Impacts of simulated atmospheric cadmium deposition on the physiological response and cadmium accumulation of Sedum plumbizincicola.

Atmospheric cadmium (Cd) deposition contributes to the accumulation of Cd in the soil-plant system. Sedum plumbizincicola is a Cd and Zn hyperaccumulator commonly used for the phytoremediation of Cd-contaminated soil. However, studies on the effects of atmospheric Cd deposition on the accumulation of Cd and physiological response in S. plumbizincicola are still limited. A Cd solution spraying pot experiment was conducted with S. plumbizincicola at three atmospheric Cd deposition concentrations (4, 8, and 12 mg/L). Each Cd concentration levels was divided into two groups, non-mulching (foliar-root uptake) and mulching (foliar uptake). The soil type used in the experiment was reddish clayey soil collected from a farmland. The results showed that compared with the non-mulching control, the fresh weight of S. plumbizincicola in non-mulching with high atmospheric Cd deposition (12 mg/L) increased by 11.35%. Compared with those in the control group, the malondialdehyde (MDA) content in the non-mulching and mulching S. plumbizincicola groups increased by 0.88-11.06 nmol/L and 0.96-1.32 nmol/L, respectively. Compared with those in the non-Cd-treated control group, the shoot Cd content in the mulching group significantly increased by 11.09-180.51 mg/kg. Under high Cd depositions, the Cd in S. plumbizincicola mainly originated from the air and was stored in the shoots (39.7-158.5%). These findings highlight that the physiological response and Cd accumulation of S. plumbizincicola were mainly affected by high Cd deposition and suggest that atmospheric Cd could directly be absorbed by S. plumbizincicola. The effect of atmospheric deposition on S. plumbizincicola cannot be ignored.

The miR-145-5p/CD36 pathway mediates PCB2-induced apoptosis in MCF-7 cells.

BACKGROUND: Procyanidin B2 (PCB2) can increase the levels of anti-inflammatory and immune mediators. OBJECTIVES: However, its molecular mechanism in human breast cancer remains unclear. This study aimed to investigate the antitumor effect of PCB2 on MCF-7 cells and to examine the underlying mechanism. METHODS: The flow cytometry and EdU incorporation assays were measured the PCB2-induced BMECs. The expression levels of inflammatory factors and immune response genes were upregulated in MCF-7 cells, high-throughput sequencing was used to detect differentially expressed genes in blank and PCB2-treated MCF-7 cells. RESULTS: The results showed that PCB2 induced the apoptosis of MCF-7 cells. CD36 profiles were affected in MCF-7 cells. Additionally, prediction software identified a miR-145-5p binding site in the CD36 sequence. Luciferase reporter assays and Western blot analysis were used to verify the regulatory relationships between the differentially expressed miRNA miR-145-5p and CD36. MiR-145-5p and its key target (CD36) constitute a potential miRNA-mRNA regulatory pair. Functional studies in MCF-7 cells revealed that CD36 promotes but miR-145-5p inhibits apoptosis. CONCLUSION: Overall, these data suggest that miR-145-5p inhibits the enhancing effect of PCB2 on CD36 expression by binding CD36 and subsequently regulating apoptosis, the immune response and anti-inflammatory pathways. These results provide theoretical and experimental support for the treatment of breast cancer.