Study Of The Expression Of Autophagy In Diabetic Rats With Pseudomonas Aeruginosa Infection

Objective 1.To study the correlation of Pseudomonas aeruginosa(PA) infection and diabetes with the expression of microtubule-associated protein light chain 3(LC3?)2.To determine the effects of rapamycin on the expression of LC3 ? in wound granulation tissue of diabetic rats with or without PA infection.Methods: Methods: 48 SD(Sprague Dawley) rats(seven weeks, about 200g) were distributed into four groups according to diabetes and PA infection: non-diabetic non-infection group(NDNI), non-diabetic infection group(NDI), diabetic non-infection group(DNI), diabetic infection group(DI), n=12 for each group.Furthermore, each group was randomly assigned into two subgroups according to the treatment of drugs: non-medication group and rapamycin group(n=6 for each subgroup). A full-thickness skin ulcer was made in all rats. Blood biochemistry were detected the day and 7 days after the models were made.Wound subcutaneous tissue was collected when the ulcer was made,and granulation tissue of each group were collected 7 days after the establishment of models. Hematoxylinstaining(HE) was used to detect the morphological changes of wound subcutaneous tissue and granulation tissue in each group. Immunohistochemistry was used to detect the expression of LC3 ? of wound subcutaneous tissue and granulation tissue in each group. More attention was paid to observe the growth of granulation tissue in rats,especially the control of infection in infectious rats, further studying the effects of diabetes, PA infection and rapamycin on the expression of autophgy.Results: There were no differences of the expression of LC3? between the eight subgroups in the subcutaneous tissue. In each group, the expression of LC3 ?was mostly located in the cytoplasm of capillary endothelial cell, neutrophile granulocyte,macrophagocyte in the granulation tissue. Seven days after establishing of models,compared with the non-diabetic non infection group, rats in diabetic non-infection group had a lower expression of LC3?[(0.18±0.015)vs.(0.28±0.030), p=0.001].Compared with the non-diabetic infection group, rats in diabetic infection group had a lower expression of LC3 ? [(0.21±0.020) vs.(0.39±0.030), p=0.000]. Compared with the non-diabetic non-infection group, rats in non-diabetic infection group had a higher expression of LC3?[(0.39±0.030) vs.(0.28±0.030), p=0.001]. Compared with the diabetic non-infection group, rats in diabetic infection group had a higher expression of LC3?[(0.21±0.020) vs.(0.18±0.010), p=0.033].In non-diabetic non-infection group, compared with the corresponding non-medication group, rats in the rapamycin group had a higher expression of LC3?[(0.37 ± 0.030) vs.(0.28 ± 0.030), p=0.004]. In non-diabetic infection group,compared with the corresponding non-medication group, rats in the rapamycin group had a higher expression of LC3?[(0.54±0.030) vs.(0.39±0.030), p=0.000]. In diabetic non-infection group, compared with the corresponding non-medication group,rats in the rapamycin group had a higher expression of LC3 ?[(0.21 ± 0.010) vs.(0.18 ± 0.010), p=0.009]. In diabetic infection group, compared with the corresponding non-medication group, rats in the rapamycin group had a higher expression of LC3 ? [(0.30 ± 0.020) vs.(0.21 ± 0.010), p=0.001]. Futhermore,compared with the non-diabetic non-infection group, rats in the diabetic non-infection group had a lower amplification of the expression of LC3?(22% vs.32%). Compared with the non-diabetic infection group, rats in the diabetic infection group had a lower amplification of the expression of LC3 ?(37% vs.39%). Compared with the non-diabetic non-infection group, rats in the non-diabetic infection group had a higher amplification of the expression of LC3?(39% vs. 32%). Compared with the diabetic non-infection group, rats in the diabetic infection group had a higher amplification of the expression of LC3?(37% vs. 22%).Conclusins: 1.The expression of LC3 ? could be induced by PA infection and inhibited by diabetes in the granulation tissue. 2.The expression of LC3?could be induced by rapamycin in the granulation tissue, which could provide a new way for the treatment of diabetic PA infection.