L1 adipocytes.

Fabrication of ZnPc/protein nanohorns for double photodynamic and hyperthermic cancer phototherapy.

Multifunctionalization of carbon nanotubules is easily achieved by attaching functional molecules that provide specific advantages for microscopic applications. We fabricated a double photodynamic therapy (PDT) and photohyperthermia (PHT) cancer phototherapy system that uses a single laser. Zinc phthalocyanine (ZnPc) was loaded onto single-wall carbon nanohorns with holes opened (SWNHox), and the protein bovine serum albumin (BSA) was attached to the carboxyl groups of SWNHox. In this system, ZnPc was the PDT agent, SWNHox was the PHT agent, and BSA enhanced biocompatibility. The double phototherapy effect was confirmed in vitro and in vivo. When ZnPc-SWNHox-BSA was injected into tumors that were subcutaneously transplanted into mice, the tumors almost disappeared upon 670-nm laser irradiation. In contrast, the tumors continued to grow when only ZnPc or SWNHox-BSA was injected. We conclude that carbon nanotubules may be a valuable new tool for use in cancer phototherapy.

[Effects of Astragalus on expression of renal angiopoietin receptor Tie-2 in diabetic rats].

OBJECTIVE: To study the expression of angiopoietin receptor Tie-2 in the renal tissue of diabetic rats and the effects of Astragalus. METHODS: SD rats were randomly divided into normal control group, diabetes group and Astragalus-treated group. The expression of receptor Tie-2 in the renal tissue was assessed by using real-time quantitative polymerase chain reaction and immunohistochemical method. RESULTS: Glomerule Tie-2 protein expression was significantly elevated in the diabetes group as compared with the normal control group (P<0.01). Glomerule Tie-2 protein expression in the Astragalus-treated group was decreased as compared with the diabetes group (P<0.01). CONCLUSION: Tie-2 may play an important role in the pathogenesis of the early stage diabetic renal injury. The reno-protection effect of Astragalus may be mediated by down-regulating the expression of Tie-2 in the kidney tissue of diabetic rats.