[Therapeutic Effect of Spleen Low Molecular Weight Extracts on Leukopenia Caused by Epirubicin in Mice and Its Mechanism].

OBJECTIVE: To investigate the therapeutic effect of spleen low molecular weight extracts on epileptics hydrochloride-induced leukopenia in mice and explore its mechanism. METHODS: The model of leukopenia in mice was established by the injection of epirubicin hydrochloride (10 mg/kg). After the injection of chemotherapeutic drugs, leukocytopenia mice were treated with different doses of spleen low molecular weight extract, Ganoderma oral solution and recombinant granulocyte colony stimulating factor (rhG-CSF). The general survival status indicators such as body weight, coat color and athletic ability of mice in each group were recorded; the tail vein blood of mice in each group was collected and the white blood cell count in them was calculated; bone marrow of mice was taken and bone marrow smears were observed. RESULTS: In the model group, the weight of the mice gradually decreased in the later period, their coat became dark and rough, and the ability to exercise decreased, while the mice in the treatment groups showed different degrees of improvement in their survival status except for the mice treated by rhG-CSF. There was no significant fluctuation in the white blood cell count of the blank control mice. After injection of epirubicin, the white blood cell count of peripheral blood in the model mice and treated mice were decreased. The white blood cell count was lower in the mice treated with high-dose low molecular weight extract and rhG-CSF than that in other experimental groups. Bone marrow smear showed that the proportion of bone marrow nucleated cells in the mice treated with the low molecular weight extract of the spleen was significantly higher than that of model mice (P<0.05). CONCLUSION: The low molecular weight spleen extracts can significantly improve the hematopoietic state of mouse bone marrow, promote the proliferation of inhibited bone marrow cells, and thus has the effect of treating leukopenia in mice.

XRN1-associated long non-coding RNAs may contribute to fungal virulence and sexual development in entomopathogenic fungus Cordyceps militaris.

BACKGROUND: Numerous long non-coding RNAs (lncRNAs) identified and characterized in mammals, plants, and fungi have been found to play critical regulatory roles in biological processes. However, little is known about the role of lncRNAs in insect pathogenic fungi. RESULTS: By profiling the transcriptomes of sexual and asexual development in the insect-pathogenic fungus Cordyceps militaris, 4140 lncRNAs were identified and found to be dynamically expressed during fungal development. The lncRNAs had shorter transcript lengths and lower numbers of exons compared to protein-coding genes. The expressed target genes (neighboring and cis-regulated) of various expressed lncRNAs were predicted, and these genes showed significant enrichment in energy metabolism and signaling pathways, such as 'Glycolysis/Gluconeogenesis' and "MAPK signaling pathway". To better understand how lncRNAs function in the fungus, xrn1, the final gene of the NMD pathway, which determines the fate of lncRNAs, was disrupted. The Δxrn1 deletion mutant displayed significant (P < 0.05) attenuation of virulence and a lower growth rate in C. militaris. Quantitative RT-PCR results revealed 10 lncRNAs with significantly higher expression, while 8 of these 10 lncRNA target genes (virulence- and sexual development-related) showed significantly lower expression in Δxrn1 compared to in the wild-type, suggesting that lncRNA expression regulates fungal virulence and sexual development by affecting gene expression. CONCLUSION: These findings suggest that lncRNAs in C. militaris play important roles in the fungal infection progress and fruiting body production, providing a broad repertoire and resource for further studies of lncRNAs. © 2019 Society of Chemical Industry.

TPX2 in malignantly transformed human bronchial epithelial cells by anti-benzo[a]pyrene-7,8-diol-9,10-epoxide.

In order to elucidate the function of the targeting protein for Xenopus kinesin-like protein 2 (Xklp2) (TPX2) in the malignant transformation of human bronchial epithelial cells induced by anti-benzo[a]pyrene-trans-7, 8-dihydrodiol-9, 10-epoxide (anti-BPDE), TPX2 was characterized in cells at both the gene and the protein levels. TPX2 was present at higher levels in 16HBE-C cells than in 16HBE cells as demonstrated by two-dimensional gel electrophoresis, immunocytochemistry, Western blot analysis and RT-PCR. TPX2 was also detected in lung squamous-cell carcinoma tissues by immunohistochemistry, but not in normal lung tissues. Depression of TPX2 by RNA interference in 16HBE-C cells led to a decrease in cell proliferation, S-phase cell cycle arrest and cell apoptosis. Abnormal TPX2 tyrosine phosphorylation was detected in 16HBE-C cells, and this could be inhibited, to different degrees, by tyrosine kinase inhibitors. Inhibiting tyrosine phosphorylation in 16HBE-C cells by three selected tyrosine protein kinase inhibitors, tyrphostin 47, AG112 and AG555, caused G(0)/G(1)-phase cell cycle arrest. Our results suggest that anti-BPDE can cause the over-expression of TPX2 and its aberrant tyrosine phosphorylation. Misregulation of TPX2 affects the cell cycle state, proliferation rates and apoptosis.