| Objective:1.In this study, we sought to observe the effect of Astragalus polysaccharidestreatment on intestinal mucosal T lymphocyte subsets, soluble IgA alteration, andpathomorphism changes of scalded rats.2.we sought to determine the functional signature of Astragalus Polysaccharidein intestinal immunity condition of scalded rats.3. we sought to find a theoretical basis for the immunotherapy of severelyburned patients，as to explore the conditioning of the function method of conditioningburn patients intestinal immune and open up new ideas for the prevention andtreatment of burn infection.Methods:The experimental subject consists of130healthy rats wighted (220±20), with amale-female ratio of50-50. The rats were randomly divided into five groups:scaldgroup(Group B,n=30)，scald with low dose Astragalus Polysaccharide (100mg.kg-1)group(Group C,n=30), with Moderate dose Astragalus Polysaccharide (200mg.kg-1)group(Group D,n=30),scold with high dose Astragalus Polysaccharide (300mg.kg-1)group(Group E,n=30)and normal control group(Group A,n=10).For control group,rats were subjected to37℃scald. For the other rats, approximately40%of bodysurface were dehaired with8%sodium sulfide one day before scald. Rats were fastedfor12hours before receiving intraperitoneal anesthesia with5%ketaminehydrochloride in a dose of2ml/kg, subsequently a homemade steam burns controllerwas used to establish scald model. The scald condition was108℃for8sec, with apressure of4Mpa, which could led to30%TBSA Ⅲ degree scald on the back ofeach rat except Group A. According to burn Parkland rehydration formula (4m1kg-1%TBSA-1), all scalded rats were subjected to anti-shock treatment byintraperitoneal injection of Ringer’s lactate immediately then the wound weresmeared with iodophor twice a day. The scalded rats of Group B，Group C，Group Dand Group E were treated with100mg.kg-1,200mg.kg-1,300mg.kg-1of Astragalus Polysaccharide or0.9%saline by intraperitoneal injection, respectively,once a dayand last14day.For Group A group,rats were sacrificed. Then all their samples werecolleted and corresponding values of indexs were set as reference values ofexperimental group. For each scalded group,10rats were sacrificed at the time pointof3,7, or14days and the cecum were taken out for subsequent detection. Intestinaltissues were made into paraffin sections and subjected to H＆E staining for observingmorphologic change. Alteration of T cell subset (CD3十, CD4十, CD8十, CD4十CD25十)in intestinal mucosa was evaluated by Flow Cytometer. Soluble IgA of intestine wasdetected by Enzyme-linked Immuno Sorbent Assay (ELISA).Results：1. The change of intestinal mucosal PP junction T lymphocyte subsets:compare with the Group A，the percentage of CD3+, CD4+and CD4+/CD8+werereduced, while percentage of CD4+CD25+and CD8+increased in the Group B, C, Dand E. Among the experimental groups, the percentage of CD3+, CD4+andCD4+/CD8+increased, while the percentage of CD4+CD25+and CD8+decreased inthe Group C compare with B, Group D compare with C, Group E compare with D.The percentage of group C, D and E treated with Astragalus Polysaccharide were amanner of dose-dependent, compared to the control group A.2. The change of intestinal soluble IgA: the Group B, C, D and E were reducedcompare with Group A. The difference of the Group C compare with B, Group Dcompare with C, Group E compare with D aggravated as the dose of AstragalusPolysaccharide increased (P<0.05).3. The change of intestinal mucosal pathomorphism: for control group, Villiepithelial cells of the intestinal mucosa were integrated and neatly arranged, withoutedema. Few lymphocytes were observed in the lamina propria, while no obviousabnormality was observed in glandular structures under the microscope. At the thirdday, severe damage of intestinal mucosal pathomorphism emerged, as severe edemawas observed in villi, and epithelium was largely necrosised and desquamated.Central chyle vessels and stromal blood vessels were expanded. Abundant neutrophilsinfiltration and glands focal necrosis were observed in the lamina propria. Repair ofintestinal mucosa was visible in scalded rats treated with Astragalus Polysaccharide. Fourteen days after scald, intestinal mucosa of rats treated with high dose AstragalusPolysaccharide (300mg.kg-1) were completely recovered, while no recovery wasobserved in that of the control group.Conclusion:1. Serious scald can destructed cellular immunity and humoral immunefunction in intestinal tract, lead to the damage of the rat intestinal barrier function.2. Intraperitoneal injection of Astragalus polysaccharide could regulate disorderof intestinal immune, promote repair of intestinal mucosa in scald rats, and ultimatelyprotect the intestinal mucosa.3. Astragalus polysaccharide can effectively regulate the intestinal immunefunction, promote intestinal immune function and intestinal mucosal recovery inscalded rats.The protective effect of Astragalus polysaccharide injection in themucosa of the rat small intestine is a dose-dependent manner within a certain doserange. |
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