Clinical practice guidelines for prevention and treatment of postoperative gastrointestinal disorder with Integrated Traditional Chinese and Western Medicine (2023).

Postoperative gastrointestinal disorder (POGD) was a common complication after surgery under anesthesia. Strategies in combination with Traditional Chinese Medicine and Western medicine showed some distinct effects but standardized clinical practice guidelines were not available. Thus, a multidisciplinary expert team from various professional bodies including the Perioperative and Anesthesia Professional Committees of the Chinese Association of Integrative Medicine (CAIM), jointly with Gansu Province Clinical Research Center of Integrative Anesthesiology/Anesthesia and Pain Medical Center of Gansu Provincial Hospital of Traditional Chinese Medicine and WHO Collaborating Center for Guideline Implementation and Knowledge Translation/Chinese Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) Center/Gansu Provincial Center for Medical Guideline Industry Technology/Evidence-based Medicine Center of Lanzhou University, was established to develop evidence-based guidelines. Clinical questions (7 background and 12 clinical questions) were identified through literature reviews and expert consensus meetings. Based on systematic reviews/meta-analyses, evidence quality was analyzed and the advantages and disadvantages of interventional measures were weighed with input from patients' preferences. Finally, 20 recommendations were developed through the Delphi-based consensus meetings. These recommendations included disease definitions, etiologies, pathogenesis, syndrome differentiation, diagnosis, and perioperative prevention and treatment.

Effects of early vitamin D supplementation on the prevention of bronchopulmonary dysplasia in preterm infants.

BACKGROUND: Bronchopulmonary dysplasia (BPD) is a respiratory dysfunction caused by poor lung bronchial development, which may lead to long-term lung disease, threatening the lives of children. Studies have shown that premature infants with low vitamin D are highly associated with BPD. In this study, we aim to obtain insights into whether early vitamin D supplementation could prevent BPD in preterm infants. METHODS: A total of 112 preterm infants were randomly divided into two groups: the control and vitamin D supplementation (VD) group. The VD group received vitamin D (800 IU/day) within 48 h at birth for consecutively 28 days. The serum levels of 25(OH)D3 and C-reactive protein (CRP), IL6, and TNF-α were measured using ELISA assay. The arterial partial pressure of oxygen (PaO2 ) and carbon dioxide (PaCO2 ) was measured using an i-STAT analyzer. RESULTS: The occurrence of BPD was decreased in the VD group compared with the control. The decreased serum 25(OH)D3 was significantly elevated by supplementation with vitamin D. In addition, the serum inflammation factors (CRP, IL6, and TNF-α) were significantly reduced by vitamin D supplementation. CONCLUSION: We demonstrated that early vitamin D supplementation could significantly reduce BPD incidence in preterm infants. We showed that early vitamin D supplementation could significantly increase serum level of 25(OH)D3 and reduce inflammatory response thereby preventing and reducing neonatal BPD. LIMITATION: Firstly, a larger sample size will be needed to be included to gain a comprehensive understanding of the protective effects of vitamin D and BPD mechanistically in preterm infants. Secondly, the pathophysiological process of BPD will need to be studied. In addition, the pathways that vitamin D is responsible for, need to be further researched.

Carnosic acid alleviates brain injury through NF­κB­regulated inflammation and Caspase­3­associated apoptosis in high fat­induced mouse models.

High fat diet (HFD) is a risk factor for various diseases in humans and animals. Metabolic disease­induced brain injury is becoming an increasingly popular research topic. Carnosic acid (CA) is a phenolic diterpene synthesized by plants belonging to the Lamiaceae family, which exhibits multiple biological activities. In the present study, a mouse model of HFD­induced metabolic syndrome was generated. The body weight, liver weight, daily food intake, daily caloric intake, serum TG, serum TC, serum insulin and serum glucose of animals treated with CA were recorded. Additionally, the gene and protein expression levels of inflammatory cytokines, NF­κB signaling componnts, and caspase­3 were evaluated in the various CA treatment groups via immunohistochemical analysis, western blotting, reverse transcription­quantitative PCR. CA treatment significantly decreased HFD­induced metabolic syndrome by decreasing the serum levels of triglycerides, total cholesterol, insulin and glucose. Furthermore, CA served a protective role against brain injury by inhibiting the inflammatory response. CA significantly decreased the protein expression levels of various pro­inflammatory cytokines in serum and brain tissues, including interleukin (IL)­1ß, IL­6 and tumor necrosis factor­α, regulated by the NF­κB signaling pathway. In addition, CA was revealed to promote the expression levels of anti­apoptotic Bcl­2, and to decrease the expression levels of pro­apoptotic Bax and matrix metallopeptidase 9. The present results suggested that CA was able to alleviate brain injury by modulating the inflammatory response and the apoptotic pathway. Administration of CA may represent a novel therapeutic strategy to treat metabolic disease­induced brain injury in the future.

Therapeutic Efficacy of the Traditional Chinese Medicine Baishaoqiwu on TNBS-induced Colitis is Associated with Down-regulation of the TLR4/MyD88/NF-κB Signaling Pathway.

BACKGROUND/AIM: The traditional Chinese medicine Baishaoqiwu (BSQW) has been previously used to clinically treat inflammatory bowel diseases. However, the mechanisms of it's therapeutic efficacy remain unclear. The aim of this study was to examine the efficacy of BSQW on ulcerative colitis (UC) and the TLR4/MyD88/NF-κB signaling pathway in a rat model of colitis. MATERIALS AND METHODS: The colitis rat model was induced by anal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS). The animals with induced colitis were treated with BSQW at a dose of 13.2 mg/kg daily, p.o. Mesalazin was used as a positive control and was given to the animals with induced colitis at a dose of 420 mg/kg daily, p.o. The untreated animals with induced colitis and normal animals served as model controls and normal controls, respectively. Macroscopic and histological assessments were performed after treatment. The expression of MyD88, NF-κB P65 and TLR4 were determined by immunohistochemical analysis. RESULTS: Administration of BSQW or Mesalazin ameliorated TNBS-induced macroscopic and histological damage in the rats with induced colitis. The macroscopic score and total colitis index were significantly reduced in the BSQW- and Mesalazin-treated groups compared to the model control group (p<0.05). BSQW or Mesalazin significantly inhibited TNBS-induced expression of the TLR4, MyD88 and NF-κB P65 genes. No treatment-related toxicity was found in either the BSQW- or the Mesalazin-treated groups. CONCLUSION: Suppression of the TLR4/MyD88/NF-κB signaling pathway may be one of the mechanisms involved in the therapeutic efficacy of BSQW against UC.