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2018 Vol. 34, No. 2

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Academician Forum
Regenerative rehabilitation medicine: new requirement, new fusion and new direction
Fu Xiaobing, Cheng Biao
2018, 34(2): 65-68. doi: 10.3760/cma.j.issn.1009-2587.2018.02.001
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Regenerative rehabilitation medicine is not just the combination of two disciplines of regenerative medicine and rehabilitation medicine but the new fusion of two disciplines, and it represents the development direction of regenerative medicine and rehabilitation medicine. With the improvement of people′s demands for tissue injury or disease recovery, new technology and means should be required, and regenerative rehabilitation medicine will emerge and develop rapidly. It will play a key role in repair, regeneration and rehabilitation of diseases or injuries in patients.
Expert Forum
Attaching importance to sepsis-induced acute kidney injury after burn
Yuan Zhiqiang, Peng Yizhi
2018, 34(2): 69-72. doi: 10.3760/cma.j.issn.1009-2587.2018.02.002
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Acute kidney injury (AKI) is a common complication after severe burn, which portends a worse prognosis. Sepsis is the leading etiology of late AKI after severe burn. The pathogenesis of sepsis-induced AKI remains incompletely understood. Although there have been numerous preventive and therapeutic measures evaluated for sepsis-induced AKI, the precise and available intervention in sepsis-induced AKI after burn has yet to be defined.
Burn Infection
Effects of application of citrate anticoagulation in bedside continuous blood purification of severe burn patients with sepsis
Ding Lingtao, Yang Minlie, Zhu Yugang, Yan Jiong, Xie Longwei, Lyu Guozhong
2018, 34(2): 73-77. doi: 10.3760/cma.j.issn.1009-2587.2018.02.003
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Objective To investigate the effects of application of citrate anticoagulation in bedside continuous blood purification (CBP) of severe burn patients with sepsis, so as to provide reference for choosing anticoagulants in CBP of these patients. Methods Thirty severe burn patients with sepsis, conforming to the study criteria, were admitted to our burn intensive care unit from January 2014 to July 2017. Patients were divided into heparin group and citrate group according to computer randomization method, with 15 cases in each group. Patients in two groups all received bedside CBP treatment. Patients in heparin group used local heparin anticoagulation, while patients in citrate group used local citrate anticoagulation. Time of predicted single-time CBP treatment, time of single-time CBP treatment, time of accumulative CBP treatment, and rate of reaching the standard of CBP treatment time were counted. Changes of prothrombin time (PT), activated partial thromboplastin time (APTT), international normalized ratio (INR), fibrinogen, serum procalcitonin, and C-reactive protein (CRP) of patients before and after treatment were monitored. Hemorrhage in wounds, incision on trachea, and arteriovenous intubation point, and other complications during and after CBP treatment were observed. Data were processed with independent sample t test and chi-square test. Results (1) Time of predicted single-time CBP treatment of patients in the two groups was equal. Time of single-time CBP treatment and time of accumulative CBP treatment of patients in citrate group were longer than those in heparin group. Rate of reaching the standard of CBP treatment time of patients in citrate group was significantly higher than that in heparin group (χ2=16.655, P<0.01). (2) There was no statistically significant difference in PT, APTT, INR, fibrinogen, serum procalcitonin, and CRP of patients in the two groups before CBP treatment (t=0.203, -1.006, 0.203, 0.039, -1.591, -0.824, P>0.05). PT and APTT of patients in citrate group after CBP treatment were (14.2±1.6) and (45±7) s, respectively, significantly shorter than (15.5±1.4) and (53±6) s in heparin group (t=2.395, 3.321, P<0.05 or P<0.01). INR of patients in citrate group after CBP treatment was 1.13±0.12, significantly lower than 1.24±0.12 in heparin group (t=2.395, P<0.05). Fibrinogen of patients in citrate group after CBP treatment was (3.5±0.6) g/L, significantly higher than (3.0±0.6) g/L in heparin group (t=-2.427, P<0.05). Serum procalcitonin and CRP of patients in citrate group after CBP treatment were significantly lower than those in heparin group (t=2.520, 2.710, P<0.05). Decreased degree of serum procalcitonin and CRP of patients in citrate group after CBP treatment were (1.8±0.6) ng/mL and (143±69) mg/L, respectively, significantly higher than (0.9±0.6) ng/mL and (95±50) mg/L in heparin group (t=-4.033, -2.170, P<0.05 or P<0.01). (3) During CBP treatment, patients in heparin group experienced 21 times of exacerbation of wound hemorrhage and 10 times of new hemorrhage, including 2 times of hemorrhage at incision on trachea and 8 times of hemorrhage at arteriovenous intubation point. No exacerbation of hemorrhage or new hemorrhage happened in patients of citrate group. After CBP treatment, no electrolyte disturbance happened in patients of heparin group, but 1 patient in citrate group experienced hypocalcemia. Conclusions Application of citrate anticoagulation in bedside CBP of severe burn patients with sepsis shows light impact on systematic coagulation status, and can effectively decrease inflammation reaction of burn sepsis with low rate of hemorrhage.
Clinical characteristics of burn patients infected with Stenotrophomonas maltophilia and antibiotic resistance of the strains
Cheng Lin, Gong Yali, Luo Xiaoqiang, Zhang Cheng, Liu Meixi, Peng Yizhi
2018, 34(2): 78-82. doi: 10.3760/cma.j.issn.1009-2587.2018.02.004
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Objective To investigate the clinical characteristics of burn patients infected with Stenotrophomonas maltophilia (SM) and antibiotic resistance of the strains. Methods Clinical data of burn patients detected with SM, admitted to our unit from July 2011 to July 2017 were retrospectively analyzed. API 20NE bacteria identification panel or fully automated microbial identification instrument was used to identify pathogen. Minimal inhibitory concentration method was used in drug sensitivity test of levofloxacin, compound sulfamethoxazole, minocycline, and cefoperazone/sulbactam. Annual detection of SM, clinical characteristics and prognosis of patients infected with SM, sample source and detection time of SM, detection of the pathogens and antibiotics application of patients before their detection of SM, and drug resistance of SM to the above four antibiotics were analyzed. The results of drug sensitivity test were analyzed by software WHONET 5.5. Results (1) There were totally 119 patients detected with SM, with 11, 12, 21, 22, 28, 13, and 12 cases from 2011 to 2017, respectively. (2) Among patients infected with SM, there were 86 (72.3%) males and 33 (27.7%) females. Patients aged more than or equal to 65 years accounted for 11.8% (14/119). Patients aged more than or equal to 18 years and less than 65 years accounted for 76.5% (91/119). Patients aged less than 18 years accounted for 11.8% (14/119). Patients with scald were the most common (totally 72 cases, accounted for 60.5%), and patients with total burn area less than or equal to 10% total body surface area were the most common (totally 35 cases, accounted for 29.4%), too. The proportion of patients with history of basic disease was 16.8% (20/119), with tracheotomy of 46.2% (55/119), with deep vein catheterization of 47.9% (57/119), with history of staying in intensive care unit (ICU) of 61.3% (73/119). Seventy-five (63.0%) patients were cured. Twenty-four (20.2%) patients were improved. Fourteen (11.8%) patients gave up treatment. Six (5.0%) patients died. (3) SM detected from wounds exudate of patients occupied the highest proportion (58.0%, 69/119), which was followed by samples of sputum (17.6%, 21/119), blood (14.3%, 17/119), wound tissue (4.2%, 5/119), catheter (4.2%, 5/119), and urine (1.7%, 2/119). The detection time of SM was 10 hours to 71 days post admission, with the average time of 12.7 days. (4) The proportion of patients detected with pathogens before detection of SM was 66.4% (79/119), and Acinetobacter baumannii and Staphylococcus aureus occupied high proportion among the strains. (5) The proportion of patients using antibiotics before detection of SM was 91.6% (109/119), and 44.0% (48/109) patients used 3 kinds of antibiotics or more. The antibiotics were applied for 271 times. The most frequently used antibiotics were glycopeptides antibiotics (63 times), followed by carbapenems antibiotics (61 times). (6) The total sensitivity rates of SM to levofloxacin and minocycline in 7 years were high (91.6% and 99.4%, respectively). The total sensitivity rate of SM to cefoperazone/sulbactam was low (52.5%). The total sensitivity rate of SM to compound sulfamethoxazole was high (77.6%), and the annual sensitivity rate was higher than 90.0% in recent 3 years. Conclusions Burn patients infecting SM have high rates of tracheotomy and deep vein catheterization, and most of them stay in ICU and use broad-spectrum antibiotics. SM has high sensitivity to levofloxacin, minocycline, and compound sulfamethoxazole.
Investigation of acquired drug-resistant genes and strains relationship in Pseudomonas aeruginosa isolated from burn patients
Fan Youfen, Cui Shengyong, Zhang Chun, Xu Xiaomin
2018, 34(2): 83-87. doi: 10.3760/cma.j.issn.1009-2587.2018.02.005
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Objective To investigate the acquired drug-resistant genes and strains relationship in 40 strains of Pseudomonas aeruginosa isolated from burn patients. Methods Forty strains of Pseudomonas aeruginosa isolated from burn patients hospitalized in our burn department from January 2014 to December 2015 were selected, with 20 strains from each year. Kirby-Bauer paper disk diffusion method was used to detect sensitivity of the isolated Pseudomonas aeruginosa to 9 kinds of antibiotics of cefotaxime, ceftazidime, cefepime, imipenem, meropenem, gentamicin, amikacin, ciprofloxacin, and levofloxacin. Polymerase chain reaction was applied to detect 9 kinds of acquired β-lactamase antibiotics-resistant genes, outer membrane porin protein oprD2 genes, 12 kinds of acquired aminoglycosides antibiotics-resistant genes, and 6 kinds of acquired disinfectant-resistant genes and genetic marker genes of mobile genetic elements. Among the above genes, positive expression genes were verified by DNA sequencing and comparison. Sequences of twenty-eight acquired drug-resistant genes of the above 40 Pseudomonas aeruginosa strains were analyzed by unweighted pair-group method with arithmetic means cluster analysis. Results Forty strains of Pseudomonas aeruginosa were resistant to the above 9 kinds of antibiotics. Two kinds of acquired β-lactamase antibiotics-resistant genes of blaTEM, blaCARB, 5 kinds of acquired aminoglycosides antibiotics-resistant genes of aac(6′)-Ⅰb, aac(6′)-Ⅱ, ant(2″)-Ⅰ, ant(3″)-Ⅰ, and rmtB, and 3 kinds of acquired disinfectant-resistant genes and genetic marker genes of mobile genetic elements of qacE△1-sul1, merA, and intⅠ1were detected in 40 strains of Pseudomonas aeruginosa with oprD2 gene deficiency. Forty strains aggregated obviously, with a total of 7 gene modes and 3 clones. Drug-resistant gene sequences of strains of number 2 to 4, 6 to 9, 11, 14, and 17 to 39 were similar and with close relationship. Drug-resistant gene sequences of number 12 and 13 strains were similar and with close relationship. Drug-resistant sequences of number 10 and 16 strains were similar and with close relationship. Conclusions Genes of blaTEM, blaCARB, aac(6′)-Ⅰb, aac(6′)-Ⅱ, ant(2″)-Ⅰ, rmtB, qacE△1-sul1, merA, and intⅠ1 were prevalent in these strains of Pseudomonas aeruginosa with oprD2 gene deficiency isolated from burn patients, which may play key roles in resistance of Pseudomonas aeruginosa to β-lactamase, aminoglycoside, and quinolone antibiotics, and the drug-resistant phenotypes were in good coincidence with genotypes. Pseudomonas aeruginosa strains isolated from burn patients were with similar acquired drug-resistant genes and close relationship.
Interventional effects of BAY11-7082 on lung inflammatory response at the early stage and acute lung injury of rats with severe burns
Li Hushan, Yang Xuekang, Hao Zhenming, Lei Jin
2018, 34(2): 88-95. doi: 10.3760/cma.j.issn.1009-2587.2018.02.006
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Objective To investigate the interventional effects of BAY11-7082 on lung inflammatory response at the early stage and acute lung injury of rats with severe burns. Methods (1) Experiment 1. Twelve Sprague-Dawley (SD) rats were divided into control (C) group and burn (B) group according to the random number table, with 3 rats in group C and 9 rats in group B. Rats in group C did not receive any special treatment. Rats in group B were inflicted with 30% total body surface area full-thickness burn on the back. Immediately after injury, rats in group B were intraperitoneally injected with normal saline in the dosage of 50 mL/kg. Abdominal aorta blood and lung tissue samples were collected from three rats in group B at post injury hour (PIH) 12, 24, and 48, respectively. The interleukin-1β (IL-1β) and the IL-18 content of serum were determined with enzyme-linked immunosorbent assay. The mRNA expressions of IL-1β and IL-18 in lung tissue were determined with real-time fluorescent quantitative reverse transcription polymerase chain reaction (RT-PCR). Sample collection and determination in rats of group C were performed as above. (2) Experiment 2. Eighteen SD rats were divided into control (C) group, simple burn (SB) group, and BAY11-7082 intervention (BI) group according to the random number table, with 6 rats in each group. Rats in group C did not receive any special treatment. Rats in groups SB and BI were inflicted with injury as in experiment 1. Immediately after injury, rats in group SB were intraperitoneally injected with normal saline in the dosage of 50 mL/kg, and those in group BI with 8 mg/mL (final mass concentration) BAY11-7082 solution in the dosage of 50 mL/kg. Lung tissue and bronchoalveolar lavage fluid (BALF) of rats with burns were collected at the optimal observation time point concluded from experiment 1. The morphology of lung tissue was observed with hematoxylin-eosin staining, and the pathological damage of lung tissue was graded. The myeloperoxidase (MPO) content of lung tissue and the total protein content of BALF were detected by microplate reader. The protein expressions of nucleotide-binding oligomerization domain-like receptor-3 (NLRP3) and cysteine-aspartic proteases 1 (caspase-1) in lung tissue were determined with Western-blotting. The mRNA expressions of IL-1β, IL-18, NLRP3, and caspase-1 in lung tissue were determined with real-time fluorescence quantitative RT-PCR. Sample collection and determination in rats of group C were performed as above. Data were processed with one-way analysis of variance and LSD-t test. Results (1) The IL-1β and IL-18 content of serum in rats of group B at PIH 12, 24, and 48 were significantly higher than those of group C (t=10.55, 22.05, 12.47, 10.60, 15.22, 11.94, P<0.01). The mRNA expressions of IL-1β and IL-18 in rats of group B at PIH 12, 24, and 48 were significantly higher than those of group C (t=3.62, 7.19, 5.28, 3.20, 12.62, 7.31, P<0.05 or P<0.01). PIH 24 was the optimal observation time point for the following experiment. (2) At PIH 24, compared with those in group SB, the inflammatory cell infiltration and erythrocyte exudates of alveolar in group BI were obviously reduced, and the pulmonary interstitial edema obviously subsided. The pathological damage score of lung tissue in rats of group SB was (9.00±1.00) points, significantly higher than (1.10±0.26) points of group C (t=13.23, P<0.01). The pathological damage score of lung tissue in rats of group BI was (4.93±0.70) points, which was significantly lower than that of group SB (t=5.76, P<0.01) but still significantly higher than that of group C (t=8.84, P<0.01). At PIH 24, the MPO content of lung tissue and the total protein content of BALF in rats of group SB were (1.83±0.15) U/mg and (1.39±0.20) mg/mL, respectively, significantly higher than (0.51±0.10) U/mg and (0.44±0.05) mg/mL of group C (t=12.50, 7.86, P<0.01). The MPO content of lung tissue and the total protein content of BALF in rats of group BI were (0.91±0.12) U/mg and (0.60±0.10) mg/mL, respectively, significantly lower than those of group SB (t=8.36, 6.06, P<0.01). At PIH 24, the protein expressions of NLRP3 and caspase-1 in lung tissue of rats of group SB were 3.10±0.09 and 2.99±0.30, respectively, significantly higher than 1.00 and 1.00 of group C (t=9.06, 11.28, P<0.01). The protein expressions of NLRP3 and caspase-1 in lung tissue of rats of group BI were 1.13±0.08 and 1.81±0.11, respectively, significantly lower than those of group SB (t=7.24, 3.91, P<0.05 or P<0.01). At PIH 24, the mRNA expressions of IL-1β, IL-18, NLRP3, and caspase-1 in lung tissue of rats in group SB were 5.0±0.4, 3.32±0.21, 3.54±0.42, and 6.3±1.0, respectively, significantly higher than 1.0, 1.00, 1.00, and 1.0 of group C (t=13.97, 14.14, 11.78, 7.13, P<0.01). The mRNA expressions of IL-1β, IL-18, NLRP3, and caspase-1 in lung tissue of rats in group BI were 2.6±0.5, 2.00±0.28, 1.39±0.21, and 2.5±0.5, respectively, significantly lower than those of group SB (t=7.11, 5.80, 9.99, 4.65, P<0.05 or P<0.01). Conclusions Applying BAY11-7082 at the early stage of acute lung injury of rats with severe burn can reduce the expression of caspase-1, decrease the levels of IL-1β and IL-18, and decrease the MPO content of lung tissue and the total protein content of BALF through inhibiting NLRP3, thus alleviating the lung inflammatory response and lung injury.
2018, 34(2): 95-95. doi: 10.3760/cma.j.issn.1009-2587.2018.02.101
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2018, 34(2): 101-101. doi: 10.3760/cma.j.issn.1009-2587.2018.02.102
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2018, 34(2): 107-110. doi: 10.3760/cma.j.issn.1009-2587.2018.02.009
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2018, 34(2): 110-110. doi: 10.3760/cma.j.issn.1009-2587.2018.02.103
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2018, 34(2): 110-110. doi: 10.3760/cma.j.issn.1009-2587.2018.02.105
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2018, 34(2): 110-110. doi: 10.3760/cma.j.issn.1009-2587.2018.02.104
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2018, 34(2): 111-113. doi: 10.3760/cma.j.issn.1009-2587.2018.02.010
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2018, 34(2): 114-116. doi: 10.3760/cma.j.issn.1009-2587.2018.02.011
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2018, 34(2): 117-119. doi: 10.3760/cma.j.issn.1009-2587.2018.02.012
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2018, 34(2): 120-121. doi: 10.3760/cma.j.issn.1009-2587.2018.02.013
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2018, 34(2): 122-123. doi: 10.3760/cma.j.issn.1009-2587.2018.02.014
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2018, 34(2): 123-124. doi: 10.3760/cma.j.issn.1009-2587.2018.02.015
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2018, 34(2): 125-126. doi: 10.3760/cma.j.issn.1009-2587.2018.02.016
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2018, 34(2): 126-127. doi: 10.3760/cma.j.issn.1009-2587.2018.02.017
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2018, 34(2): 128-128. doi: 10.3760/cma.j.issn.1009-2587.2018.02.018
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Original Article
Effects of denatured collagen type Ⅰ on differentiation of human fibroblasts into myofibroblasts
Wang Zhiyong, Wang Xiqiao, Liu Yingkai, Yuan Bo, Dong Jiaoyun, Song Fei, Jiang Yuzhi, Lu Shuliang
2018, 34(2): 96-101. doi: 10.3760/cma.j.issn.1009-2587.2018.02.007
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Objective To investigate the effects of denatured collagen type Ⅰ on differentiation of human fibroblasts into myofibroblasts. Methods A small amount of normal skin donated by burn patients undergoing scar surgery was collected. Human fibroblasts were obtained by method of explant culture and then sub-cultured. The fourth passage of cells were used in the following experiments. (1) Fibroblasts were divided into normal collagen group and denatured collagen group according to the random number table, with 10 wells in each group. Fibroblasts in normal collagen group were cultured on normal collagen type Ⅰ coated coverslips. Fibroblasts in denatured collagen group were cultured on denatured type Ⅰ collagen coated coverslips. Expression of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemical method, and the percentage of PCNA positive cells was calculated. (2) Another batch of fibroblasts were grouped and treated as in (1), with 12 wells in each group. Proliferation activity of cells was determined with methyl-thiazolyl-tetrazolium colorimetry method. (3) Another batch of fibroblasts were grouped and treated as in (1), and the microfilament morphology of cells was observed by rhodamine-phalloidin staining. (4) Another batch of fibroblasts were grouped and treated as in (1). Expression of α smooth muscle actin (α-SMA) of cells was detected by immunohistochemical method, and expression of OB-cadherin of cells was detected by immunofluorescence method. (5) Another batch of fibroblasts were divided into normal collagen, denatured collagen, and common coverslips groups according to the random number table, with 6 wells in each group. Fibroblasts in normal collagen and denatured collagen groups were treated as in (1), while fibroblasts in common coverslips group were cultured on coverslips without collagen coating. Expressions of α-SMA and OB-cadherin of cells were determined with Western blotting. (6) Another batch of fibroblasts were grouped and treated as in (5), and then the mRNA expressions of collagen type Ⅰ, collagen type Ⅲ, and α-SMA of cells were determined with real-time fluorescent quantitative reverse transcription polymerase chain reaction. Data were processed with t test, one way analysis of variance, and least-significant difference test. Results (1) The percentage of PCNA positive cells in denatured collagen group was (83±9)%, significantly higher than (29±9)% in normal collagen group (t=13.53, P<0.01). (2) The proliferation activity of fibroblasts in denatured collagen group was 0.32±0.06, significantly higher than 0.25±0.05 in normal collagen group (t=3.06, P<0.01). (3) The microfilament of fibroblasts in normal collagen group was arranged vertically and in parallel way, paralleling the long axis of cells. The microfilament of fibroblasts in denatured collagen group was denser and thicker. (4) Most fibroblasts in normal collagen group showed long shuttle-like shape typically. Morphology of fibroblasts in denatured collagen group changed, and cells were obviously spreading. Expressions of α-SMA and OB-cadherin of fibroblasts in denatured collagen group were stronger than those in normal collagen group. (5) Expressions of α-SMA of fibroblasts in denatured collagen, normal collagen, and common coverslips groups were respectively 1.69±0.41, 0.89±0.27, and 1.46±0.42. Expression of α-SMA of fibroblasts in denatured collagen group was significantly higher than that in normal collagen group (P<0.01). Expressions of OB-cadherin of fibroblasts in denatured collagen, normal collagen, and common coverslips groups were respectively 5.17±0.28, 2.21±0.10, and 4.01±0.56. Expression of OB-cadherin of fibroblasts in denatured group was significantly higher than that in normal collagen group (P<0.01). (6) There was no significant difference in mRNA expression of collagen type Ⅰ of fibroblasts in denatured collagen, normal collagen, and common coverslips groups (F=2.71, P>0.05). The mRNA expressions of collagen type Ⅲ and α-SMA of fibroblasts in normal collagen group were significantly lower than those in denatured collagen group (P<0.01). Conclusions Denatured collagen type Ⅰ may influence the activity of fibroblasts, thus inducing fibroblasts differentiating into myofibroblasts.
Mechanism of cell autophagy for regulating skeletal muscle wasting of rats after severe burns
Zhao Yannan, Li Zongyu, Kan Kan, Su Haitao
2018, 34(2): 102-106. doi: 10.3760/cma.j.issn.1009-2587.2018.02.008
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Objective To investigate the mechanism of cell autophagy for regulating skeletal muscle wasting of rats after severe burns. Methods Seventy-two Sprague-Dawley rats were collected and divided into sham injury group, simple burn group, burn+ phosphate buffer solution (PBS) group, and burn+ 3-methyladenine (3-MA) group according to the random number table, with 18 rats in each group. Rats in simple burn group, burn+ PBS group, and burn+ 3-MA group were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns). Rats in sham injury group were sham injured. Immediately after burns and fluid resuscitation, rats in burn+ PBS group were intraperitoneally injected with 1 mL PBS, and rats in burn+ 3-MA group were intraperitoneally injected with 1 mL 3-MA (125 g/L). On post injury day 3 and 7, the weights of anterior tibial muscle of right hind limbs and body of rats were measured to calculate percentage of anterior tibial muscle of right hind limbs weight. Protein expressions of microtubule related protein 1 light chain 3A (LC3A) and Beclin-1 of anterior tibial muscle were observed by immunofluorescence method and detected by Western blotting, and ratio of microtubule related protein 1 LC3A-Ⅱ to LC3A-Ⅰ was calculated. Data were processed with analysis of variance of factorial design, one-way analysis of variance, t-test and Bonferroni correction. Results On post injury day 3 and 7, percentages of anterior tibial muscle of right hind limbs weight of rats in simple burn group were (0.148±0.009)% and (0.134±0.018)%, respectively, which were significantly lower than those in sham injury group [(0.203±0.009)%, (0.181±0.015)%, t=10.585, 4.913, P<0.01]. Percentages of anterior tibial muscle of right hind limbs weight of rats in burn+ 3-MA group were (0.187±0.004)% and (0.192±0.009)%, respectively, which were obviously higher than those in burn+ PBS group [(0.162±0.005)%, (0.167±0.005)%, t=9.564, 5.948, P<0.01]. On post injury day 3 and 7, protein expressions of Beclin-1 and microtubule related protein 1 LC3A of anterior tibial muscle of rats in simple burn group were significantly higher than those in sham injury group, while protein expressions of Beclin-1 and microtubule related protein 1 LC3A of anterior tibial muscle of rats in burn+ 3-MA group were significantly lower than those in burn+ PBS group. Ratios of microtubule related protein 1 LC3A-Ⅱ to LC3A-Ⅰ of anterior tibial muscle of rats in simple burn group were significantly higher than those in sham injury group (t=3.461, 3.353, P<0.05), while ratios of microtubule related protein 1 LC3A-Ⅱ to LC3A-Ⅰ of anterior tibial muscle of rats in burn+ 3-MA group were significantly lower than those in burn+ PBS group (t=3.129, 3.977, P<0.05). Conclusions Cell autophagy induced by severe burns is involved in the process of skeletal muscle wasting of rats, and inhibition of cell autophagy may contribute to the remission of skeletal muscle wasting of rats induced by burns.

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