Red nucleus IL-33 facilitates the early development of mononeuropathic pain in male rats by inducing TNF-α through activating ERK, p38 MAPK, and JAK2/STAT3.

BACKGROUND: Our recent studies have identified that the red nucleus (RN) dual-directionally modulates the development and maintenance of mononeuropathic pain through secreting proinflammatory and anti-inflammatory cytokines. Here, we further explored the action of red nucleus IL-33 in the early development of mononeuropathic pain. METHODS: In this study, male rats with spared nerve injury (SNI) were used as mononeuropathic pain model. Immunohistochemistry, Western blotting, and behavioral testing were used to assess the expressions, cellular distributions, and actions of red nucleus IL-33 and its related downstream signaling molecules. RESULTS: IL-33 and its receptor ST2 were constitutively expressed in the RN in naive rats. After SNI, both IL-33 and ST2 were upregulated significantly at 3 days and peaked at 1 week post-injury, especially in RN neurons, oligodendrocytes, and microglia. Blockade of red nucleus IL-33 with anti-IL-33 neutralizing antibody attenuated SNI-induced mononeuropathic pain, while intrarubral administration of exogenous IL-33 evoked mechanical hypersensitivity in naive rats. Red nucleus IL-33 generated an algesic effect in the early development of SNI-induced mononeuropathic pain through activating NF-κB, ERK, p38 MAPK, and JAK2/STAT3, suppression of NF-κB, ERK, p38 MAPK, and JAK2/STAT3 with corresponding inhibitors markedly attenuated SNI-induced mononeuropathic pain or IL-33-evoked mechanical hypersensitivity in naive rats. Red nucleus IL-33 contributed to SNI-induced mononeuropathic pain by stimulating TNF-α expression, which could be abolished by administration of inhibitors against ERK, p38 MAPK, and JAK2/STAT3, but not NF-κB. CONCLUSIONS: These results suggest that red nucleus IL-33 facilitates the early development of mononeuropathic pain through activating NF-κB, ERK, p38 MAPK, and JAK2/STAT3. IL-33 mediates algesic effect partly by inducing TNF-α through activating ERK, p38 MAPK and JAK2/STAT3.

[Study on GLI values of Polygonatum odoratum base on multi-temporal of unmanned aerial vehicle remote sensing].

Unmanned aerial vehicle(UAV) remote sensing and vegetation index have great potential in the field of Chinese herbal medicine planting. In this study, the visible light image of Polygonatum odoratum planting area in Changyi district of Jilin province were acquired by UAV, and the real-time monitoring of P. odoratum planting area was realized. The green leaf index(GLI) was established, and GLI values of P. odoratum were collected used the spatial sampling points. To compare the GLI values in different periods, it was found that the GLI values of P. odoratum have three stages changing rule of rising-gentle-falling related to the germination, vigorous growth and withered of P. odoratum growth. Meanwhile, the GLI values were compared with four biomass data of P. odoratum, including plant height, leaf area, chlorophyll a and chlorophyll b content in leaves, and it was found that the GLI value was related to the growth potential of P. odoratum. The GLI value with a rapid increase in rising stage or at a high level in the gentle stage means the P. odoratum was in a better growth potential. GLI value has a same change trend with plant height, and has certain correlation with plant height and leaf area. However, there is no obvious relationship between chlorophyll a and chlorophyll b contents in leaves and GLI value. The study clarified the change rule of GLI value of P. odoratum, explained the reason for the change of GLI value, and expanded the application range of GLI. The research shows that UAV and vegetation index can be applied to monitoring the Chinese herbal medicines planting, and provides a new idea for exploring more effective information extraction methods of Chinese herbal medicines.

Effect of nicotine on Staphylococcus aureus biofilm formation and virulence factors.

Staphylococcus aureus is a common pathogen in chronic rhinosinusitis (CRS) patients, the pathogenesis of which involves the ability to form biofilms and produce various virulence factors. Tobacco smoke, another risk factor of CRS, facilitates S. aureus biofilm formation; however, the mechanisms involved are unclear. Here, we studied the effect of nicotine on S. aureus biofilm formation and the expression of virulence-related genes. S. aureus strains isolated from CRS patients and a USA300 strain were treated with nicotine or were untreated (control). Nicotine-treated S. aureus strains showed dose-dependent increases in biofilm formation, lower virulence, enhanced initial attachment, increased extracellular DNA release, and a higher autolysis rate, involving dysregulation of the accessory gene regulator (Agr) quorum-sensing system. Consequently, the expression of autolysis-related genes lytN and atlA, and the percentage of dead cells in biofilms was increased. However, the expression of virulence-related genes, including hla, hlb, pvl, nuc, ssp, spa, sigB, coa, and crtN was downregulated and there was reduced bacterial invasion of A549 human alveolar epithelial cells. The results of this study indicate that nicotine treatment enhances S. aureus biofilm formation by promoting initial attachment and extracellular DNA release but inhibits the virulence of this bacterium.