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Objective To explore the improvement effect of myricitrin on bone defect in rats with bacterial osteomyelitis(OM)through vascular endothelial growth factor A(VEGFA)/stromal cell-derived factor(SDF-1)/C-X-C chemokine receptor 4(CXCR4)pathway.Methods Rats were randomly divided into the sham operation group,the OM group,the myricitrin group[50 mg/(kg·d)],PX-478 group[25 mg/(kg·d)VEGFA/SDF-1/CXCR4 signaling pathway inhibitor PX-478],and the myricitrin+PX-478 group[50 mg/(kg·d)myricitrin and 25 mg/(kg·d)PX-478],18 mice per group.Bilateral proximal tibia bone defects were used to construct bacterial OM rat model.After 12 weeks of continuous treatment,the wound healing degree of rats was observed,and anal temperature of rats was measured.The serum inflammatory factors interleukin(IL)-6,IL-1β,IL-17 and bone metabolism indexes bone alkaline phosphatase(BALP),osteocalcin(BGP)and C-terminal telopeptide of type Ⅰ collagen(CTX-Ⅰ)were measured by enzyma-linked immunosorbent assay(ELISA).The bacterial load of tissue around the lesion was detected.HE staining was used to detect the pathological changes of the tissue around lesions.The expression of CD31 was detected by immunofluorescence staining.Western blot assay was used to detect the expression of VEGFA/SDF-1/CXCR4 signal pathway related proteins.Results Compared with the sham operation group,the number of rats with grade A wound healing,BALP and BGP levels,CD31 positive area,VEGFA,SDF-1 and CXCR4 protein levels were decreased in the OM group(P＜0.005 or P＜0.05),and the anal temperature,bacterial load,IL-6,IL-1β,IL-17 and CTX-Ⅰlevels were increased(P＜0.05).Compared with the OM group,the BALP and BGP levels,CD31 positive area,VEGFA,SDF-1 and CXCR4 protein levels were increased,and the anal temperature,bacterial load,IL-6,IL-1β,IL-17 and CTX-Ⅰlevels were decreased in the myricitrin group(P＜0.05).Results of PX-478 group showed the opposite trend.PX-478 reversed the effect of myricitrin on the improvement of bone defects in bacterial OM rats.Conclusion Myricitrin may improve bone defect of OM rats by activating the VEGFA/SDF-1/CXCR4 signal pathway.
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Objective To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH).Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table,with 6 rats in each group.The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna.Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein.Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment.Rats in normal group received no treatment.Rats were sacrificed to harvest basilar artery after 7 days.The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining.The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry.Caspase-3 activity was measured by a fluorometric assay.The expressions of Bax and Bcl-2 were determined by Western Blot.Intracellular reactive oxygen species (ROS) was detected by H2DCFDA.Results Compared with normal group,increased thickness of vessel wall (μm:27.72 ± 1.94 vs.18.30 ± 1.10,P＜0.05),decreased lumen area (μm2:26 115 ± 1 991 vs.55 080 ± 2 091,P＜0.05),and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) ％ vs.(5.93 ± 1.53) ％,P＜ 0.05] were found in model group.Compared with model group,decreased thickness of vessel wall (μm:22.55 ± 1.50 vs.27.72 ± 1.94,P＜0.05),increase of lumen area (μm2:48 115 ±2 460 vs.26 115 ± 1 991,P＜0.05),and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) ％ vs.(35.05 ± 5.54) ％,P＜ 0.05] were found in HSH treatment group.Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)％,(163.50 ± 17.02)％,(208.71 ± 26.04)％ and (44.52 ± 9.61) ％ of those of normal group,and the differences of these parameters between model and normal groups were statistically significant (all P＜0.05).Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)％,(119.44 ± 11.50)％,(139.20 ± 18.04)％ and (85.35 ± 13.12)％ of those of normal group,respectively,and the differences of these parameters between HSH treatment and model groups were statistically significant (all P＜0.05).The differences of all measurements between sham and normal groups were not statistically significant.Conclusion The current results demonstrate that HSH attenuates the SAH-induced CVS,alleviates thickness of vessel wall,and increases lumen area via inhibition of VSMCs apoptosis.
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@# Neuropathic pain is an intractable pain condition that initiated or caused by a primary lesion or dysfunction in the nervous system. Because the underlying molecular mechanisms of neuropathic pain are largely unknown, routine pharmacologic treatment is often insufficient. It has become a rather tough problem bothering both physicians and patients. Recently, with the development of molecular biology, the study of neuropathic pain stepped into the post-genomic period which is characterized by study of proteome. A number of proteomic studies have been performed using different animal neuropathy models. The Results of these proteomic approaches are summarized in this review to provide a better overview of proteins that are involved in the mechanisms of neuropathic pain. This might allow a better understanding of the pathogenesis of neuropathic pain, and facilitate the discovery of specific therapies and new treatment target.
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Objective To compare the hemodynamic responses to orotracheal intubation with GlideScope video laryngoscope (GSVL), Macintosh laryngoscope (MDLS) and fiberoptic bronchoscope (FOB) .Methods Sixty ASAⅠorⅡpatients (21 male, 39 female) aged 18-50 yrs weighing 45-90 kg scheduled for elective plastic surgery under general anesthesia with tracheal intubation and mechanical ventilation were randomly divided into 3 groups ( n = 20 each): GSVL group; MDLS group and FOB group. The patients were premedicated with intramuscular scopolamine 0.3 mg. Anesthesia was induced with midazolam 0.05 mg?kg-1 , fentanyl 2?g?kg-1 , propofol 2 mg?kg-1 and vecuronium 0.1 mg?kg-1 and maintained with 1% isoflurane and 60% N2O-40% O2 . Orotracheal intubation was performed at 2 min after intravenous vecuronium. Noninvasive BP and HR were recorded before and after induction of anesthesia, during tracheal intubation and at 1, 2, 3, 4, 5 min after tracheal intubation was completed. The HR and SBP product (RPP) was calculated. Results The intubation time was significantly longer in FOB group than in MDLS group (P