An aqueous extract of Prunella vulgaris L. ameliorates cadmium-induced bone loss by promoting osteogenic differentiation in female rats.

Cadmium (Cd) causes bone loss, concerning inhibiting osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Prunella vulgaris L. (PV) has the potential for promoting osteogenic differentiation, but its influence on Cd-induced bone loss is unclear. This study investigated the effect of PV aqueous extract (PVE) on Cd-induced bone loss and its underlying mechanisms. Eight-week-old female SD rats were randomly assigned into four groups and treated for 16 weeks: Control, Cd (50 mg/L of Cd chloride), Cd + PV Low (125 mg/kg bw of PVE), and Cd + PV High (250 mg/kg bw of PVE). PV ameliorated femoral bone loss in Cd-treated rats manifested as increases in bone mineral density, bone volume, trabecular thickness, number, and area, and decreases in trabecular separation. Compared with Cd group, PV-treatment groups had higher serum levels of bone formation markers (ALP, BGP). Additionally, in PV-treatment groups, expressions of bone formation markers (Osterix, Runx2) and molecules involved in osteogenic differentiation signal pathway BMP/Smad (BMP4, Smad1/5/9) in the tibia of rats and isolated rat primary BMSCs were upregulated. These results suggest that PV alleviates Cd-induced bone loss by promoting osteogenic differentiation, which is likely associated with BMP/Smad pathway.

A new model to accurately measure the radon exhalation rate from soil using AlphaGUARD.

Radon exhalation rate from soil is a critical factor in evaluating environmental radon levels. However, AlphaGUARD PQ2000PRO may have some sensitivity towards thoron, which can have a significant impact on radon measurement. The traditional radon exhalation models generally ignore the presence of thoron, leading to an overestimation of the radon exhalation rate from soil. To handle this issue, a new model was proposed based on an analysis of several previous studies on radon exhalation theories. To prove the feasibility of the model, the radon exhalation rate measurements were performed by two different types of detectors-AlphaGUARD PQ2000PRO and RAD7. The radon exhalation rate obtained by using the new model is in good agreement with that obtained by using the theoretical model of radon exhalation of RAD7 within one standard error. This new model can be applied to accurately measure radon exhalation rate from soil by the PIC detector (PQ2000PRO).

Design of intermittent continuous measurement of radon concentration in water.

The U.S. Environmental Protection Agency established the maximum contaminant level limit for radon concentration in drinking water as 11.1 Bq L-1. A new device based on the bubbling method with a 290 mL sample bottle was designed for intermittent continuous measurement of water radon concentration. A STM32 is used to control the switch of the water pump and the valves. The Water-Radon-Measurement software written in C# is to connect RAD7 and calculate the water radon concentration automatically.

Cadmium contributes to atherosclerosis by affecting macrophage polarization.

Chronic cadmium (Cd) exposure contributes to the progression of atherosclerosis, but the direct role of Cd and its mechanisms in atherosclerosis remains incompletely understood. Atherosclerosis is a chronic inflammatory disease promoting macrophage polarization to M1 phenotype and producing pro-inflammations that are vital in regulating the inflammatory response. Herein, through a case-control study, we found that Cd exposure may promote the occurrence of carotid plaque via inflammation, where interleukin-6 (IL-6) may play an important role. We also combined in vivo and in vitro experiments to explore the underlying mechanism of Cd-promoted plaque formation and the production of IL-6. With or without cadmium chloride (CdCl2) fed ApoE-/- mouse and treated RAW264.7 cells, we found Cd accumulated in the aortas which significantly increased the plaque area in atherosclerotic mice, macrophage accumulation, and lipid accumulation, and Cd promoted M1 phenotype macrophage polarization reflected by the increased expression of CD86 which produced tumor necrosis factor-α (TNF-α) and IL-6. However, the influences on M2 phenotype and anti-inflammatory cytokines interleukin-4 (IL-4) and interferon-γ (IFN-γ) were non-significant. Moreover, we found that JAK2/STAT3 pathway was greatly activated in the plaques and CdCl2-treated macrophages. The inhibition of JAK2/STAT3 substantially reversed the Cd-stimulated macrophage M1 phenotype macrophage polarization and the expression of pro-inflammatory cytokines including TNF-α and IL-6. Altogether, Cd intensifies atherosclerosis by modulating macrophage polarization via JAK2/STAT3 to up-regulated the expression of IL-6.