Objective:To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), and to study the intervention effect and mechanism of N-acetylcysteine (NAC) on ultrafine carbon black-induced oxidative damage in BEAS-2B cells.Methods:In March 2023, BEAS-2B cells were used as research object, an in vitro airway model exposed to ultrafine carbon black was constructed. A control group and three carbon black exposure groups (50, 100, 200 μg/ml) were set up, and the cells were treated with corresponding concentrations of ultrafine carbon black for 24 hours. In addition, the experiment was divided into control group, NAC+ control group, 100 μg/ml carbon black exposure group and NAC+ exposure group. The corresponding groups were treated with 2 mmol/L NAC for 1 h and 100 μg/ml ultrafine carbon black for 24 h, respectively. Cell viability was measured by CCK-8 assay. Intracellular reactive oxygen species (ROS) level was detected by chemical fluorescence method. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the content of malondialdehyde (MDA) were detected by colorimetry. The mRNA and protein expressions of autophagy-related genes[Atg5, Atg7, Beclin1, microtubule-associated protein light chain 3B (LC3B), p62 and lysosome-associated membrane protein 2 (LAMP2) ] and apoptosis-related genes [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and poly (ADP-ribose) polymerase 1 (PARP1) ] were determined by fluorescence quantitative PCR and Western blot. Cell apoptosis was determined by flow cytometry.Results:Compared with the control group, the relative survival rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly decreased, the levels of ROS and MDA were significantly increased, and the activities of SOD, GSH-Px and CAT were significantly decreased ( P<0.05). The relative survival rate, ROS and MDA levels, SOD, GSH-Px and CAT activities were significantly correlated with the exposure dose of ultrafine carbon black ( rs=-0.755, 0.826, 0.934, -0.810, -0.880, -0.840, P<0.05). Compared with the control group, the relative expression levels of Atg5, Atg7, Beclin1, LC3B, p62, LAMP2, Bax, Caspase3, Caspase9, PARP1 mRNA and Atg5, Atg7, Beclin1, LC3BⅡ, p62, LAMP2, Bax, cleaved Caspase3 (C-Caspase3), cleaved Caspase9 (C-Caspase9), cleaved PARP1 (C-PARP1) protein and the ratio of LC3BⅡ/LC3BⅠ in 50, 100 and 200 μg/ml carbon black exposure groups were significantly increased, while the relative expression levels of Bcl-2 mRNA and protein were significantly decreased ( P<0.05). The changes of the above indexes were significantly correlated with the exposure dose of carbon black ( rs=0.892, 0.879, 0.944, 0.892, 0.828, 0.880, 0.814, 0.794, 0.931, 0.918, 0.813, 0.866, 0.774, 0.695, 0.918, 0.761, 0.794, 0.944, 0.833, 0.866, 0.905, -0.886, -0.748, P<0.05). Compared with 100 μg/ml carbon black exposure group, the relative survival rate, the activities of SOD, GSH-Px and CAT in NAC+exposure group were significantly increased, while the levels of ROS and MDA were significantly decreased, and the relative expression levels of LC3B, p62 and Caspase3 mRNA and protein as well as the ratio of LC3BⅡ/LC3BⅠ were significantly decreased, and the differences were statistically significant ( P<0.05). Compared with the control group, the apoptosis rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly increased ( P<0.05), and there was a significant positive correlation between ultrafine carbon black exposure dose and cell apoptosis rate ( rs=0.944, P<0.05). While compared with 100 μg/ml carbon black exposure group, the apoptosis rate of NAC+exposure group was significantly decreased, and the difference was statistically significant ( P<0.05) . Conclusion:Cell autophagy and apoptosis may be important pathophysiological mechanisms of ultrafine carbon black-induced oxidative damage in BEAS-2B cells. NAC can alleviate the occurrence of BEAS-2B cell damage caused by ultrafine carbon black by regulating oxidative stress and the cascading autophagy and apoptosis pathways.

Objective:To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), and to study the intervention effect and mechanism of N-acetylcysteine (NAC) on ultrafine carbon black-induced oxidative damage in BEAS-2B cells.Methods:In March 2023, BEAS-2B cells were used as research object, an in vitro airway model exposed to ultrafine carbon black was constructed. A control group and three carbon black exposure groups (50, 100, 200 μg/ml) were set up, and the cells were treated with corresponding concentrations of ultrafine carbon black for 24 hours. In addition, the experiment was divided into control group, NAC+ control group, 100 μg/ml carbon black exposure group and NAC+ exposure group. The corresponding groups were treated with 2 mmol/L NAC for 1 h and 100 μg/ml ultrafine carbon black for 24 h, respectively. Cell viability was measured by CCK-8 assay. Intracellular reactive oxygen species (ROS) level was detected by chemical fluorescence method. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the content of malondialdehyde (MDA) were detected by colorimetry. The mRNA and protein expressions of autophagy-related genes[Atg5, Atg7, Beclin1, microtubule-associated protein light chain 3B (LC3B), p62 and lysosome-associated membrane protein 2 (LAMP2) ] and apoptosis-related genes [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and poly (ADP-ribose) polymerase 1 (PARP1) ] were determined by fluorescence quantitative PCR and Western blot. Cell apoptosis was determined by flow cytometry.Results:Compared with the control group, the relative survival rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly decreased, the levels of ROS and MDA were significantly increased, and the activities of SOD, GSH-Px and CAT were significantly decreased ( P<0.05). The relative survival rate, ROS and MDA levels, SOD, GSH-Px and CAT activities were significantly correlated with the exposure dose of ultrafine carbon black ( rs=-0.755, 0.826, 0.934, -0.810, -0.880, -0.840, P<0.05). Compared with the control group, the relative expression levels of Atg5, Atg7, Beclin1, LC3B, p62, LAMP2, Bax, Caspase3, Caspase9, PARP1 mRNA and Atg5, Atg7, Beclin1, LC3BⅡ, p62, LAMP2, Bax, cleaved Caspase3 (C-Caspase3), cleaved Caspase9 (C-Caspase9), cleaved PARP1 (C-PARP1) protein and the ratio of LC3BⅡ/LC3BⅠ in 50, 100 and 200 μg/ml carbon black exposure groups were significantly increased, while the relative expression levels of Bcl-2 mRNA and protein were significantly decreased ( P<0.05). The changes of the above indexes were significantly correlated with the exposure dose of carbon black ( rs=0.892, 0.879, 0.944, 0.892, 0.828, 0.880, 0.814, 0.794, 0.931, 0.918, 0.813, 0.866, 0.774, 0.695, 0.918, 0.761, 0.794, 0.944, 0.833, 0.866, 0.905, -0.886, -0.748, P<0.05). Compared with 100 μg/ml carbon black exposure group, the relative survival rate, the activities of SOD, GSH-Px and CAT in NAC+exposure group were significantly increased, while the levels of ROS and MDA were significantly decreased, and the relative expression levels of LC3B, p62 and Caspase3 mRNA and protein as well as the ratio of LC3BⅡ/LC3BⅠ were significantly decreased, and the differences were statistically significant ( P<0.05). Compared with the control group, the apoptosis rates of BEAS-2B cells in 50, 100, 200 μg/ml carbon black exposure groups were significantly increased ( P<0.05), and there was a significant positive correlation between ultrafine carbon black exposure dose and cell apoptosis rate ( rs=0.944, P<0.05). While compared with 100 μg/ml carbon black exposure group, the apoptosis rate of NAC+exposure group was significantly decreased, and the difference was statistically significant ( P<0.05) . Conclusion:Cell autophagy and apoptosis may be important pathophysiological mechanisms of ultrafine carbon black-induced oxidative damage in BEAS-2B cells. NAC can alleviate the occurrence of BEAS-2B cell damage caused by ultrafine carbon black by regulating oxidative stress and the cascading autophagy and apoptosis pathways.

BACKGROUND: LY01005 (Goserelin acetate sustained-release microsphere injection) is a modified gonadotropin-releasing hormone (GnRH) agonist injected monthly. This phase III trial study aimed to evaluated the efficacy and safety of LY01005 in Chinese patients with prostate cancer. METHODS: We conducted a randomized controlled, open-label, non-inferiority trial across 49 sites in China. This study included 290 patients with prostate cancer who received either LY01005 or goserelin implants every 28 days for three injections. The primary efficacy endpoints were the percentage of patients with testosterone suppression ≤50 ng/dL at day 29 and the cumulative probability of testosterone ≤50 ng/dL from day 29 to 85. Non-inferiority was prespecified at a margin of -10%. Secondary endpoints included significant castration (≤20 ng/dL), testosterone surge within 72 h following repeated dosing, and changes in luteinizing hormone, follicle-stimulating hormone, and prostate specific antigen levels. RESULTS: On day 29, in the LY01005 and goserelin implant groups, testosterone concentrations fell below medical-castration levels in 99.3% (142/143) and 100% (140/140) of patients, respectively, with a difference of -0.7% (95% confidence interval [CI], -3.9% to 2.0%) between the two groups. The cumulative probabilities of maintaining castration from days 29 to 85 were 99.3% and 97.8%, respectively, with a between-group difference of 1.5% (95% CI, -1.3% to 4.4%). Both results met the criterion for non-inferiority. Secondary endpoints were similar between groups. Both treatments were well-tolerated. LY01005 was associated with fewer injection-site reactions than the goserelin implant (0% vs . 1.4% [2/145]). CONCLUSION: LY01005 is as effective as goserelin implants in reducing testosterone to castration levels, with a similar safety profile. TRIAL REGISTRATION ClinicalTrials.gov, NCT04563936.
Humans ; Male ; Antineoplastic Agents, Hormonal/therapeutic use* ; East Asian People ; Gonadotropin-Releasing Hormone/agonists* ; Goserelin/therapeutic use* ; Prostate-Specific Antigen ; Prostatic Neoplasms/drug therapy* ; Testosterone

Antibody-mediated rejection (AMR) is one of the major causes of graft loss after transplantation. Recently, the regulation of B cell differentiation and the prevention of donor-specific antibody (DSA) production have gained increased attention in transplant research. Herein, we established a secondary allogeneic in vivo skin transplant model to study the effects of romidepsin (FK228) on DSA. The survival of grafted skins was monitored daily. The serum levels of DSA and the number of relevant immunocytes in the recipient spleens were evaluated by flow cytometry. Then, we isolated and purified B cells from B6 mouse spleens in vitro by magnetic bead sorting. The B cells were cultured with interleukin-4 (IL-4) and anti-clusters of differentiation 40 (CD40) antibody with or without FK228 treatment. The immunoglobulin G1 (IgG1) and IgM levels in the supernatant were evaluated by enzyme-linked immunosorbent assay (ELISA). Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and western blotting were conducted to determine the corresponding levels of messenger RNA (mRNA) and protein expression in cultured cells and the recipient spleens. The results showed that FK228 significantly improved the survival of allogeneic skin grafts. Moreover, FK228 inhibited DSA production in the serum along with the suppression of histone deacetylase 1 (HADC1) and HDAC2 and the upregulation of the acetylation of histones H2A and H3. It also inhibited the differentiation of B cells to plasma cells, decreased the transcription of positive regulatory domain-containing 1 (Prdm1) and X-box-binding protein 1 (Xbp1), and decreased the expression of phosphorylated inositol-requiring enzyme 1 α (p-IRE1α), XBP1, and B lymphocyte-induced maturation protein-1 (Blimp-1). In conclusion, FK228 could decrease the production of antibodies by B cells via inhibition of the IRE1α-XBP1 signaling pathway. Thus, FK228 is considered as a promising therapeutic agent for the clinical treatment of AMR.
Animals ; Depsipeptides ; Endoribonucleases ; Hematopoietic Stem Cell Transplantation ; Histone Deacetylase Inhibitors/pharmacology* ; Mice ; Protein Serine-Threonine Kinases ; Skin Transplantation

ObjectiveTo study the changes of primary metabolites and phenols in the fruits of Acanthopanax senticosus at different development stages, so as to provide a theoretical basis for the rational utilization of A. senticosus fruit resources. MethodThe primary metabolites and phenols in the fruits at different development stages were determined via gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS) and then compared by multivariate statistical analysis. ResultA total of 274 chromatographic peaks were obtained by GC-MS-based non-targeted metabonomics and 24 differential metabolites were screened out by multivariate statistical analysis. The differential metabolites were mainly concentrated in pentose phosphate pathway, galactose metabolism, ascorbic acid and aldose metabolism pathways. After color conversion, the pentose phosphate pathway and galactose metabolism were activated and increasing sugars were accumulated. The ascorbic acid and aldose metabolism pathways were active before color conversion, with high accumulation of the end product ascorbic acid. The ultra-high liquid chromatography-mass spectrometry (UPLC-MS) identified 28 phenols in the fruits at different development stages. Flavonoids were accumulated mainly at the green ripening stage before color conversion, and phenolic acids were accumulated mainly after color conversion. ConclusionThe accumulation of primary metabolites and phenols in A. senticosus fruits varies significantly among different development stages

OBJECTIVES: Neuropathic pain (NP) is a chronic pain caused by somatosensory neuropathy or disease, and genistein (Gen) might be a potential drug for the treatment of NP. Therefore, this study aims to investigate the effect of Gen on lipopolysaccharide (LPS)-induced inflammatory injury of dorsal root ganglion neuron (DRGn) in rats and the possible molecular mechanism. METHODS: The DRGn of 1-day-old juvenile rats were taken for isolation and culture. The DRGn in logarithmic growth phase were divided into a control group, a LPS group, a tubastatin hydrochloride (TSA)+LPS group, a Gen1+LPS group, a Gen2+LPS group, a Gen2+LPS+TSA group, a Gen2+pcDNA-histone deacetylase 6 (HDAC6)+LPS group, and a Gen2+pcDNA3.1+LPS group. The LPS group was treated with 1 μg/mL LPS for 24 h; the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group were treated with 5 μmol/L TSA, 5 μmol/L Gen, 10 μmol/L Gen respectively for 0.5 h, and then added 1 μg/mL LPS for 24 h; the Gen2+TSA+LPS group was treated with 10 μmol/L Gen and 5 μmol/L TSA for 0.5 h and then added 1 μg/mL LPS for 24 h; the Gen2+pcDNA-HDAC6+LPS group and the Gen2+pcDNA3.1+LPS group received 100 nmol/L pcDNA-HDAC6 and pcDNA3.1 plasmids respectively, and 24 h after transfection, 10 μmol/L Gen was pretreated for 0.5 h, and then added 1 μg/mL LPS for 24 h. Real-time RT-PCR was used to detect the HDAC6 mRNA expression in DRGn; CCK-8 method was used to detect cell viability of DRGn; flow cytometry was used to detect cell apoptosis of DRGn; ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in DRGn culture supernatant; Western blotting was used to detect the protein expression of HDAC6, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF-κB p65 in DRGn. RESULTS: Compared with the control group, the expression levels of HDAC6 mRNA and protein, the expression levels of TLR4 and MyD88 protein in DRGn of LPS group rats were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, and the activity of DRGn was significantly decreased, the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05). Compared with the LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group and the Gen2+TSA+LPS group were significantly down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly decreased, the activity of DRGn was significantly increased, the apoptosis rate was significantly decreased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly decreased (all P<0.05), and the above changes were most obvious in the Gen2+TSA+LPS group. Compared with the Gen2+LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the Gen2+pcDNA-HDAC6+LPS group were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, the activity of DRGn was significantly decreased, and the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05). CONCLUSIONS Gen can alleviate LPS-induced DRGn inflammatory injury in rats, which might be related to down-regulating the expression of HDAC6 and further inhibiting the activation of TLR4/MyD88/NF-κB signaling pathway.
Animals ; Ganglia, Spinal ; Genistein/pharmacology* ; Histone Deacetylase 6/metabolism* ; Interleukin-6/metabolism* ; Lipopolysaccharides ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism* ; Neurons/metabolism* ; RNA, Messenger ; Rats ; Toll-Like Receptor 4/metabolism* ; Tumor Necrosis Factor-alpha/metabolism*

Background: Antimicrobial peptides (AMPs) have been identified as promising compounds for consideration as novel antimicrobial agents. Objectives: This study analyzed the efficacy of cecropin B against Haemophilus parasuis isolates through scanning electron microscopy (SEM) and atomic force microscopy (AFM) experiments. Results: Cecropin B exhibited broad inhibition activity against 15 standard Haemophilus parasuis (HPS) strains and 5 of the clinical isolates had minimum inhibition concentrations (MICs) ranging from 2 to 16 μg/mL. Microelectrophoresis and hexadecane adsorption assays indicated that the more hydrophobic and the higher the isoelectric point (IEP) of the strain, the more sensitive it was to cecropin B. Through SEM, multiple blisters of various shapes and dents on the cell surface were observed. Protrusions and leakage were detected by AFM. Conclusions Based on the results, cecropin B could inhibit HPS via a pore-forming mechanism by interacting with the cytoplasmic membrane of bacteria. Moreover, as cecropin B concentration increased, the bacteria membrane was more seriously damaged. Thus, cecropin B could be developed as an effective anti-HPS agent for use in clinical applications.

Objective:To explore the causes of in premature infants with gestational age of 28 to 34 weeks in Neonatal Intensive Care Unit (NICU) , and to observe the influence of interruption of enteral nutrition, parenteral nutrition replacement or abandonment events on the clinical outcome of premature infants.Methods:A retrospective study was used to select 310 premature infants with gestational age of 28 to 34 weeks who were admitted to NICU of Children's Hospital of Shanxi (Women Health Center of Shanxi) and hospitalized for enteral nutrition and parenteral nutrition from January to June 2019. The effect of interruption on the clinical outcomes of premature infants was statistically analyzed.Results:All 310 preterm infants had received more than 24 hours of enteral nutrition support during the NICU. A total of 280 cases (397 times) of enteral nutrition interruption occurred, for a total of 4 367 hours. Among 280 premature infants with interruption of enteral nutrition, the interruption time of enteral nutrition in 123 premature infants was longer than 12 h/d, and the interruption time of enteral nutrition in 157 cases was less than 12 h/d. There were significant differences in time to regain birth weight, duration of ventilator use, average length of hospital stays, incidence of parenteral nutrition replacement or abandonment, and incidence of extrauterine growth retardation among premature infants with different duration of enteral nutrition interruption ( P<0.05) . Conclusions:The nutritional status of premature infants with gestational age of 28 to 34 weeks in NICU is not ideal during hospitalization. Feeding intolerance, iatrogenic manipulation, necrotizing enterocolitis, out-of-care examinations, rescue, and surgery are the main causes of nutritional interruption. Among them, the nutritional interruption time >12 h/d has a greater impact on the clinical outcome of preterm infants. It is recommended that preterm infants need reasonable and standardized enteral nutrition and parenteral nutrition during the NICU, and actively promote breastfeeding of preterm infants to promote the efficiency of enteral nutrition in preterm infants, improve the ability of preterm infants to resist infection, and reduce the occurrence of extrauterine growth retardation Rate, and ultimately achieve the goal of reducing the morbidity and mortality of premature infants.

Objective:To explore the fluid resuscitation strategy in shock stage in severely burned children with different burn areas in different age groups, and to evaluate the curative effect.Methods:A retrospective cohort study was conducted. From January 2015 to June 2020, 235 children with severe and above burns who met the inclusion criteria were hospitalized in the First Affiliated Hospital of Nanchang University, including 150 males and 85 females, aged 3 months to 12 years. After admission, it was planned to rehydrate the children with electrolyte, colloid, and water according to the domestic rehydration formula for pediatric burn shock, and the rehydration volume and speed were adjusted according to the children's mental state, peripheral circulation, heart rate, blood pressure, and urine output, etc. The actual input volume and planned input volume of electrolyte, colloid, water, and total fluid of all the children were recorded during the 8 hours since fluid replacement and the first and second 24 hours after injury. According to urine output during the 8 hours since fluid replacement, all the children were divided into satisfactory urine output maintenance group (119 cases) with urine output ≥1 mL·kg -1·h -1 and unsatisfactory urine output maintenance group (116 cases) with urine output <1 mL·kg -1·h -1, and the electrolyte coefficient, colloid coefficient, and water coefficient of the children were calculated during the 8 hours since fluid replacement. According to the total burn area, children aged <3 years (155 cases) and 3-12 years (80 cases) were divided into 15%-25% total body surface area (TBSA) group and >25%TBSA group, respectively. The electrolyte coefficient, colloid coefficient, water coefficient, and urine output of the children were calculated or counted during the first and second 24 hours after injury, and the non-invasive monitoring indicators of body temperature, heart rate, respiratory rate, and percutaneous arterial oxygen saturation and efficacy indicators of hematocrit, platelet count, hemoglobin, albumin, creatinine, and alanine aminotransferase (ALT) of the children were recorded 48 hours after injury. The prognosis and outcome indicators of all the children during the treatment were counted, including complications, cure, improvement and discharge, automatic discharge, and death. Data were statistically analyzed with independent sample or paired sample t test, Mann-Whitney U test, chi-square test, and Fisher's exact probability test. Results:During the 8 hours since fluid replacement, the actual input volume of electrolyte of all the children was significantly more than the planned input volume, and the actual input volumes of colloid, water, and total fluid were significantly less than the planned input volumes ( Z=13.094, 5.096, 13.256, 7.742, P<0.01). During the first and second 24 hours after injury, the actual input volumes of electrolyte of all the children were significantly more than the planned input volumes, and the actual input volumes of water and total fluid were significantly less than the planned input volumes ( Z=13.288, -13.252, 3.867, 13.183, -13.191, 10.091, P<0.01), while the actual input volumes of colloid were close to the planned input volumes ( P>0.05). During the 8 hours since fluid replacement, compared with those in unsatisfactory urine output maintenance group, there was no significant change in electrolyte coefficient or colloid coefficient of children in satisfactory urine output maintenance group ( P>0.05), while the water coefficient was significantly increased ( Z=2.574, P<0.05). Among children <3 years old, compared with those in >25%TBSA group, the electrolyte coefficient and water coefficient of children were significantly increased and the urine output of children was significantly decreased in 15%-25%TBSA group during the first and second 24 hours after injury ( Z=-3.867, -6.993, -3.417, -5.396, -5.062, 1.503, P<0.05 or P<0.01), while the colloid coefficient did not change significantly ( P>0.05); the levels of efficacy indicators of hematocrit, platelet count, and hemoglobin at 48 h after injury were significantly increased, while ALT level was significantly decreased ( Z=-2.720, -3.099, -2.063, -2.481, P<0.05 or P<0.01); the levels of the rest of the efficacy indicators and non-invasive monitoring indicators at 48 h after injury did not change significantly ( P>0.05). Among children aged 3-12 years, compared with those in >25%TBSA group, the electrolyte coefficient and water coefficient of children in 15%-25%TBSA group were significantly increased during the first and second 24 hours after injury, the colloid coefficient during the second 24 h was significantly decreased ( Z=-2.042, -4.884, -2.297, -3.448, -2.480, P<0.05 or P<0.01), while the colloid coefficient during the first 24 hours after injury, urine output during the first and second 24 hours after injury, and the non-invasive monitoring indicators and efficacy indicators at 48 hours after injury did not change significantly ( P>0.05). Complications occurred in 17 children during the treatment. Among the 235 children, 211 cases were cured, accounting for 89.79%, 5 cases were improved and discharged, accounting for 2.13%, 16 cases were discharged automatically, accounting for 6.81%, and 3 cases died, accounting for 1.28%. Conclusions:The electrolyte volume in early fluid resuscitation in severely burned children exceeding the volume calculated by the formula can obtain a good therapeutic effect. Among children <3 years old, the volume of fluid resuscitation should be appropriately increased in children with extremely severe burns compared with children with severe burns during fluid resuscitation; among children aged 3-12 years, the colloid volume should be appropriately increased in children with extremely severe burns compared with children with severe burns during fluid resuscitation; non-invasive monitoring indicators can be used to monitor hemodynamics and guide fluid resuscitation in severely burned children.