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Knee osteoarthritis (KOA) is one of the most common degenerative joint diseases in the elderly worldwide. The primary lesion in patients with KOA is the degeneration of articular cartilage. This study aimed to observe the biological effects of cyclic negative pressure on C28/I2 chondrocytes and to elucidate the underlying molecular mechanisms. We designed a bi-directional intelligent micro-pressure control device for cyclic negative pressure intervention on C28/I2 chondrocytes. Chondrocyte vitality and proliferation were assessed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays. The extracellular matrix was analyzed using real-time fluorescence quantitative polymerase chain reaction (PCR) and western blot, while the molecular mechanism of the chondrocyte response to cyclic negative pressure was explored through mRNA sequencing. Experimental data demonstrated that cyclic negative pressure promoted chondrocyte proliferation and upregulated the expression of chondrocyte-specific protein, namely the collagen type II alpha 1 chain (COL2A1) protein, and the transcription factor SRY-box transcription factor 9 (SOX9). Additionally, RNA sequencing analysis revealed that the gene levels of insulin-like growth factor 2 (IGF-2) and early growth response 1 (EGR-1) were significantly elevated in the cyclic negative pressure group. This study demonstrates that cyclic negative pressure stimulates the proliferation of C28/I2 chondrocytes by promoting the expression of EGR-1 and IGF-2. This new discovery may provide novel insights into cartilage health and KOA prevention.

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Background: Exercise is recommended as the first-line management for knee osteoarthritis (KOA); however, it is difficult to determine which specific exercises are more effective. This study aimed to explore the potential mechanism and effectiveness of a leg-swinging exercise practiced in China, called 'KOA pendulum therapy' (KOAPT). Intraarticular hydrostatic and dynamic pressure (IHDP) are suggested to partially explain the signs and symptoms of KOA. As such this paper set out to explore this mechanism in vivo in minipigs and in human volunteers alongside a feasibility clinical trial. The objective of this study is 1) to analyze the effect of KOAPT on local mechanical and circulation environment of the knee in experimental animals and healthy volunteers; and 2) to test if it is feasible to run a large sample, randomized/single blind clinical trial. Methods: IHDP of the knee was measured in ten minipigs and ten volunteers (five healthy and five KOA patients). The effect of leg swinging on synovial blood flow and synovial fluid content depletion in minipigs were also measured. Fifty KOA patients were randomly divided into two groups for a feasibility clinical trial. One group performed KOAPT (targeting 1000 swings/leg/day), and the other performed walking exercise (targeting 4000 steps/day) for 12 weeks with 12 weeks of follow-up. Results: The results showed dynamic intra-articular pressure changes in the knee joint, increases in local blood flow, and depletion of synovial fluid contents during pendulum leg swinging in minipigs. The intra-articular pressure in healthy human knee joints was -11.32 ± 0.21 (cmH2O), whereas in KOA patients, it was -3.52 ± 0.34 (cmH2O). Measures were completed by 100% of participants in all groups with 95-98% adherence to training in both groups in the feasibility clinical trial. There were significant decreases in the Oxford knee score in both KOAPT and walking groups after intervention (p < 0.01), but no significant differences between the two groups. Conclusion: We conclude that KOAPT exhibited potential as an intervention to improve symptoms of KOA possibly through a mechanism of normalising mechanical pressure in the knee; however, optimisation of the method, longer-term intervention and a large sample randomized-single blind clinical trial with a minimal 524 cases are needed to demonstrate whether there is any superior benefit over other exercises. The translational potential of this article: The research aimed to investigate the effect of an ancient leg-swinging exercise on knee osteoarthritis. A minipig animal model was used to establish the potential mechanism underlying the exercise of knee osteoarthritis pendulum therapy, followed by a randomised, single-blind feasibility clinical trial in comparison with a commonly-practised walking exercise regimen. Based on the results of the feasibility trial, a large sample clinical trial is proposed for future research, in order to develop an effective exercise therapy for KOA.

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The aim of this study was to examine whether administration of valproic acid (VPA), a histone deacetylase inhibitor, inhibits proinflammatory mediators and ameliorate visceral vasopermeability both in a rat model of major burn, and also in rat cultured endothelial cells stimulated with permeability evoking mediators. SD rats were subjected to a 50% TBSA full-thickness scald injury, and treated with either saline or VPA (300 mg/kg) intraperitoneally. Pulmonary vascular endothelial growth factor (VEGF), myeloperoxidase (MPO), pulmonary microvascular permeability, water content, and acetylation of histone H3K9 of lungs were evaluated. In addition, pulmonary microvascular endothelial cells (PMECs) from male SD rats were cultured. With then, MPO, VEGF, histone acetylation, and the permeability of PMECs were investigated. Lethal scald injury resulted in a significant increase in microvascular permeability and water content of lung, accompanied by a significant elevation of the content of VEGF and activity of MPO, and a decrease of histone acetylation. VPA treatment significantly alleviated the microvascular permeability and water content of lung, lowered the levels of VEGF and MPO, and promoted acetylation of histone H3K9 following scald injury. Moreover, VPA reduced permeability of monolayer PMECs subjected to scald serum challenge, reduced the level of MPO and VEGF in supernatants, and promoted acetylation of histone H3K9 in PMECs. These results indicated that VPA can protect pulmonary microvascular endothelial barrier, alleviate proinflammatory mediators-evoked vascular hyperpermeability and tissue edema and improve the survival rate of rats subjected to lethal scald injury.

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A pH-sensitive copolymer PAsp(DIP)-b-PAsp(MEA) (PDPM) was synthesized and self-assembled to micelle loading chemotherapeutic drug doxorubicin (DOX) and introducing a gold nanocage structure for photothermo-chemotherapy and photoacoustic imaging. After further surface modification with polyethylene glycol (PEG), the DOX-loaded pH-sensitive gold nanocage (D-PGNC) around 100 nm possessed a uniform spherical structure with a pH-sensitive core of PAsp(DIP) incorporating DOX, an interlayer crosslinked via disulfide bonds and decorated with discontinuous gold shell, and a PEG corona. The release of DOX from D-PGNC was turned off in bloodstream due to the cross-linking and gold decoration of interlayer but turned on inside tumor tissue by multiple stimulations including the low pH value of tumor tissue (≈6.8), the low lysosomal pH value of cancer cells (≈5.0) and near-infrared (NIR) irradiation. The gold nanocage receiving NIR irradiation could generate hyperthermia to ablate tumor cells. Moreover, the photoacoustic (PA) imaging and analysis of DOX fluorescence inside tumor tissue demonstrated that photothermal therapy based on the gold nanocage effectively drove DOX penetration inside tumor. Owing to the rapid intratumor release and deep tissue penetration of drug favorable for killing cancer cells survived the photothermal therapy, the combined therapy based on D-PGNC via NIR irradiation exhibited a synergistic treatment effect superior to either chemotherapy or NIR-induced photothermal therapy alone. STATEMENT OF SIGNIFICANCE: The novelty of the manuscript is its multifunctional system which incorporates anticancer drug DOX in its pH-sensitive core and acts as a template to introduce a gold nanocage. This nanomedicine presents potentials of sequestrating drug molecules in blood circulation but releasing them inside tumor upon responding to the acidic microenvironment therein. Exposure to NIR laser further expedited the pH-sensitive DOX release and promoted DOX penetration into cancer tissues far away from the vasculature. Consequently, the combined photothermo-chemotherapy showed synergistic effects to inhibit tumor growth and prolong animal survival in nude mice bearing human SKOV-3 ovarian tumor. Moreover, owing to the decoration with gold nanocage, the tumor accumulation and intratumor diffusion of the micelles were easily trackable using photoacoustic imaging.

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OBJECTIVE: To study the early effects of ulinastatin (UTI) by aerosol inhalation on rabbits with acute lung injury induced by LPS, and to observe the early diagnostic value of 320-slice CT. METHODS: According to the random number table, 18 specific pathogen free New Zealand white rabbits were divided into normal control group, group LPS, and group UTI, with 6 rabbits in each group. Rabbits in group LPS and group UTI were given 15 mL lipopolysaccharide (0.16 mg/mL, in the dose of 0.8 mg/kg) to reproduce acute lung injury model. Rabbits in normal control group were given equal volume of normal saline. Rabbits in UTI group were treated with UTI by aerosol inhalation for 10 min from 30 min after injury, while those in the other two groups received normal saline by aerosol inhalation. Rabbits in group LPS and group UTI were scanned by 320-slice CT at post injury hour (PIH) 6 and 24. After anesthesia, heart blood of rabbits in group LPS and group UTI was collected for determination of serum levels of TNF-α, IL-1ß, and IL-6 by ELISA at PBH 24. At PBH 24, lung tissue samples were harvested for gross observation and histomorphological observation, measurement of wet to dry weight ratio, and detection of mRNA expressions of TNF-α, IL-1ß, and IL-6 with RT-PCR. Above-mentioned indexes were detected in rabbits of normal control group at the same time point. Data were processed with one-way analysis of variance and LSD test. RESULTS: (1) CT perfusion (CTP) image. The difference in CTP image of rabbits in group LPS between PBH 6 and PBH 24 was obvious, while that of rabbits in group UTI and normal control group was slight and not obvious respectively. (2) There were statistically significant differences in the serum levels of TNF-α, IL-1ß, and IL-6 of rabbits among the three groups (with F values from 843.896 to 2 564.336, P values below 0.001). The serum levels of TNF-α, IL-1ß, and IL-6 in group UTI were respectively (225 ± 9), (190 ± 8), (227 ± 6) pg/mL, and they were significantly lower than those in group LPS [(710 ± 25), (306 ± 16), (422 ± 16) pg/mL, with P values below 0.001]. (3) Gross observation. In group UTI, the degrees of pulmonary edema and pneumorrhagia of rabbits were lower than those in group LSP. (4) Histological observation. The damage to alveolar wall in group UTI was milder, and alveolar space hemorrhage and inflammatory cell infiltration were significantly less intense as compared with those in group LPS. (5) Compared with that in normal control group, the wet to dry weight ratio of lung tissue was increased in group LPS (P < 0.001). The wet to dry weight ratio of lung tissue in group UTI was significantly higher than that in normal control group but lower than that in group LPS (P values below 0.001). (6) There were statistically significant differences in mRNA levels of TNF-α, IL-1ß, and IL-6 in lung tissue of rabbits among three groups (with F values from 24.700 to 69.538, P values below 0.001). The mRNA levels of TNF-α, IL-1ß, and IL-6 in lung tissue of rabbits in group UTI were respectively (31.4 ± 2.7), (21.2 ± 3.3), (13.9 ± 2.4) pg/mL, which were significantly lower than those in group LPS [ (58.5 ± 10.0) , (35.1 ± 5.1), (20.7 ± 3.2) pg/mL, P values below 0.001]. CONCLUSIONS: UTI by aerosol inhalation can mitigate pulmonary edema and hemorrhage and inhibit inflammatory response. 320-slice CT may be used for detection of early lung injury.

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OBJECTIVES: The regulatory mechanism of microRNA (miRNA) within macrophage innative response to Mycobacterium tuberculosis infection is not clear yet. METHODS: The expression profile of cellular miRNAs during Mycobacterium bovis BCG infection was analyzed by using microarray. The expression of miR-146a was evaluated in alveolar macrophages (AMs) of bronchoalveolar lavage solution from pulmonary tuberculosis (PTB) patients and healthy volunteers respectively. Inhibitor experiment and promoter analysis were used to investigate the pathway involved in the induction of miR-146a. Examination of miR-146a function in macrophages was performed by overexpression and inhibition of miR-146a. RESULTS: Among the altered miRNAs, 10 were downregulated whereas 8 were upregulated in M. bovis BCG-infected macrophage. MiR-146a was high expressed in cultured macrophage respond to M. bovis BCG but decreased in AMs of PTB patients, and stated a negative correlation with degree of smear-positive. Nuclear factor-κB pathway was required for the induction of miR-146a. Overexpression of miR-146a results in significant reduction of PTGS2 and enhanced the killing ability of THP-1 cells to intracellular M. bovis BCG, and miR-146a negatively regulated TNF-α release in feedback manner. CONCLUSIONS: Our findings suggest an important role of miR-146a in M. bovis BCG infection that helps to fine-tune the inflammation response of MTB infection.

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BACKGROUND: Helicobacter pylori is a major human pathogenic bacterium in the gastric mucosa, but to date the regulatory mechanism of the H. pylori-induced inflammatory response is not clear. MicroRNAs have recently emerged as key post-transcriptional regulators of gene expression. We have previously reported that miR-146a negatively regulates the H. pylori-induced inflammatory response, but its molecular mechanism is just beginning to be explored. Our aim was to further explore the key targets of miR-146a and its role of regulation in H. pylori infection. METHODS: The potential targets of miR-146a were screened through bioinformatic approaches and identified by luciferase reporter assays and green fluorescent protein (GFP) repression experiments. Overexpression and inhibition of miR-146a were used to examine the impacts of miR-146a on its target gene, determined by quantitative real-time polymerase chain reaction (PCR) and western blotting. RESULTS: Prostaglandin endoperoxide synthase 2 (PTGS2) is a target gene of miR-146a, and miR-146a decreased PTGS2 expression by degradation of its mRNA, suggesting that the miR-146a-mediated inhibition is a post-transcriptional event. Furthermore, miR-146a and PTGS2 were significantly increased in H. pylori -infected human gastric epithelial cells. Overexpression of miR-146a resulted in significantly reduced PTGS2 production induced by H. pylori infection. CONCLUSIONS: These results suggest that miR-146a may be involved in negatively regulating H. pylori-induced PTGS2 expression in human gastric epithelial cells.

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BACKGROUND: The aim of this study was to examine whether administration of ulinastatin inhibits pro-inflammatory mediators and ameliorate visceral vasopermeability both in a rat model of major burn, and also in rat cultured endothelial cells stimulated with permeability-evoking mediators. METHODS: Plasma levels of tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), myeloperoxidase (MPO), microvascular permeability, and water content of organ tissues were evaluated in a rodent model of a 55% TBSA full-thickness scald injury. Microvascular permeability was also evaluated with a cultured pulmonary microvascular endothelial cells (PMECs) monolayer after stimulation with trypsin, bradykinin, histamine, prostaglandin E2 and burn serum. RESULTS: We found that the plasma levels of TNF-α, CRP, MPO, vascular permeability and water content of heart, lung, kidney, and small intestine tissues were significantly increased in animals after scald injury, and administration of ulinastatin lowered the levels TNF-α, CRP, MPO, vascular permeability and water content of those organ tissues. In vitro, ulinastatin lowered the levels of TNF-α, interleukin-6 (IL-6) and attenuated permeability in PMEC monolayers after being stimulated with burn serum or trypsin, but not by bradykinin, histamine or prostaglandin E2. CONCLUSIONS: These results indicate that ulinastatin attenuates the systemic inflammatory response and visceral vasopermeability both in vivo and vitro, and may serve as a therapeutic agent for prevention of systemic inflammatory response and leakage of fluid into tissue after major burn.

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The objective of this study is to investigate the effect of oral feeding of an electrolyte glucose mosapride solution for resuscitation in dogs with shock after a 35% TBSA full-thickness burn and the effect of mosapride on gastric emptying time. Eighteen male Beagle dogs were randomly divided into intravenous isotonic solution group, intragastric hypertonic solution group, and mosapride group after they were subjected to a 35% TBSA full-thickness flame injury. In intravenous isotonic solution group (I group), isotonic electrolyte glucose solution was given through vein with adoption of the Parkland formula. The resuscitation fluid in intragastric hypertonic solution group (H group) and mosapride group (M group) consisted of 1.8% NaCl and 5% glucose, the total fluid volume was one half of that for I group, and it was given in divided amount every 2 hours. Mosapride was added to the resuscitation fluid in mosapride group. Fluid replacement was begun 30 minutes after the injury in all the groups. Mean arterial pressure (MAP), cardiac output index (CI), intrathoracic blood volume index (ITBI), blood volume (BV), serum sodium concentration, intestinal mucosal blood flow (IMBF), gastric emptying, and serum motilin levels were determined at different time points. The urinary output of all animals was measured immediately after burn upto 360 minutes postburn. CI, ITBI, BV, and IMBF were all decreased obviously after burn. In I group and M group, CI, ITBI, BV, and IMBF were increased gradually after resuscitation, and they were significantly higher than that of H group (P < .05). MAP in all three groups was lowered significantly and then gradually recovered, showing no significant difference among groups. The urinary output in M group was similar to that in I group (P > .05), and it was higher than that in H group (P < .05). Serum sodium level in H group and M group increased in varying degrees and were markedly higher compared with the I group (P < .05). Postburn gastric emptying in H group was much more delayed (P < .05), but in M group it was much faster. Motilin level in the latter group also increased gradually postburn and was markedly higher than that of the other two groups (P < .05). At the early stage of 35% TBSA third-degree burns, gavage of 1.8% hypertonic electrolytes glucose ends in slow gastric emptying, resulting in delayed recovery from shock. When a prokinetic drug mosapride was added to the solution, gastric emptying could be accelerated and a resuscitation effect similar to that of intravenous isotonic fluid resuscitation can be achieved, while total fluid volume can be decreased by half.

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BACKGROUND: To observe the influence of carbachol on inflammatory cytokine release and its protective role on organ function in rat endotoxemia model, and, furthermore, to investigate its receptor mechanism in rat peritoneal macrophages in vitro. METHODS: In the animal experiments, Wistar rats were subjected to lipopolysaccharide (LPS) injection (5 mg/kg body weight) to establish an endotoxemia animal model, and carbachol/nicotine was given 15 minutes after LPS injection. Serum contents of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 were determined with enzyme-linked immunosorbent assay 4 hours after LPS injection. Plasma alanine aminotransferase, creatine kinase-MB, and diamine oxidase contents were detected 24 hours after LPS injection. In cell experiments, rat peritoneal macrophages were collected and initially pretreated with atropine (muscarinic cholinergic receptor antagonist) or α-Bungarotoxin (an antagonist that specifically binds α7 subunit of nicotinic cholinergic receptor), then with carbachol or nicotine, and finally stimulated with LPS. Contents of TNF-α, IL-6, and IL-10 in supernatant were assayed by enzyme-linked immunosorbent assay. Furthermore, macrophages were exposed to nicotine and carbachol of high concentration and then stained with fluorescein isothiocyanate-labeled α-bungarotoxin and observed with fluorescent confocal microscopy. RESULTS: Carbachol inhibited expression of TNF-α and IL-6 after LPS injection and had no significant effect on IL-10 in rat endotoxemia model. It also inhibited the increase of plasma alanine aminotransferase and creatine kinase-MB contents whereas restored the inhibited plasma diamine oxidase activity. Cell experiments also showed that increases of TNF-α and IL-6 after LPS stimulation could be significantly inhibited by carbachol or nicotine, whereas IL-10 was not apparently altered. Atropine did not downregulate the inhibitive effects of both carbachol and nicotine, whereas α-bungarotoxin significantly downregulated these effects. Fluorescent confocal microscopy showed that nicotine and carbachol pretreatment markedly reduced the intensity of binding between fluorescein isothiocyanate-labeled α-bungarotoxin and macrophages. CONCLUSION: The results suggested that both carbachol and nicotine play a role in the anti-inflammatory process and organ function protection through the α7 subunit of nicotinic cholinergic receptor.

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OBJECTIVE: To investigate the effects of oral rehydration with glucose electrolyte solution(GES) on intestinal ischemia injury in 40% blood volume loss in rats. METHODS: SD rats were randomly divided into three groups (n=24): oral rehydration without hemorrhage (GES), hemorrhage without oral rehydration (HS), hemorrhage resuscitated with oral GES(HS + GES). About 4% of total blood volume was bled from the right common carotid artery of rats to produce a model of hemorrhagic shock. GES, which volume was three times of blood loss was given to GES group and HS + GES group in 0.5 h, 1 h and 6 h by a gastric tube post bleeding. The intestinal blood flow(IBF) were measured by laser Doppler at 2 h, 4 h and 24 h post hemorrhage. Animals were sacrificed, and specimens of intestinal tissue was taken for evaluation of Na+ -K+ -ATPase, diamine oxidase (DAO) and the rate of tissue water content, and assessment of the intestinal pathological changes. RESULTS: The IBF and the activity of Na+ -K+ -ATPase in HS+ GES group were dramatically higher than those in HS group (P < 0.05), and lower than those in GES group (P < 0.05). The water content of intestinal tissue in HS group were dramatically higher than those in GES group (P < 0.05), and lower than those at 2 h and 4 h, but dramatically higher than those at 24 h in HS + GES group. The activity of DAO at 24 h in HS+ GES group was higher than those in HS group (P < 0.05), and lower than those in GES group (P < 0.05). Less edema and hyperemia were found in HS + GES group than those in HS group at 24 h after bleeding. CONCLUSION: It is indicated that oral rehydration alleviate edema and ischemia injury in gut by increasing intestinal blood flow and the activity of Na+ -K+ -ATPase and DAO in the resuscitation of hemorrhagic shock.

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We investigated the effect of carbachol (CAR, a cholinergic agent) on intestinal mucosal blood flow (IMBF), activity of Na-K-ATPase, expression of aquaporin (AQP)-1, and intestinal absorption rate during enteral resuscitation of a 35%TBSA scald in rats with a glucose electrolyte solution (GES). One hundred male Wistar rats were randomly divided into five groups: sham scald (N group); scald without fluid resuscitation (S group); scald resuscitated with enteral GES alone (GES group); scald resuscitated with enteral CAR alone (CAR group); and scald resuscitated with enteral CAR plus GES (GES/CAR group). The rats were inflicted 35%TBSA third degree of scald injury on the back with boiling water (100 degrees C, 15 seconds) in all groups, except the sham scald group. A catheter was inserted into the proximal duodenum (5 cm distal to pylorus) and distal ileum (5 cm proximal to cecum), of each rats through laparotomy, thus a segment of intestine was virtually isolated to form a loop for inlet and outlet of introduced fluid. In N, GES, and GES/CAR groups, fluids were introduced 30 minutes after scald injury. The speed of fluid infusion was 4 ml/kg/1%TBSA for 4 hours. CAR (60 microg/kg) was injected into the intestinal lumen at 30-minute after injury in CAR and GES/CAR groups. At 2 and 4 hours after scald, intestinal absorption rate of water and Na, and IMBF were determined, respectively. Then, animals were killed, and specimens of intestinal tissue were obtained for the determination of the activity of Na-K-ATPase, hematoxylin-eosin coloring, and expression of AQP-1. The intestinal absorption rate was reduced markedly in GES group compared with sham scald group at 2 and 4 hours after scald, and absorption rate of small intestine in GES/CAR was significantly higher than that in GES group (P < .05). It was also found that there was significant decrease in IMBF, activity of Na-K-ATPase, and expression of AQP-1 in scald group compared with the sham group. However, in GES/CAR group, the levels of these parameters were significantly increased compared with scald groups (P < .05). The results indicate that CAR promotes intestinal absorption rate of water and Na by improving IMBF, ATPase activity, and AQP-1 expression in gut mucosa during resuscitation with enteral GES of burn shock in rats.

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In the title coordination polymer, [Sm(C(10)H(13)N(2)O(8))(H(2)O)](n), each samarium(III) centre is nine-coordinated by six O and two N atoms from three N'-(carboxy-meth-yl)ethyl-enediamine-N,N,N'-triacetate ligands and one O atom of a water mol-ecule, forming polymeric chains running parallel to the a axis. The packing is governed by inter-molecular O-H⋯O hydrogen-bonding inter-actions.

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OBJECTIVE: To investigate the influence of escharectomy at different time-points after burn injury on the lymphocyte apoptosis and the antigen presentation function of monocytes in peripheral blood of scalded rats. METHODS: One hundred and thirty-six Wistar rats were randomly divided into normal control ( C,n = 8 ), scald ( S, n = 64,without treatment after scald) , A ( n = 40, with escharectomy at 36 post-burn hour( PSH) ) , B ( n = 24, with escharectomy at 72 PSH ) groups. The rats in A , B, S groups were inflicted with 30% TBSA full-thickness scald. The rats in S group were sacrificed on 6,12,24,72,120,168,216, 288 PSH, while those in A and B groups were sacrificed at 72 -288 PSH, 168 -288PSH, respectively. The rats in C group were also sacrificed as control. The apoptotic rate of peripheral lymphocytes, the positive expression rate of MHC- II in mononuclear cells, the changes in concentration of IL-4 and gamma-IFN were determined in each group. The correlation of above indices were also analyzed. RESULTS: (1) The apoptotic rate of peripheral lymphocyte in S group were increased dramatically at 6PSH, peaking at 24 PSH( 18. 19+/-1.42% ) , then decreasing gradually, reaching the lowest level at 72 PSH(8. 25+/-0.56% ) , then it increased gradually again, approaching almost the peak value at 288 PSH( 17.81 +/- 1.99% ). The values were all obviously higher than those in C group( P <0.05). The apoptotic rates of peripheral lymphocyte in A and B groups were evidently lower than that in S group ( P <0. 01). (2) The positive expression rate of MHC-II in monocyte was decreased sharply at 6 PSH, and it was 20% lower than that in C group (37. 2 +/- 2. 4% ) at 24 PSH. It then increased gradually, but it was significantly lower than that in A, B groups at 288 PSH (18. 8 +/-2. 8, P <0.01). (3) The plasma level of y-IFN in S group increased gradually from 6 PSH on, peaking at 24 PSH(440. 8 +/-25. 1 )ng/L,then decreasing gradually , and it reached the lowest level at 288 PSH (51.3 +/-37.0) ng/L. The IL-4 level in S group was increased gradually ,peaking at 288 PSH (78. 1+/-2. 8) ng/L. (4) There was negative correlation between the expression rate of MHC- II in S group and IL-4/gamma-IFN ratio in escharectomy groups during 72 - 288 PSH ( r = - 0. 96, P < 0. 05). CONCLUSION: Eacharectomy after scald can inhibit peripheral lymphocyte apoptosis, slow down the insertional tendency of IL-4/gamma-IFN , and ameliorate the antigen presentation function of monocytes. Moreover, escharectomy during shock stage can markedly promote the immune function of monocytes.

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