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Shi-Liang Wang

Publications and source records attributed to Shi-Liang Wang.

7 recordsLinked to original sources

[Effects of enteral supplementation with glutamine on mitochondria respiratory function of intestinal epithelium in burned rats].

OBJECTIVE: To investigate the effects of enteral supplementation with glutamine on mitochondria respiratory function of intestinal epithelium in burned rats. METHODS: Wistar rats inflicted with 30% total body surface area (TBSA) full thickness thermal injury were randomly divided into three groups, i.e. burn with enteral nutrition (EN), burn with glutamine treatment (GLN), and normal control (C) groups. Burned rats were infused 732.2 kJ.kg-1.d-1 solution for intravenous nutrition and oral administration, in which the supply energy ratio of glucose, fat and protein was 55:30:15 respectively, glucose was 15.3% and the proportion of calorie to nitrogen was 183:1. The following indices including respiratory control rate (RCR), oxygen extraction (Oext), P/O ratio and intestine mucosal blood flow (IMBF) were measured on postburn days 1, 3, 5, 7, 10. RESULTS: After burn injury, the RCR, Oext, P/O ratio, and IMBF were significant decreased in both EN and GLN groups, but all above indices were markedly increased in GLN group compared to those in EN group. CONCLUSION: After burn injury, the IMBF and Oext were declined, resulting in mitochondria respiratory oxidative dysfunction and phosphorylation discoupling in intestinal epithelium. GLN supplementation appears to be beneficial to improving IMBF, increasing Oext, abating the extent of mitochondria respiration dysfunction, and promoting oxidative phosphorylation.

Animals↗

[The isolation and purification of 19S regulator compound and the change of its protein level in rat skeletal muscle after severe scalding].

OBJECTIVE: To explore the role of 19S regulator compound protein in the degradation of skeletal muscle protein in scalded rats. METHODS: Wistar rats were scalded and they were randomly divided into normal and 1, 2, 3, 5, and 7 postburn day (PBD) groups with 8 rats in each group. The 19S regulator compound of skeletal muscle in scalded rats was isolated and purified with chromatography. Rabbit-anti-rat antibody IgG of 19S regulator compound was prepared conventionally. The antibody was injected to rats in injection group (I) in which 19S antibody in dose of 3 mg/kg BW was injected for two times via tail vein with 6-hour interval. The rats in I group were decapitated on 1, 2 and 3 post-injection days, respectively. The scalded rats in control group (C) were treated in the same way, except that the antibody was replaced by normal saline. The change in content of 19S regulator compound was determined by western-blot. Meanwhile, the releasing rate of tyrosine from the skeletal muscle of scalded rats was also detected by fluorescent photography. RESULTS: 19S regulator compound with high purity was obtained. The content of 19S regulator compound in rat skeletal muscle was increased significantly after 2 PBD. But the protein degradation rate was also obviously increased on 2 PBD. The antibody of 19S compound might inhibit the enhancement of protein degradation. CONCLUSION: Burn injury might up-regulate the protein level of skeletal muscle 19S regulator compound, which therefore activated the protein degradation by 26S protease compound. This might be an important factor leading to postburn negative nitrogen balance.

Adenosine Triphosphatases↗

[The changes in the prostaglandin level and the prostaglandin transfer factor mRNA expression in the intestinal mucosa in scalded rats].

OBJECTIVE: To explore the changes in the PGE(2) and PGI(2), TXA(2) levels and PGT mRNA expression in the intestinal mucosa in scalded rats. METHODS: Wistar rats inflicted with TBSA 30% III degree scald were employed as the model. The PGE(2) and PGI(2) and TXA(2) contents in the intestinal mucosa were measured by radioimmunoassay, and the expression of PGT mRNA was detected by in situ hybridization. RESULTS: The PGE(2) and PGI(2) levels in intestinal mucosa were increased at 12 postburn hours (PBHs) and thereafter decreased dramatically (P < 0.05). The TXA(2) level in intestinal mucosa of scalded rats was obviously higher than that of normal level at 24 and 48 PBHs (P < 0.05), and the expression of PGT mRNA seemed to be increased after scalding. CONCLUSION: The decrease of PGE(2) level and the increase of TXA(2) level in the intestinal mucosa of scalded rats might be involved in rat mucosal injury, and PGT played an important role in the regulation of PGs levels.

Animals↗

[Experimental study on the effects of intestinal trefoil factor on intestinal epithelial proliferation and its signal transduction mechanism].

OBJECTIVE: To explore the effects of intestinal trefoil factor (ITF) on intestinal epithelial proliferation and its possible signal transduction mechanism. METHODS: 1). The intestinal epithelial cytoplasmic membrane was isolated and harvested from Wistar rats, and it was treated with various doses of ITF in the concentration of 0.01, 0.10, 1.00 and 10.00 micro g/ml. The tyrosine protein kinase (TPK) activity from cytoplasmic membrane ITF receptor was determined by membrane-bound method. 2). The intestinal epithelial cells 6 (IEC-6) cultured in vitro were employed in the study. Some of the cells were used as normal control, while a group of cells were stimulated by 1 micro g/ml ITF, and others were treated by PD098059, SB202190 and SB202474, respectively. The last three agents were inhibitors of three members of mitogen-activated protein kinase family (MAPKs), i.e. extracellular signal regulated protein kinases (ERKs), protein kinase p38 (p38), and stress-activated protein kinase (SAPK). They were used before the addition of 1 micro g/ml of ITF. The changes in DNA synthetic rate and the MAPK activity of IEC-6 after being treated by above agents were assessed by (3)H-TdR incorporation method. RESULTS: ITF receptor possessed TPK activity. TPK activity of ITF receptor, MAPKs activity and DNA synthetic rate of IEC-6 were increased obviously under the stimulation of ITF (P < 0.01). The above ITF effects could be evidently blocked by PD098059 and partially attenuated by SB202474. But SB202190 showed no effect in this respect. CONCLUSION: ITF could promote intestinal epithelial proliferation and transmit extracellular signals mainly by means of ERKs signalling pathway.

Animals↗