Sulforaphane decreases serum selenoprotein P levels through enhancement of lysosomal degradation independent of Nrf2.

Selenoprotein P (SeP) is a major selenoprotein in serum predominantly produced in the liver. Excess SeP impairs insulin secretion from the pancreas and insulin sensitivity in skeletal muscle, thus inhibition of SeP could be a therapeutic strategy for type 2 diabetes. In this study, we examine the effect of sulforaphane (SFN), a phytochemical of broccoli sprouts and an Nrf2 activator, on SeP expression in vitro and in vivo. Treatment of HepG2 cells with SFN decreases inter- and intra-cellular SeP levels. SFN enhances lysosomal acidification and expression of V-ATPase, and inhibition of this process cancels the decrease of SeP by SFN. SFN activates Nrf2 in the cells, while Nrf2 siRNA does not affect the decrease of SeP by SFN or lysosomal acidification. These results indicate that SFN decreases SeP by enhancing lysosomal degradation, independent of Nrf2. Injection of SFN to mice results in induction of cathepsin and a decrease of SeP in serum. The findings from this study are expected to contribute to developing SeP inhibitors in the future, thereby contributing to treating and preventing diseases related to increased SeP.

Distribution Law of Corrosion Products in a Marine Chloride Environment.

Steel corrosion is the main cause of reinforced concrete cracking. Conventionally, concrete is considered to crack when the circumferential tensile stress reaches the tensile strength of the concrete. However, few analyses have considered the fracture criteria of the internal cross-section of concrete. Based on the von Mises distribution of angle probabilities, this paper proposes a new probability distribution function for investigating the distribution law of corrosion products. The cracking process of experimental samples was numerically analyzed, and the results were consistent with those of the theoretical model. The effect of the dry-wet cycle ratio on the corrosion products was preliminarily investigated by microscopic observation of the reinforced concrete under different dry-wet cycle corrosion environments.

DNAJC2 is reversely regulated by miR­627­3p, promoting the proliferation of colorectal cancer.

Colorectal cancer (CRC) is one of the most common malignancies among human, which is often connected with increased incidence and mortality rate. DnaJ Heat Shock Protein Family (Hsp40) Member C2 (DNAJC2) is an epigenetic factor, which is involved in a number of cytological functions, such as transcriptional regulation and ubiquitination. A number of studies reveal that DNAJC2 is closely associated with several tumors. However, the function and mechanism of DNAJC2 in CRC remains to be elucidated. In the present study, the expression of DNAJC2 was detected in CRC tissues and adjacent normal tissues. The results indicated that DNAJC2 was increased in CRC tissues and the expression level of DNAJC2 was significantly associated with tumor size. Cell function was detected via Cell Counting Kit­8, 5­ethynyl­2'­deoxyuridine, colony formation assays and flow cytometry by upregulating or knocking down of DNAJC2. Overexpression of DNAJC2 could accelerate cell proliferation while suppression of DNAJC2 decreased cell proliferation, possibly via the regulation of cell cycle regulation in vitro. It was also found that the function of DNAJC2 was reversely regulated by miR­672­3p, causing the promoting of cell proliferation through the activation of AKT/P21 signal pathway in CRC cells. These results suggested that DNAJC2 is a tumor­regulated protein in the progression of CRC and may represent a novel target for CRC detection and therapy.