Objective To observe and analyze the clinical efficacy of Hewei Jiangni Formula in treating patients with non-erosive gastroesophageal reflux disease(NERD)and cold-heat complex syndrome and explore its regulatory mechanism on visceral hypersensitivity.Methods Sixty patients with NERD and cold-heat complex syndrome diagnosed at the Gastroenterology Clinic of Dongfang Hospital,Beijing University of Chinese Medicine from January 2021 to Decemer 2023,were randomly divided into the Hewei Jiangni Formula group and omeprazole group,with 30 patients per group.The Hewei Jiangni Formula group was treated with Hewei Jiangni Formula and omeprazole enteric-coated tablets placebo,whereas the omeprazole group was treated with omeprazole enteric-coated tablets and Hewei Jiangni Formula placebo.The treatment period was scheduled to last for 8 weeks.The primary outcome indicators(Gastroesophageal Reflux Disease Quality of Life Questionnaire(GERD-Q)scale score:response rate,total score,and single symptom score)and secondary outcome indicators(traditional Chinese medicine clinical scores scale)were recorded before and after treatment in both groups.Ten healthy individuals were recruited from the Physical Examination Center of Dongfang Hospital,Beijing University of Chinese Medicine,as the healthy control group.The expression levels of mast cell tryptase(MCT),protease-activated receptor 2(PAR2),transient receptor potential vanilloid 1(TRPV1),substance P(SP),calcitonin gene-related peptide(CGRP),5-hydroxytryptamine(5-HT),and 5-hydroxytryptamine 3 receptor(5-HT3R)were recorded.These indicators were then used for the following comparisons:the NERD patients vs.the healthy group before treatment;the Hewei Jiangni Formula group vs.the omeprazole group after treatment;the intra-group comparisons within both NERD groups.Changes in serum levels of these indicators were observed before and after treatment in both NERD groups.Results According to the GERD-Q scores before and after treatment,the effective rate was 90.00%in the Hewei Jiangni Formula group and 86.67%in the omeprazole group,with no significant differences.Both groups exhibited improved symptoms of heartburn,regurgitation,upper abdominal pain,and sleep disorders caused by heartburn or regurgitation(P<0.05);however,neither group exhibited significantly improved nausea(P>0.05).Before treatment,MCT,PAR2,TRPV1,SP,CGRP,5-HT,and 5-HT3R expression levels in both NERD groups were significantly higher than those in the healthy control group(P<0.05).After treatment with Hewei Jiangni Formula or omeprazole enteric-coated tablets,the expression levels of these indicators decreased in both groups(P<0.05).The omeprazole group was superior to Hewei Jiangni Formula in reducing 5-HT3R expression(P<0.05).Conclusion Hewei Jiangni Formula significantly improves the symptoms of patients with NERD and cold-heat complex syndrome,with efficacy comparable to that of omeprazole enteric-coated tablets.It is superior to omeprazole in improving symptoms of spleen yang deficiency,such as loss of appetite,fatigue,borborygmus with loose stools,and cold extremities.Hewei Jiangni Formula reduces MCT,PAR2,TRPV1,SP,CGRP,5-HT,and 5-HT3R expression levels,regulates related signaling pathways,and alleviates visceral hypersensitivity.

Objective To observe and analyze the clinical efficacy of Hewei Jiangni Formula in treating patients with non-erosive gastroesophageal reflux disease(NERD)and cold-heat complex syndrome and explore its regulatory mechanism on visceral hypersensitivity.Methods Sixty patients with NERD and cold-heat complex syndrome diagnosed at the Gastroenterology Clinic of Dongfang Hospital,Beijing University of Chinese Medicine from January 2021 to Decemer 2023,were randomly divided into the Hewei Jiangni Formula group and omeprazole group,with 30 patients per group.The Hewei Jiangni Formula group was treated with Hewei Jiangni Formula and omeprazole enteric-coated tablets placebo,whereas the omeprazole group was treated with omeprazole enteric-coated tablets and Hewei Jiangni Formula placebo.The treatment period was scheduled to last for 8 weeks.The primary outcome indicators(Gastroesophageal Reflux Disease Quality of Life Questionnaire(GERD-Q)scale score:response rate,total score,and single symptom score)and secondary outcome indicators(traditional Chinese medicine clinical scores scale)were recorded before and after treatment in both groups.Ten healthy individuals were recruited from the Physical Examination Center of Dongfang Hospital,Beijing University of Chinese Medicine,as the healthy control group.The expression levels of mast cell tryptase(MCT),protease-activated receptor 2(PAR2),transient receptor potential vanilloid 1(TRPV1),substance P(SP),calcitonin gene-related peptide(CGRP),5-hydroxytryptamine(5-HT),and 5-hydroxytryptamine 3 receptor(5-HT3R)were recorded.These indicators were then used for the following comparisons:the NERD patients vs.the healthy group before treatment;the Hewei Jiangni Formula group vs.the omeprazole group after treatment;the intra-group comparisons within both NERD groups.Changes in serum levels of these indicators were observed before and after treatment in both NERD groups.Results According to the GERD-Q scores before and after treatment,the effective rate was 90.00%in the Hewei Jiangni Formula group and 86.67%in the omeprazole group,with no significant differences.Both groups exhibited improved symptoms of heartburn,regurgitation,upper abdominal pain,and sleep disorders caused by heartburn or regurgitation(P<0.05);however,neither group exhibited significantly improved nausea(P>0.05).Before treatment,MCT,PAR2,TRPV1,SP,CGRP,5-HT,and 5-HT3R expression levels in both NERD groups were significantly higher than those in the healthy control group(P<0.05).After treatment with Hewei Jiangni Formula or omeprazole enteric-coated tablets,the expression levels of these indicators decreased in both groups(P<0.05).The omeprazole group was superior to Hewei Jiangni Formula in reducing 5-HT3R expression(P<0.05).Conclusion Hewei Jiangni Formula significantly improves the symptoms of patients with NERD and cold-heat complex syndrome,with efficacy comparable to that of omeprazole enteric-coated tablets.It is superior to omeprazole in improving symptoms of spleen yang deficiency,such as loss of appetite,fatigue,borborygmus with loose stools,and cold extremities.Hewei Jiangni Formula reduces MCT,PAR2,TRPV1,SP,CGRP,5-HT,and 5-HT3R expression levels,regulates related signaling pathways,and alleviates visceral hypersensitivity.

PURPOSE: Molecular mechanisms leading to asthma is still ill-defined. Though the function of microRNAs (miRNAs) in asthma was previously reported, the involvement of miR-155 in important features of this disease remains unknown. The present study was designed to uncover the probable involvement of miR-155-5p in the proliferation and migration of IL-13-induced human bronchial smooth muscle cells (BSMCs) and the intrinsic regulatory mechanism. METHODS: The effects of different concentrations of IL-13 on the proliferation and migration of BSMCs as well as the expression of miR-155-5p and its predicted target transforming growth factor (TGF)-β-activated kinase 1/MAP3K7-binding protein 2 (TAB2) were investigated. The effects of miR-155-5p on the proliferation and migration of interleukin (IL)-13-induced BSMCs was determined in vitro using BSMCs transfected with miR-155 mimic/inhibitor and induced by a high concentration of IL-13. The quantitative real-time polymerase chain reaction (qRTPCR) was employed for determining the expression of miR-155-5p and TAB2. Western blotting was applied to analyze the expression of TAB2 at the protein level. Cell proliferation and migration were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell assays, respectively. RESULTS: The proliferation and migration of BSMCs were dose-dependently increased with IL-13 treatment. Contrariwise, IL-13 dose-dependently inhibited the expression of miR-155-5p in BSMCs. Mechanistic studies showed that inhibition of miR-155-5p further promoted the stimulatory effects of IL-13, whereas overexpression of miR-155 significantly inhibited these effects. In silico studies and luciferase reporter assays indicated that TAB2 was a negatively regulated miR-155-5p target. CONCLUSIONS: These results suggested that miR-155-5p-inhibit the IL-13-induced proliferation and migration of BSMCs by targeting TAB2 and that the IL-13/miR-155/TAB2 pathway could serve as a therapeutic target for pulmonary diseases, especially asthma.
Asthma ; Blotting, Western ; Cell Proliferation ; Computer Simulation ; Humans* ; In Vitro Techniques ; Interleukin-13 ; Interleukins ; Luciferases ; Lung Diseases ; MicroRNAs ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Phosphotransferases* ; Real-Time Polymerase Chain Reaction ; Transforming Growth Factors