This study investigated the neuroprotective effects and underlying mechanism of Liujing Toutong Tablets(LJTT) on a rat model of permanent middle cerebral artery occlusion(pMCAO). The pMCAO model was established using the suture method. Eighty-four male SPF-grade SD rats were randomly divided into a sham operation group, a model group, a nimodipine group(0.020 g·kg~(-1)), and high-, medium-, and low-dose LJTT groups(2.8, 1.4, and 0.7 g·kg~(-1)). The Longa score, adhesive removal test and laser speckle contrast imaging technique were used to evaluate the degree of neurological functional impairment and changes in local cerebral blood flow. The survival and mortality of rats in each group were recorded daily. After seven days of continuous administration following the model induction, the rats in each group were euthanized, and brain tissue and blood samples were collected for corresponding parameter measurements. Nissl staining was used to examine pathological changes in brain tissue neurons. The levels of tumor necrosis factor-alpha(TNF-α), interleukin-6(IL-6), IL-1β, vascular endothelial growth factor(VEGF), calcitonin gene-related peptide(CGRP), beta-endorphin(β-EP), and endogenous nitric oxide(NO) in rat serum were measured using specific assay kits. The entropy weight method was used to analyze the weights of various indicators. The protein expression levels of nuclear factor kappa-B(NF-κB), inhibitor kappaB alpha(IκBα), phosphorylated IκBα(p-IκBα), and phosphorylated inhibitor of NF-κB kinase alpha(p-IKKα) in brain tissue were determined using Western blot. Immunohistochemistry was used to detect the protein expression of chemokine-like factor 1(CKLF1) and C-C chemokine receptor 5(CCR5) in rat brain tissue. Compared with the sham operation group, the model group showed significantly higher neurological functional impairment scores, prolonged adhesive removal time, decreased cerebral blood flow, increased neuronal damage, reduced survival rate, significantly increased levels of TNF-α, IL-1β, IL-6, CGRP, and NO in serum, significantly decreased levels of VEGF and β-EP, significantly increased expression levels of NF-κB p65, p-IκBα/IκBα, and p-IKKα in rat brain tissue, and significantly upregulated protein expression of CKLF1 and CCR5. Compared with the model group, the high-dose LJTT group significantly improved the neurological functional score of pMCAO rats after oral administration for 7 days. LJTT at all doses significantly reduced adhesive removal time and restored cerebral blood flow. The high-and medium-dose LJTT groups significantly improved neuronal damage. The LJTT groups at all doses showed reduced levels of TNF-α, IL-1β, IL-6, CGRP, and NO in rat serum, increased VEGF and β-EP levels, and significantly decreased expression levels of NF-κB p65, p-IκBα/IκBα, p-IKKα, and CCR5 protein in rat brain tissue. The entropy weight analysis revealed that CGRP and β-EP were significantly affected during the model induction, and LJTT exhibited a strong effect in reducing the release of inflammatory factors such as TNF-α and IL-1β. LJTT may exert a neuroprotective effect on rats with permanent cerebral ischemia by reducing neuroinflammatory damage, and its mechanism may be related to the inhibition of the NF-κB signaling pathway and the regulation of the CKLF1/CCR5 axis. Additionally, LJTT may exert certain analgesic effects by reducing CGRP and NO levels and increasing β-EP levels.
Rats ; Male ; Animals ; NF-kappa B/metabolism* ; NF-KappaB Inhibitor alpha/metabolism* ; Vascular Endothelial Growth Factor A/genetics* ; I-kappa B Kinase/pharmacology* ; Tumor Necrosis Factor-alpha/pharmacology* ; Interleukin-6/genetics* ; Calcitonin Gene-Related Peptide/pharmacology* ; Rats, Sprague-Dawley ; Signal Transduction ; Brain Ischemia/drug therapy* ; Tablets

Our previous studies have shown that calcitonin gene-related peptide (CGRP) exerts protective effects on the acute lung injury induced by oxidative stress. This study was aimed to investigate whether autophagy was involved in the protection of CGRP against oxidative stress-induced lung injury in neonatal rats. Newborn Sprague-Dawley (SD) rats were randomly divided into five groups: Control group, oxidative stress model group (Model group), Model + CGRP group, Model + CGRP + Rapamycin (an autophagy agonist) group, and Model + CGRP + LY294002 (an autophagy inhibitor) group. The model of hyperoxia-induced lung injury was established by continuous inhalation of oxygen (FiO₂ = 90%-95%) for 14 days in neonatal SD rats. Pathological changes of lung tissue were observed by hematoxylin and eosin (HE) staining, and mean linear intercept (MLI) was measured. The quantitative changes of autophagic vesicles (AV) in type II alveolar epithelial cells (AECII) were measured under the transmission electron microscope. The protein expressions of Caspase-3, Bcl-2, mTOR, and Beclin-1 in lung tissue lysates were detected by Western blot. The results showed that, compared to the Model group at the same time point, the number of AV in AECII and the expression level of Beclin-1 protein of the lung tissue were increased, while the expression level of mTOR protein was decreased, with alleviated pathological changes, reduced MLI value and Caspase-3 protein expression level, increased Bcl-2 protein expression level in the lung tissue of Model + CGRP group. In addition, we found that the protective effect of CGRP on hyperoxia-induced lung injury could be enhanced by autophagy activator Rapamycin and abolished by autophagy inhibitor LY294002. Together, these findings indicate that CGRP could attenuate hyperoxia-induced lung injury in neonatal rats by enhancing autophagy.
Acute Lung Injury/pathology* ; Animals ; Animals, Newborn ; Autophagy ; Calcitonin/metabolism* ; Calcitonin Gene-Related Peptide/metabolism* ; Caspase 3/metabolism* ; Hyperoxia/pathology* ; Lung/pathology* ; Lung Injury/prevention & control* ; Oxidative Stress ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Rats ; Rats, Sprague-Dawley ; Sirolimus/pharmacology*

OBJECTIVE: To investigate the changes of skin temperature, blood infusion and inflammatory cytokines of cutaneous tissue in the sensitized area of colitis model rats, as well as the relationship between sensory and sympathetic nerves and the formation of sensitized area, and to initially reveal the partial physical-chemical characteristics of the sensitized area in the colitis model rats. METHODS: Thirty-five male SD rats were randomly divided into a control group (n=10), a model group (n=18) and a guanethidine group (n=7). 5% dextran sulfate sodium (DSS) was adopted for 6-day free drinking to establish colitis model in the model group and the guanethidine group. On day 6 and 7, in the guanethidine group, guanethidine solution (30 mg/kg) was injected intraperitoneally for sympathetic block. On day 7, after injection of evans blue (EB) solution, the EB extravasation areas on the body surface were observed to investigate the distribution and physical-chemical characteristics of the sensitized area. The control area was set up, 0.5 cm away from the sensitized area, and with the same nerve segment innervation. Disease activity index (DAI) score of rats was compared between the normal group and the model group, and the morphological changes in the colon tissue were investigated with HE method. Using infrared thermal imaging technology and laser speckle flow imaging technology, skin temperature and blood infusion were determined in the sensitized area and the control area of the rats in the model group. Immunofluorescence technique was adopted to observe the expression levels of the positive nerve fibers of substance P (SP), calcitonin gene-related peptide (CGRP) and tyrosine hydroxylase (TH), and the correlation with blood vessels; as well as the expression levels of SP positive nerve fibers/tryptase⁺ mast cells, and tryptase⁺ mast cells/5-hydroxytryptamine (5-HT) in skin tissue in the sensitized area and the control area of the rats in the model group. MSD multi-level factorial method and ELISA were applied to determine the contents of pro-inflammatory and anti-inflammatory cytokines (e.g. TNF-α, IL-1β, IL-6, IL-4 and IL-10) and anti-inflammatory substance corticosterone (CORT). RESULTS: Sensitization occurred at the T₁₂-S₁ segments of the colitis model rats, especially at L₂-L₅ segments. Compared with the normal group, DAI score was increased in the rats of the model group (P<0.05), and the colonic mucosal damage was obvious, with the epithelial cells disordered, even disappeared, crypt destructed, submucosal edema and a large number of inflammatory cells infiltrated. In comparison with the control area, the skin temperature and blood infusion were increased in the sensitized area of the model group (P<0.05, P<0.01); as well as the expression levels of the positive nerve fibers of SP, CGRP and TH of skin tissue (P<0.05), which was specially distributed in peripheral vessels, the expression levels of SP positive nerve fibers/tryptase⁺ mast cells, and tryptase⁺ mast cells/5-HT of the skin tissue were all expanded (P<0.05) in the sensitized area of the model group. Compared with the model group, the number of sensitized areas was reduced in the guanethidine group (P<0.05). In comparison with the control area of the model group, in the sensitized area, the contents of pro-inflammatory cytokines, e.g. TNF-α, IL-1β and IL-6, and the anti-inflammatory substance CORT of skin tissue were all increased (P<0.05); and the contents of IL-6 and TNF-α were negatively correlated with CORT (P<0.05). CONCLUSION The sensitized areas on the body surface of colitis rats are mainly distributed in the L₂-L₅ segments. Sensory and sympathetic nerves are involved in the acupoint sensitization, and the sensitized areas may have the dynamic changes in pro-inflammatory and anti-inflammatory substances.
Animals ; Anti-Inflammatory Agents ; Calcitonin Gene-Related Peptide/metabolism* ; Colitis/metabolism* ; Cytokines/metabolism* ; Guanethidine ; Interleukin-6 ; Male ; Rats ; Rats, Sprague-Dawley ; Serotonin ; Skin Temperature ; Substance P/genetics* ; Tryptases ; Tumor Necrosis Factor-alpha

OBJECTIVE: To discuss the clinical significance of antibacterial peptide LL-37 in the early diagnosis of patients with sepsis in emergency department. METHODS: Forty patients diagnosed with sepsis in the emergency department of the Affiliated Hospital of Zunyi Medical College from December 2017 to March 2018 were enrolled as sepsis group. Twenty healthy volunteers were enrolled contemporaneously in our hospital at medical center as healthy control group. Peripheral blood was collected immediately after diagnosis in sepsis group or during physical examination in healthy control group. The expression of antibacterial peptide LL-37 was determined by enzyme-linked immunosorbent assay (ELISA). Meanwhile, serum procalcitonin (PCT) and C-reactive protein (CRP) levels were determined. The differences in antibacterial peptide LL-37, PCT and CRP levels between the two groups were compared. Pearson correlation method was used to analyze the correlation between antibacterial peptide LL-37, PCT and CRP. Receiver operating characteristic (ROC) curve was drawn, and the early individually or jointly diagnostic value of each detected index for sepsis was analyzed. RESULTS: The levels of antimicrobial peptide LL-37, PCT and CRP in peripheral blood of sepsis group were significantly higher than those of healthy control group [LL-37 (μg/L): 1.34±0.69 vs. 0.10±0.06, PCT (μg/L): 46.67±39.51 vs. 0.03±0.02, CRP (mg/L): 129.68±49.83 vs. 3.16±2.85], with statistically significant differences (all P < 0.05). Pearson correlation analysis showed that the expression of antimicrobial peptide LL-37 was positively correlated with PCT and CRP levels (r₁ = 0.835, r₂ = 0.932, both P < 0.01). ROC curve analysis showed that the area under ROC curve (AUC) of LL-37, PCT and CRP for early diagnosis of sepsis was 0.885, 0.963 and 0.983, respectively, and the AUC of combined diagnosis of the three parameters was as high as 0.994, indicating that the value of combined diagnosis of sepsis was greater than that of single diagnosis; when the combined prediction probability of the three parameters was 0.92, the sensitivity was 97.5%, and the specificity was 95.0%. CONCLUSIONS Antibacterial peptide LL-37 has certain clinical value in early diagnosis of patients with sepsis, which can be used as early routine monitoring indicators for patients with early sepsis when combined with PCT and CRP.
Antimicrobial Cationic Peptides/metabolism* ; C-Reactive Protein ; Calcitonin ; Calcitonin Gene-Related Peptide ; Early Diagnosis ; Emergency Service, Hospital ; Humans ; Protein Precursors ; ROC Curve ; Sepsis/metabolism* ; Cathelicidins

OBJECTIVEPrevious studies have clarified that calcitonin gene-related peptide (CGRP) can promote the biologi- cal activity of osteoblasts. To further reveal the role of CGRP in bone repair, we studied its influence on osteogenic differentia- tion of mouse bone marrow stromal cells (BMSCs) and initially explored the effect of the Hippo signaling pathway with this process.

METHODSBMSCs were induced to osteogenic differentiate osteoblasts by different concentrations of CGRP for a screening of the optimal concentration. CGRP was added in BMSCs, then the activity of alkaline phosphatase (ALP) and the number of mineralized nodules were examined by specific ALP kits after 48 hours and alizarin red staining fluid after 7 days, respectively. The protein expression of p-Mst1/2 was measured by Western blot. Verteporfin was used to block the downstream Yap signaling. The mRNA expression of collagen type I (Col I) and runt-related transcription factor 2 (Runx2) were detected by reverse transcription-polymerase chain reaction.

RESULTSCompared to the blank group, different concentrations of CGRP (10⁻⁹, 10⁻⁸, 10⁻⁷ mol · L⁻¹), especially 10⁻⁸ mol · L⁻¹, significantly increased the ALP activity of BMSCs (P < 0.05). Alizarin red staining also showed more mineralized nodules in 10⁻⁸ mol · L⁻¹ group. The expression of p-Mst1/2 increased in the CGRP group (P < 0.05). Verteporfin treatment effectively decreased the mRNA expression of Runx2 and Col I (P < 0.05).

CONCLUSIONThe Hippo signaling pathway plays a role in CGRP-induced osteogenic differentiation in mouse BMSCs.

Alkaline Phosphatase ; Animals ; Calcitonin ; genetics ; metabolism ; Calcitonin Gene-Related Peptide ; metabolism ; Cell Differentiation ; Cells, Cultured ; Collagen Type I ; Core Binding Factor Alpha 1 Subunit ; Mesenchymal Stromal Cells ; physiology ; Mice ; Osteoblasts ; Osteogenesis ; physiology ; Signal Transduction

PURPOSE: The pathophysiology of discogenic low back pain is not fully understood. Tetrodotoxin-sensitive voltage-gated sodium (NaV) channels are associated with primary sensory nerve transmission, and the NaV1.7 channel has emerged as an analgesic target. Previously, we found increased NaV1.7 expression in dorsal root ganglion (DRG) neurons innervating injured discs. This study aimed to examine the effect of blocking NaV1.7 on sensory nerves after disc injury. MATERIALS AND METHODS: Rat DRG neurons innervating the L5/6 disc were labeled with Fluoro-Gold (FG) neurotracer. Twenty-four rats underwent intervertebral disc puncture (puncture group) and 12 rats underwent sham surgery (non-puncture group). The injury group was divided into a saline infusion group (puncture+saline group) and a NaV1.7 inhibition group, injected with anti-NaV1.7 antibody (puncture+anti-NaV1.7 group); n=12 per group. Seven and 14 days post-surgery, L1 to L6 DRGs were harvested and immunostained for calcitonin gene-related peptide (CGRP) (an inflammatory pain marker), and the proportion of CGRP-immunoreactive (IR) DRG neurons of all FG-positive neurons was evaluated. RESULTS: The ratio of CGRP-IR DRG neurons to total FG-labeled neurons in the puncture+saline group significantly increased at 7 and 14 days, compared with the non-puncture group, respectively (p<0.05). Application of anti-NaV1.7 into the disc significantly decreased the ratio of CGRP-IR DRG neurons to total FG-labeled neurons after disc puncture at 7 and 14 days (40% and 37%, respectively; p<0.05). CONCLUSION: NaV1.7 antibody suppressed CGRP expression in disc DRG neurons. Anti-NaV1.7 antibody is a potential therapeutic target for pain control in patients with lumbar disc degeneration.
Animals ; Antibodies ; Calcitonin Gene-Related Peptide/metabolism ; Disease Models, Animal ; Ganglia, Spinal/*metabolism ; Intervertebral Disc/*drug effects/*injuries ; Intervertebral Disc Degeneration/metabolism ; Low Back Pain/*physiopathology ; Lumbar Vertebrae/injuries ; Male ; NAV1.7 Voltage-Gated Sodium Channel/*metabolism ; Neurons/*metabolism ; Pain/metabolism ; Rats ; Rats, Sprague-Dawley ; Stilbamidines

OBJECTIVETo investigate the nerve growth factor (NGF) regulating the expression of calcitonin gene-related peptide (CGRP) in promoting the proliferation of osteoblast-like cell (MG-63) and thus illustrate the mechanism of the NGF in wound healing.

METHODSDifferent concentrations of NGF were used to stimulate MG-63. The expression of CGRP was detected by real-time quantitative polymerase chain reaction (RT-QPCR) and enzyme-linked immunosorbent assay after 1, 2, 3, and 4 days. The proliferation of MG-63 was detected by cell counting kit-8 (CCK-8). The expression of CGRP mRNA and the proliferation of MG-63 were then detected by RT-QPCR and CCK-8 after adding the NGF receptor blocker.

RESULTSCompared with the blank control group, the expression of CGRP significantly increased by stimulating the NGF. The expression of CGRP was positively related to the concentration of NGF (P<0.05). Moreover, the expression of CGRP increased by prolonging the NGF stimulation time. The proliferation of MG-63 increased after stimulating the NGF (P<0.05). After adding the NGF receptor blocker, the expression of CGRP and the proliferation of MG-63 correspondingly decreased (P<0.05).

CONCLUSIONNGF can up-regulate the expression of CGRP and increase the proliferation of MG-63. Therefore, NGF plays a significant role in wound healing.

Animals ; Calcitonin ; Calcitonin Gene-Related Peptide ; metabolism ; Cell Line ; Ganglia, Spinal ; Humans ; Nerve Growth Factor ; metabolism ; Rats, Sprague-Dawley ; Receptor, Nerve Growth Factor ; Signal Transduction ; Up-Regulation

OBJECTIVETo observe the neurological protection effects of "paraplegia-triple-needling method" on rats with incomplete spinal cord injury (SCI), so as to make a preliminary exploration on its mechanism.

METHODSA total of 45 SD rats were randomly divided into a paraplegia-triple-needling method group (group A), a regular acupuncture group (group B) and a model group (group C), 15 rats in each one. The rats model of incomplete spinal cord injury was established by modified Allen's method. The acupoints of governor vessel and back-shu points next to the vertebras of upper end and lower end of injured segment as well as motor points in key muscle of lower extremities were treated with acupuncture in the group A; the acupoints of governor vessel and back-shu points next to the vertebras of upper end and lower end of injured segment as well as "Huantiao" (GB 30), "Housanli" (ST 36), "Yanglingquan" (GB 34) and "Genduan"(Extra) were treated with acupuncture in the group B; rats in the group C received no treatment after model establishment but grabbing and immobilization. The needles were retained for 15 min in the group A and group B, once a day for 14 times. 1 d, 7 d and 14 d after model establishment, Basso Beattie Bresnahan (BBB) scores were observed in each group; the morphologic change of injured spinal cord and expression of positive cells of calcitonin gene-related peptide (CGRP) were observed. Results (1) One day after SCI, there was no significant difference of BBB scores among three groups (P> 0. 05); 7 days and 14 days after SCI, BBB scores in the group A and group B were significantly superior to those in the group C (all P<0. 05), and the BBB scores in the group A were superior to those in the group B ( both P<0. 05). (2) There was expression of CGRP positive cells in all three groups, and that in the group A and group B was significantly higher than that in group C (both P<0. 05); 14 days after treatment, the expression in the group A was higher than that in the group B (P<0. 05).

CONCLUSIONThe "paraplegia-triple-needling method" could obviously! improve the motor function of rats with SCI, especially the expression of neuroprotective factor CGRP, which is likely to be one of the mechanisms of neurological protection effect.

Acupuncture Points ; Acupuncture Therapy ; instrumentation ; methods ; Animals ; Calcitonin Gene-Related Peptide ; genetics ; metabolism ; Disease Models, Animal ; Humans ; Male ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; genetics ; metabolism ; therapy

OBJECTIVETo explore the molecular mechanism of pain associated with chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) in the rat model of prostatic inflammation.

METHODSThirty-six male SD rats were equally randomized to an experimental and a control group, the former injected with 50 μl of 3% λ-carrageenan into the ventral prostate to make the model of non-bacterial prostatic inflammation, while the latter with the same volume of sterile saline solution. At 1, 2 and 4 weeks after modeling, the prostate, L6-S1 dorsal root ganglion (DRG) and spinal cord were harvested for examination of the expressions of the nerve growth factor (NGF), transient receptor potential ankyrin 1 (TRPA1), and calcitonin-gene-related peptide (CGRP) by immunohistochemistry and Western blot.

RESULTSThe expressions of NGF, TRPA1 and CGRP in the prostatic tissue were all significantly increased in the experimental group as compared with the control (P <0.05), with a gradual decrease with the prolonging of time (P <0.05). In the L6-S1 DRG and spinal cord, the expressions of NGF, TRPA1 and CGRP exhibited no significant differences between the experimental and control groups at 1 week after modeling (P >0.05) and kept at high levels in the experimental group at 2 and 4 weeks, though not significantly different from those at 1 week (P >0.05). Statistically significant differences were observed in the expressions of the three proteins in the experimental rats among different time points (P <0.05), but not between the two groups at any time point (P >0.05).

CONCLUSIONThe molecular mechanism of CP/CPPS can be evaluated in the rat model of prostatic inflammation established by injecting λ-carrageenan into the prostate. TRPA1 may play an important role in connecting the upstream and down-stream pathways of CP/CPPS-associated pain.

Animals ; Calcitonin Gene-Related Peptide ; metabolism ; Carrageenan ; Chronic Disease ; Chronic Pain ; metabolism ; Ganglia, Spinal ; metabolism ; Humans ; Male ; Nerve Growth Factor ; metabolism ; Pelvic Pain ; metabolism ; Prostatitis ; chemically induced ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism ; TRPA1 Cation Channel ; TRPC Cation Channels ; metabolism

OBJECTIVETo explore the effects of oral administration of mixed enteral nutritional agent on intestinal mucosal barrier of patients with severe burn injury at early stage.

METHODSTwenty-four patients with severe burn injury admitted to our burn ward from August 2013 to September 2014, conforming to the study criteria, were divided into conventional therapy group (n = 12) and early enteral feeding group (n = 12) according to the random number table. Patients in conventional therapy group received conventional treatment immediately after admission, while those in early enteral feeding group were orally given 100 mL of a mixture of glutamine, probiotics, and prebiotics once a day besides conventional treatment for 7 days. Serum levels of diamine oxidase (DAO) and procalcitonin (PCT) and plasma level of LPS were determined by ELISA before treatment and on treatment day (TD) 1, 3, 7, 14, and 21. Wound secretion and blood samples were collected for bacterial culture within the 21 TD. The incidence of MODS within the 21 TD was observed. Data were processed with Fisher's exact test, rank sum test, analysis of variance for repeated measurement, and LSD-t test.

RESULTS(1) Serum levels of DAO in patients of early enteral feeding group on TD 7, 14, and 21 were respectively (14.9 ± 3.7), (12.4 ± 3.1), and (9.5 ± 0.7) ng/mL, which were significantly lower than those of conventional therapy group [(17.5 ± 4.0), (16.3 ± 3.3), and (13.0 ± 1.1) ng/mL, with t values from 2.913 to 15.304, P values below 0.01]. Serum levels of DAO at the other time points were close between the two groups (with t values from -0.598 to 0.139, P values above 0.05). (2) Compared with serum levels of PCT in patients of conventional therapy group [(11.7 ± 20.9) and (12.9 ± 23.9) ng/mL], those of early enteral feeding group were significantly lower on TD 7 and 14 [(2.7 ± 8.1) and (2.0 ± 5.6) ng/mL, with Z values respectively -2.919 and -2.139, P < 0.05 or P < 0.01]. Serum levels of PCT at the other time points were close between the two groups (with Z values from -1.833 to -0.346, P values above 0.05). (3) Plasma level of LPS in patients of early enteral feeding group on TD 7 was (33 ± 56) pg/mL, which was significantly lower than that of conventional therapy group [(102 ± 108) pg/mL, Z = -2.046, P < 0.05]. Plasma levels of LPS at the other time points between the two groups showed no significant difference (with Z values from -2.003~-0.526, P values above 0.05). (4) Positive results in bacterial culture of wound secretion were approximately the same between the two groups (P > 0.05). Bacterial culture of blood was positive in 7 patients of conventional therapy group and 1 patient of early enteral feeding group, showing significantly statistical difference (P < 0.05). MODS was observed in 1 patient of conventional therapy group, showing no significantly statistical difference with that of early enteral feeding group (no patient, P > 0.05).

CONCLUSIONSEarly intestinal feeding of mixed enteral nutritional agent in addition to conventional therapy can effectively promote repair of the impairment of intestinal mucosal barrier, protect integrity of intestinal mucosa, reduce damage to intestines, and alleviate inflammatory response in patients suffering from severe burn injury.

Administration, Oral ; Amine Oxidase (Copper-Containing) ; blood ; Burns ; metabolism ; therapy ; Calcitonin ; blood ; Calcitonin Gene-Related Peptide ; Enteral Nutrition ; methods ; Female ; Glutamine ; administration & dosage ; pharmacology ; Humans ; Intestinal Mucosa ; drug effects ; metabolism ; Protein Precursors ; blood ; Treatment Outcome ; Wound Healing