ABSTRACT
Objective To evaluate the changes in the expression of Nogo-A protein in the dorsal root ganglion (DRG) and spinal dorsal horn in a rat model of inflammatory pain.Methods One hundred and twenty male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 2 groups (n =60 each):control group (group C) and formalin group (group F).The inflammatory pain was induced by injection of 3％ formalin 100 μl into the plantar surface of left hindpaw in group F.The equal volume of normal saline was given instead of formalin in group C.Mechanical withdrawal threshold to yon Frey filament stimulation was measured at 1 h and 1,2,3 and 7 days after injection.Twelve rats in each group were chosen at each time point and sacrificed.The L5 DRG and L4,5 segment of spinal cord on the operated side were removed for determination of Nogo-A protein expression by immunofluorescence and Western blot.Remlts Compared with group C,the mechanical withdrawal threshold was significantly decreased at 1 h,1,2,3 and 7 days after injection,and the expression of Nogo-A protein in the DRG and L4,5 segment of spinal cord was up-regulated at 1 h and 2,3 and 7 days after injection in group F (P ＜0.05).Conclusion Up-regulation of Nogo-A protein in the DRG and spinal dorsal horn may play an important role in the development of formalin-induced inflammatory pain in rats.
ABSTRACT
Both innate and adaptive immunity contribute to the pathogenesis of ischemia-reperfusion injury (IRI).During acute phase of kidney IRI,kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability,and tubular epithelial cells increase complement C3 binding and Toll-like receptor 2 and Toll-like receptor 4 expression.Early activation of kidney dendritic cells initiates a cascade of events leading to accumulation of neutrophils,macrophage,natural killer cells,CD4 + T cells and B cells in the early phase of renal IRI.Soluble components of the immune system,such as complement activation production,cytokines and chemokines,also are implicated in the injury and repair of post-ischemic kidneys.Foxp3 + regulatory T cells and alternatively activated macrophage participate in attenuating the inflammation and initiating the repair of kidney IRI,while B lymphocytes limit repair of kidney IRI.
ABSTRACT
Nitric oxide (NO) has been considered a key molecule in infammation. OBJECTIVE: The aim of this study was to evaluate the effect of treatment with L-NAME and sodium nitroprussiate, substances that inhibit and release NO, respectively, on tissue tolerance to endodontic irrigants. MATERIAL AND METHODS: The vital dye exudation method was used in a rat subcutaneous tissue model. Injections of 2 percent Evans blue were administered intravenously into the dorsal penial vein of 14 male rats (200-300 g). The NO inhibitor and donor substances were injected into the subcutaneous tissue in the dorsal region, forming two groups of animals: G1 was inoculated with L-NAME and G2 with sodium nitroprussiate. Both groups received injections of the test endodontic irrigants: acetic acid, 15 percent citric acid, 17 percent EDTA-T and saline (control). After 30 min, analysis of the extravasated dye was performed by light absorption spectrophotometry (620 nm). RESULTS: There was statistically signifcant difference (p<0.05) between groups 1 and 2 for all irrigants. L-NAME produced a less intense infammatory reaction and nitroprussiate intensifed this process. CONCLUSIONS: Independently of the administration of NO inhibitors and donors, EDTA-T produced the highest irritating potential in vital tissue among the tested irrigating solutions.
Subject(s)
Animals , Male , Rats , Enzyme Inhibitors/therapeutic use , NG-Nitroarginine Methyl Ester/therapeutic use , Nitric Oxide Donors/therapeutic use , Nitric Oxide/antagonists & inhibitors , Nitroprusside/therapeutic use , Root Canal Irrigants/adverse effects , Acetic Acid/adverse effects , Anti-Inflammatory Agents/therapeutic use , Citric Acid/adverse effects , Edetic Acid/adverse effects , Inflammation/chemically induced , Inflammation/drug therapy , Rats, Wistar , Sodium Chloride/adverse effectsABSTRACT
Tongmal Wanji consisting of several components of traditional medicines may protect thromboangiitis obliterans (TAO), and its total clinical curative effects is about 95.90%, In order to explore the mechanism anti-TAO effect of Tongmal Wanji, an inflammation exudation and proliferation process have been studied with inflammatory edema of phalange and granular sacs models in rats. The results suggested that these inflammatory alterations were significantly inhibited by Tongmal wanji. The swelling ratio of phalange decreased more significantly in treated group than in the control group (P