ABSTRACT
Interleukin-33 (IL-33),a novel member of IL-1 family,is a multifunctional cytokine.IL-33 can act as a transcriptional repressor.It can also bind to growth stimulation expressed gene 2 protein (ST2) to induce the activation of some inflammatory cells.IL-33 is extensively expressed in nervous system.Some studies showed that the levels of IL-33 and ST2 were significantly changed in pain.Some reports demonstrated that the IL-33/ST2 signaling pathway played critical roles in them.This present article will review the biological characteristics of IL-33/ST2 and their expressions in nervous system and significance of interventional pain related diseases.
ABSTRACT
Objective To investigate whether hydrogen-rich saline could ameliorate the expressions of cytokines in a rat model of inflammatory pain through activating heme oxygenase-1 (HO-1).Methods Eighty male Sprague-Dawley (SD) rats,weighing 180 ～ 220 g,were randomly divided into five groups (n =16 in each group):Control group (Con),inflammation pain group (CFA),inflammation pain + hydrogen-rich saline group (CFA + H2),inflammation pain + HO-1 inhibitor Znpp-Ⅸ group (CFA + Znpp-Ⅸ),and inflammation pain + hydrogen-rich saline + HO-1inhibitor Znpp-Ⅸ group (CFA + H2 + Znpp-Ⅸ).The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were tested on days 1 (T1),2 (T2),3 (T3),5 (T4),7 (T5),and 14 (T6) after inflammation pain.The expressions of spinal HO-1 mRNA and protein were measured with real-time quantitative polymerase chain reaction (RT-PCR) and Western blot,and spinal inflammatory cytokines were measured with enzyme-linked immunosorbent assay (ELISA) on day 7 after inflammatory pain.Results Compared to Con group,MWT and TWL were significantly reduced;the spinal HO-1 mRNA level,protein expression and activity were increased;and the levels of tumor necrosis factor-α (TNF-α),interleukin (IL)-1β,IL-6 and IL-10 in spinal tissues were also increased in CFA group (P ＜ 0.05).Compared to CFA group,MWT and TWL were significantly increased;the spinal HO-1 mRNA level,protein expression and activity were further increased;and the levels of TNF-α,IL-1β and IL-6 were decreased,while IL-10 was further increased in CFA + H2group (P ＜ 0.05).Compared to CFA + H2 group,MWT and TWL were decreased;the spinal HO-1 mR-NA level,protein expression and activity were decreased;and the levels of TNF-α,IL-1β and IL-6 in spinal tissue were significantly increased,while IL-10 was decreased in CFA + H2 + Znpp-Ⅸ group (P ＜0.05).Conclusions Hydrogen-rich saline can ameliorate the mechanical and thermal allodynia in a rat model of inflammatory pain,and reduce the release of inflammatory cytokines via activating HO-1.
ABSTRACT
Objective To investigate the effect of leptin on transcription factor nuclear-κB (NF-κB) activity of pancreatic tissue and blood inflammatory cytokines (TNF-α,IL-1β) in severe acute pancreatitis. Methods Thirty-six rats were randomly divided into three groups, including sham group (group A, n = 12), AP model group(group B, n = 12) and Leptin treatment group (group C, n = 12). SAP was induced by intraductal injection of 5% sodium taurocholate into the pancreatic duct. Exogenous leptin was injected I. P. Fifteen minutes later. The concentration of serum amylase, leptin, TNF-α, IL-1βwere measured by radioimmunoassay 6 hours later. NF-κB activity of the pancreatic tissue were measured by immunohistochemistry. The changes of pathology of the pancreas were observed. Results The levels of serum amylase, cytokine TNF-αand IL-1βwere significantly reduced in group C, and the levels of serum leptin were significantly increased in group C. NF-κB activity in the pancreatic tissue in group B were significantly higher than that in group A. However, NF-κB activity of the pancreatic tissue in group C were significantly lower than that in group B. Furthermore, the extent of necrosis of the pancreatic tissue was re-lieved. Conclusion Exogenous leptin protected the rats pancreas against damage by sodium taurocholate. The protective effects of exoge-nous leptin were attributive to the reduction in cytokines TNF-α, IL-1β. The possible protective mechanism was that leptin decreased NF-κB activity.