Dietary supplementation with arginine and glutamic acid alters the expression of amino acid transporters in skeletal muscle of growing pigs.

Sixty Duroc × Large White × Landrace pigs with an average initial body weight (BW) of 77.1 ± 1.3 kg were selected to investigate the effects of dietary supplementation with arginine (Arg) and/or glutamic acid (Glu) on free amino acid (FAA) profiles, expression of AA transporters, and growth-related genes in skeletal muscle. The animals were randomly assigned to one of five treatment groups (basic diet, iso-nitrogenous, Arg, Glu, and Arg + Glu groups). The results showed that plasma Glu concentration was lowest in the Arg + Glu group and highest in the Glu group (P < 0.05). In the longissimus dorsi (LD) muscle, the concentrations of histidine, Arg, and taurine in the Arg + Glu group were higher, and the concentrations of 3-methylhistidine was lower, than in the basic diet group (P < 0.05). The mRNA levels of ASC amino acid transporter-2 (ASCT2), L-type AA transporter 1, and sodium-coupled neutral amino acid transporter 2 in the LD muscle, as well as the mRNA levels of ASCT2 and proton-assisted amino acid transporter in the biceps femoris (BF) muscle, were higher in the Arg + Glu group compared to the basic diet group (P < 0.05). The mRNA levels of the muscle-specific RING finger-1 and muscle atrophy F-box genes in the LD muscle were downregulated in the Glu and Arg + Glu groups compared to the basic diet group (P < 0.05). Collectively, these findings suggest that dietary supplementation with both Arg and Glu increases intramuscular FAA concentrations and decreases the mRNA levels of genes involved in protein degradation in skeletal muscle.

[The relationship between dietary pattern and serum C-reactive protein concentration].

In order to explore the relationship between dietary pattern and C-reactive protein (CRP) in Xiamen residents, 2 904 subjects from 3 districts of Xiamen City were selected by a multi-stage stratified random sampling method. The food frequency questionnaire was used for dietary survey and serum CRP concentration was determined simultaneously. The dietary model was established by factor analysis and the relationship between different dietary patterns and serum CRP concentration was analyzed. Five dietary patterns were obtained by the factor analysis. After the adjustment of gender, age, occupation, education, marriage status, income, smoking, drinking and body mass index, the healthy dietary pattern was negative associated with the serum CRP concentration [OR(95%CI):0.62(0.42-0.90)]. The Serum CRP concentration of residents with a healthy dietary pattern is lower.

Andrographolide suppresses RANKL-induced osteoclastogenesis in vitro and prevents inflammatory bone loss in vivo.

BACKGROUND AND PURPOSE: Osteoclasts play a pivotal role in diseases such as osteoporosis, rheumatoid arthritis and tumour bone metastasis. Thus, searching for natural compounds that may suppress osteoclast formation and/or function is promising for the treatment of osteoclast-related diseases. Here, we examined changes in osteoclastogenesis and LPS-induced osteolysis in response to andrographolide (AP), a diterpenoid lactone isolated from the traditional Chinese and Indian medicinal plant Andrographis paniculata. EXPERIMENTAL APPROACH: Effects of AP on osteoclast differentiation and bone resorption were measured in vitro. Western blots and RT-PCR techniques were used to examine the underlying molecular mechanisms. The bone protective activity of AP in vivo was assessed in a mouse model of osteolysis. KEY RESULTS: AP concentration-dependently suppressed RANKL-mediated osteoclast differentiation and bone resorption in vitro and reduced the expression of osteoclast-specific markers, including tartrate-resistant acid phosphatase, calcitonin receptors and cathepsin K. Further molecular analysis revealed that AP impaired RANKL-induced NF-κB signalling by inhibiting the phosphorylation of TGF-ß-activated kinase 1, suppressing the phosphorylation and degradation of IκBα, and subsequently preventing the nuclear translocation of the NF-κB p65 subunit. AP also inhibited the ERK/MAPK signalling pathway without affecting p38 or JNK signalling. CONCLUSIONS AND IMPLICATIONS: AP suppressed RANKL-induced osteoclastogenesis through attenuating NF-κB and ERK/MAPK signalling pathways in vitro, thus preventing bone loss in vivo. These data indicated that AP is a promising natural compound for the treatment of osteoclast-related bone diseases.

Effects of dicalcium silicate coating ionic dissolution products on human mesenchymal stem-cell proliferation and osteogenic differentiation.

This study investigated the effects of ionic dissolution products released from dicalcium silicate (DS) coatings on human mesenchymal stem cells (hMSC), cultured in the presence or absence of the dissolution products, with or without osteogenic supplements (OS). DS(+) medium promoted cell proliferation during the first 4 days, but then inhibited proliferation. DS(+)OS(-) medium increased alkaline phosphatase (ALP) activity on day 14, and upregulated runt-related transcription factor 2 and osteonectin mRNA on days 7 and 14, respectively. The addition of osteogenic supplements (DS(+)OS(+)) led to a significant increase in ALP activity from days 7 to 21, upregulation of osteogenic markers on day 14, and formation of more mineralized nodules on day 28. The results demonstrated that the ionic dissolution products from DS coating alone can partly induce osteogenic differentiation of hMSC, and that the addition of osteogenic supplements further enhances osteoblast-specific gene expression and mineralization in hMSC.

[An animal experiment and clinical investigation on the protective effect of selenium on the microcirculation induced by free radical damaged RBCs].

UNLABELLED: Fluorescent labeling image analysis was used to evaluate the changes in cerebral arteriole and veinlet diameters (D), circulation velocities (FV) and permeability (VP) in rats; while in clinics, a laser-doppler device was used for assessing changes of skins and muscles microcirculation. The results show that in control rats, equal volume perfusion of free radical damaged RBCs resulted in decreases of D and FV significantly but VP was increased, whereas in the case when free radical damaged RBCs were perfused together with selenium, no disturbances in the D and VP were observed with FV even improved. In the human control group, either average skin microcirculative perfusions (ASMP) at 25 degrees C or maximal skin microcirculative perfusions (MSMP) at 42 degrees C were evidently decreased during myocardial ischemia/reperfusion period, while ASMP at 24th hour of post-surgery was kept reducing. At the same time, the changes in muscles microcirculative perfusions (MMP) tended to be similar to the skin, but overloaded than the pre-surgery levels at 24th hour of post-surgery period. In the selenium group before surgery, the ratio of MSMP to ASMP was obviously increased than the control group (3.95 in Se group vs 1.74 in control group, P < 0.05), but did not have significantly differences in ASMP, MSMP and MMP between the two groups during surgery period. RBC deformabilities were not changed. At 24th hour post-surgery, the ASMP were almost restored to pre-surgery levels. However, MMP were still lower than the pre-surgery levels. CONCLUSIONS: (1) free radical damaged RBC perfusion leads to damage of microcirculation; (2) selenium is highly efficient in protecting microcirculation from free radical damaged RBC disturbance; and (3) Oral administration of selenium may improve pre-surgery maximal skin microcirculative perfusion and promote recovery of the worsened skin microcirculation in addition to prevent the occurrence of RBC deformability.