Our results provided direct evidence that forest bathing has therapeutic effects on human hypertension and induces inhibition of the renin-angiotensin system and inflammation, and thus inspiring its preventive efficacy against cardiovascular disorders.

Tartrate-resistant acid phosphatase 5b (TRACP 5b) has been used as a biomarker of bone resorption and cancer metastasis. TRACP 5b has also been suggested to be a reliable marker of osteoclast number. In this study, the correlation of TRACP 5b level and osteoclast-like cell number was investigated in RAW 264.7 cells treated with receptor-activated nuclear factor κB ligand (RANKL). RAW 264.7 cells were cultured with α-MEM containing RANKL (40 ng/ml) for 3, 5 and 7 days. Osteoclast formation and TRACP 5b levels were determined by TRACP staining, scanning electron microscopy and enzyme-linked immunosorbent assay. The RAW 264.7 cells that were not exposed to RANKL did not secrete TRACP 5b. RANKL induced the RAW 264.7 cells to differentiate into osteoclasts and to secrete TRACP 5b. The TRACP 5b level in the RAW 264.7 cells treated with RANKL was significantly correlated with the number and volume of osteoclasts (r=0.95 and r=0.92, respectively; P<0.0001). TRACP 5b is a good marker of RANKL-induced osteoclast formation in RAW 264.7 cells. TRACP 5b analysis may be used as an alternative to osteoclast counting in vitro.

The present paper was designed to investigate the effect of pine pollen against aging in human diploid fibroblast 2BS cells and in an accelerated aging model, which was established by subcutaneous injections with D-galactose daily for 8 weeks in C57BL/6J mice. Pine pollen (1 mg/mL and 2 mg/mL) is proved to delay the replicative senescence of 2BS cells as evidenced by enhanced cell proliferation, decreased SA-β-Gal activity, and reversed expression of senescence-associated molecular markers, such as p53, p21Waf1, p16INK4a, PTEN, and p27Kip1 in late PD cells. Besides, pine pollen reversed D-galactose-induced aging effects in neural activity and inflammatory cytokine levels, as indicated by improved memory latency time and reduced error rate in step-down test and decreased concentrations of IL-6 and TNF-α in model mice. Similar to the role of AGEs (advanced glycation endproducts) formation inhibitor aminoguanidine (AG), pine pollen inhibited D-galactose-induced increment of AGEs levels thus reversed the aging phenotypes in model mice. Furthermore, the declined antioxidant activity was obviously reversed upon pine pollen treatment, which may account for its inhibitory effect on nonenzymatic glycation (NEG) in vivo. Our finding presents pine pollen as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.

Abstract. Acute lung injury (ALI) is characterized by severe lung edema and an increase in the inflammatory reaction. Considerable evidence has indicated that microRNAs (miRNAs or miRs) are involved in various human diseases; however, the expression profile and function of miRNAs in ALI have been rarely reported. The present study used miRNA microarray and reverse transcription-quantitative polymerase chain reaction to demonstrate that miR-181b is the one of the most significantly upregulated miRNA after lipopolysaccharide (LPS) stimulation in human bronchial epithelial cells, BEAS-2B. To elaborate the role of miR-181b in ALI, an assay was performed to investigate the overexpression of miR-181b in BEAS-2B cells, and the expression of inflammatory factors was then analyzed. The overexpression of miR-181b resulted in the induction of an increment in interleukin (IL)-6 levels. p65 was identified to be a primary component of NF-κB, since it was upregulated in the miR-181b overexpression in the BEAS-2B cells, while pyrrolidine dithiocarbamate, a specific inhibitor of NF-κB, was found to be able to abrogate the upregulation of the expression of p65. In conclusion, the findings of the present study suggested that miR-181b may be involved in the process of LPS-induced inflammation in BEAS-2B cells by activating the NF-κB signaling pathway, which implies that it may serve as a potential therapeutic target for ALI.

Cadmium (Cd) can induce bone loss and osteoporosis. Histologic methods have shown that Cd can induce microarchitecture change of the trabecular bone. The aim of this study is to evaluate the imaging biomarkers of osteoporosis induced by Cd using micro-computed tomography (micro-CT). Twenty-four male Sprague-Dawley rats were randomly divided into four groups that were exposed to Cd via drinking water at concentrations of 0, 2, 10, and 50 mg/L for 3 months. Before sacrifice, micro-CT scanning was performed on the proximal tibia. Three-dimensional images were analyzed by using commercial software to measure apparent bone mineral density (ABMD), tissue bone mineral density (TBMD), bone volume/total volume fraction (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), trabecular separation (Tb.Sp), and structural model index (SMI) as imaging biomarkers. Histologic analyses were performed using hematoxylin and eosin (HE) and Goldner's trichrome stain. Exposure to Cd resulted in a marked decrease of ABMD, BV/TV, and Tb.N and an increase of Tb.Sp and SMI compared with control, especially for those treated with 50 mg Cd/L (p < 0.05). Decreased Tb.N and increased Tb.Sp compared to that of control were also observed in histologic findings. The micro-CT imaging is a promising tool for assessing the bone damage induced by Cd, and Tb.N, Tb.Sp, and SMI may be the potential sensitive imaging biomarkers.