Abstrakt: |
Boron is one of the essential trace elements in animals. Although boron supplementation can enhance immune function and promote cell proliferation, high-dose boron supplementation can negatively affect immune function and inhibit cell proliferation. Furthermore, its action pathway is unknown. In this study, ERK1/2, JNK, and p38MAPK signaling pathways were blocked using specific blockers to investigate the impact of low-dose and high-dose boron on proliferation, apoptosis, and immune function of lymphocytes, and the expression of genes related to cell proliferation and apoptosis in rats. The addition of 0.4 mmol/L boron did not affect the ratio of CD4+/CD8+ T cells (P>0.05), IgG and IFN-γ contents (P>0.05), the proliferation rate of lymphocytes (P>0.05), and mRNA and protein expressions of PCNA (P>0.05) in the spleen after ERK1/2 signal pathway was selectively inhibited. Moreover, the addition of 40 mmol/L boron did not affect the proportion of CD4+ T cells, contents of IgG and cytokines (IL-2 and IL-4), proliferation and apoptosis rates of lymphocytes, and expression of proliferation- and apoptosis-related genes in the spleen. Meanwhile, the addition of 0.4 mmol/l boron increased the ratio of CD4+/CD8+ T cells (P<0.05 or P<0.01), IFN-γ or IgG contents (P<0.05), and the proliferation rate of lymphocytes (P<0.05) in spleen after selective inhibition of JNK or p38MAPK signaling pathways, while the protein expression of Caspase-3 decreased (P<0.05 or P<0.01). Furthermore, 40 mmol/L boron decreased the proportion of lymphocyte subsets, cytokine contents, proliferation rate of lymphocytes, and mRNA and protein expressions of PCNA. In contrast, the mRNA and protein expressions of Caspase-3 and protein expression of Bax were increased. These results indicate that ERK1/2 signaling pathway mainly regulates the effects of low-dose and high-dose boron on proliferation, apoptosis, and immune function of splenic lymphocytes. [ABSTRACT FROM AUTHOR] |