Cocoa tea (Camellia ptilophylla) is a naturally decaffeinated tea plant. Previously we found that cocoa tea demonstrated a beneficial effect against high-fat diet induced obesity, hepatic steatosis, and hyperlipidemia in mice. The present study aimed to investigate the anti-adipogenic effect of cocoa tea in vitro using preadipocytes 3T3-L1. Adipogenic differentiation was confirmed by Oil Red O stain, qPCR and Western blot. Our results demonstrated that cocoa tea significantly inhibited triglyceride accumulation in mature adipocytes in a dose-dependent manner. Cocoa tea was shown to suppress the expressions of key adipogenic transcription factors, including peroxisome proliferator-activated receptor gamma (PPAR γ) and CCAAT/enhancer binding protein (C/EBP α). The tea extract was subsequently found to reduce the expressions of adipocyte-specific genes such as sterol regulatory element binding transcription factor 1c (SREBP-1c), fatty acid synthase (FAS), Acetyl-CoA carboxylase (ACC), fatty acid translocase (FAT) and stearoylcoenzyme A desaturase-1 (SCD-1). In addition, JNK, ERK and p38 phosphorylation were inhibited during cocoa tea inhibition of 3T3-L1 adipogenic differentiation. Taken together, this is the first study that demonstrates cocoa tea has the capacity to suppress adipogenesis in pre-adipocyte 3T3-L1 similar to traditional green tea

This study reports the proportioning and standardized mixing procedures for preparing a hydroxylapatite cement (tetracalcium phosphate and dicalcium phosphate) of desired viscosity and mechanical strength reproducibly for application in trauma surgery. The behavior and the biomechanical properties of the resulting bone cement in screw augmentation were then evaluated in our osteopenic goat model. The use of a shaker standardized the mixing procedure. The optimal volume of Na2HPO4 used to prepare the injectable cement was 0.45 mL/g, with averaged in vitro compressive strength of 48.29 +/- 5.62 MPa. Histology showed increasing tightly-coupled bone apposition on the cement surface without fibrous encapsulation as observed in the screw-only controls with time in the osteopenic goat model. The cement increased the initial screw pull-out force (54.7%, p = 0.005) significantly and the energy required to failure (54.7%, p < 0.05) significantly, and remained higher than the screw-only controls after 3 months (9.8% and 20.2%, respectively) and 6 months (20.2% and 44.7%, respectively). These results imply potential in the prevention of interfacial micromotions and subsequent fibrous tissue formation at the implant-bone interface resulting in a decreased risk of implant failure. The optimized cement in this study may serve as a good candidate for augmenting fixation of osteoporotic bone.

Recent studies suggested that green tea has the potential to protect against diet-induced obesity. The presence of caffeine within green tea has caused limitations. Cocoa tea (Camellia ptilophylla) is a naturally decaffeinated tea plant. To determine whether cocoa tea supplementation results in an improvement in high-fat diet-induced obesity, hyperlipidemia and hepatic steatosis, and whether such effects would be comparable to those of green tea extract, we studied six groups (n = 10) of C57BL/6 mice that were fed with (1) normal chow (N); (2) high-fat diet (21% butterfat + 0.15% cholesterol, wt/wt) (HF); (3) a high-fat diet supplemented with 2% green tea extract (HFLG); (4) a high-fat diet supplemented with 4% green tea extract (HFHG); (5) a high-fat diet supplemented with 2% cocoa tea extract (HFLC); and (6) a high-fat diet supplemented with 4% cocoa tea extract (HFHC). From the results, 2% and 4% dietary cocoa tea supplementation caused a dose-dependent decrease in (a) body weight, (b) fat pad mass, (c) liver weight, (d) total liver lipid, (e) liver triglyceride and cholesterol, and (f) plasma lipids (triglyceride and cholesterol). These data indicate that dietary cocoa tea, being naturally decaffeinated, has a beneficial effect on high-fat diet-induced obesity, hepatomegaly, hepatic steatosis, and elevated plasma lipid levels in mice, which are comparable to green tea. The present findings have provided the proof of concept that dietary cocoa tea might be of therapeutic value and could therefore provide a safer and cost effective option for patients with diet-induced metabolic syndrome.

There is no clear evidence to show the direct causal relationship between passive cigarette smoking and osteoporosis. Furthermore, the underlying mechanism is unknown. The objective of this study is to demonstrate the effects of long-term passive cigarette smoking on bone metabolism and microstructure by a mouse model and cell culture systems. BALB/c mice were exposed to 2 or 4 % cigarette smoke for 14 weeks. The bone turnover biochemical markers in urine and serum and also the bone micro-architecture by micro-CT were compared with the control group exposed to normal ambient air. In the cell culture experiments, mouse MC3T3-E1 and RAW264.7 cell lines to be employed as osteoblast and osteoclast, respectively, were treated with the sera obtained from 4 % smoking or control mice. Their actions on cell viability, differentiation, and function on these bone cells were assessed. The urinary mineral and deoxypyridinoline (DPD) levels, and also the serum alkaline phosphatase activity, were significantly higher in the 4 % smoking group when compared with the control group, indicating an elevated bone metabolism after cigarette smoking. In addition, femoral osteopenic condition was observed in the 4 % smoking group, as shown by the decrease of relative bone volume and trabecular thickness. In isolated cell studies, osteoblast differentiation and bone formation were inhibited while osteoclast differentiation was increased. The current mouse smoking model and the isolated cell studies demonstrate that passive cigarette smoke could induce osteopenia by exerting a direct detrimental effect on bone cells differentiation and further on bone remodeling process.

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Bone mineral density (BMD) is commonly used to predict osteoporotic fracture risk without considering the geometry of the bone. However, geometric parameters are also important in determination of bone strength. An index including both material and geometric properties may be therefore more relevant in prediction of fracture risk. We studied the correlation between parameters measured by noninvasive peripheral quantitative computed tomography (pQCT) and bone bending strength of the diaphysis of 45 fresh goat humeri and 27 femora. Multislice pQCT was used for measuring volumetric diaphyseal cortical BMD, total BMD, diaphyseal and cortical cross-sectional area (CSA), and cross-sectional moment of inertia (CSMI) and their derived bone strength indices (BSIs), including BSI(CSMI) (cortical BMD x CSMI) and BSI(CSA) (cortical BMD x cortical CSA). Conventional dual-energy absorptiometry (DXA) was also conducted to measure areal BMD of diaphysis for comparison. Ultimate fracture load was obtained via three-point bending test. Results showed that for femora, fracture load was correlated better with BSI(CSA) ( r = 0.697, P < 0.001) than cortical BMD ( r = 0.304, P > 0.05) and total BMD ( r = 0.387, P > 0.05) measured using pQCT and areal BMD ( r = 0.612, P < 0.001) measured using DXA. For humeri, fracture load was also correlated with BSI(CSA) ( r = 0.579, P < 0.001) but not with other pQCT parameters including cortical BMD and total BMD ( r = 0.282 and 0.305, respectively; P > 0.05, both). The best correlation was found with areal BMD measured by DXA ( r = 0.760, P < 0.001). In conclusion, pQCT noninvasive BSI(CSA) derived from cortical BMD (material) and its cortical CSA (bone geometry or distribution) may serve as an important noninvasive index for predicting long bone bending strength. The bending strength was also predicted by bone mass (areal BMD) measured by DXA, an integration of bone mineral and geometry. Further clinical studies are needed to validate the predictive value of BSI in long bone osteoporotic fracture.

BackgroundFructus Ligustri Lucidi (FLL) is a commonly used herb for treating bone disorders in Chinese medicine. The present study investigates the anti-osteoporotic activity of FLL aqueous extract in the model of postmenopausal bone loss in aged ovariectomized (OVX) female rats.MethodsAfter eight weeks of treatment of FLL or water, the lumbar spine was scanned by peripheral quantitative computed tomography (pQCT). Effects of FLL water extract on osteogenic and adipogenic differentiations in rat mesenchymal stem cells (MSCs) were assessed by biochemical methods and staining.ResultsFLL aqueous extract significantly inhibited bone mineral density (BMD) loss in total, trabecular and cortical bones without affecting body weight and uterus wet weight. FLL extract significantly promoted osteogenesis and suppressed adipogenesis in MSCs as indicated by the elevated alkaline phosphatase activity, calcium deposition levels and decreased adipocyte number in a dose-dependent manner without cytotoxic effects. Real-time PCR analysis revealed significant increase of osteoprotegerin (OPG)-to-receptor activator for nuclear factor-κB ligand (RANKL) mRNA, indicating a decrease in osteoclastogenesis.ConclusionThe present study demonstrates the osteoprotective effects of FLL aqueous extract on aged OVX rats, stimulation of osteogenesis, inhibition of adipogenesis and osteoclastogenesis in MSCs.

Introduction The biological role of mesenchymal stem cells (MSCs) in wound healing has been demonstrated. However, there were limited studies on the healing effect of secretome which consists of many biological factors secreted by MSCs. In this study, we aimed to compare the therapeutic effects of secretome with MSCs on facilitating wound healing. Methods Green fluorescent protein labelled adipose-derived MSCs (GFP-ADMSCs) or secretome was injected in the full-thickness skin excision model on SD rats. The wound healing process was evaluated by calculating the healing rate and the histological examinations on skin biopsy. The cell viability, proliferation and mobility of the rat dermal fibroblasts were compared after different treatments. The inflammatory response in macrophages was indicated by the level of nitric oxide (NO) and inflammatory cytokines through NO assay and ELISA. Results On day 5 and day 14, both MSCs and secretome accelerated the wound healing, secretome further enhanced the process. GFP-MSCs were detected 10 days after transplantation. The level of IL-6 and TNF-α in blood was reduced after MSCs and secretome treatments. The expressions of VEGF and PCNA were increased after treatment, higher intensity of VEGF was observed in secretome-injected tissue. The concentrations of total protein and VEGF in secretome were 2.2 ± 0.5 mg/mL and 882.0 ± 72.7 pg/mL, respectively. The cell viability and proliferation of FR were promoted significantly after the treatment. The scratch test showed that secretome accelerated the wound healing speed. Secretome reduced the metabolism of macrophages remarkably, but it did not decrease the level of macrophage-secreted NO. The expression of the pro-inflammatory cytokines (IL-6, MCP-1 and TNF-α) was downregulated significantly. Conclusion Our study indicated both MSCs and MSCs-derived secretome enhanced the wound healing process in early phase. Secretome further promoted the healing effects through promoting the fibroblast proliferation and migration and suppressing the inflammatory response.