AIM To investigate the stability of salvianolic acid B.METHODS HPLC was adopted in the content determination of salvianolic acid B,after which the chemical stability in different pH of buffer solutions,oxidation stability in different concentrations of H2O2,and biological stability in artificial gastric fluid,artificial intestinal fluid and biological matrices were analyzed,and its degradation kinetics was fitted.RESULTS Salvianolic acid B was stable in acidic and weakly acidic buffer solutions and artificial gastric fluid,which demonstrated poor stability in neutral and alkaline buffer solutions,artificial intestinal fluid,H2O2 and biological matrices.The degradation process of this constituent accorded with the first-order kinetic model in ileum homogenate,and the second-order kinetic model in pH 7.4 buffer solution,artificial intestinal fluid,H2O2 and stomach,duodenum,jejunum,colon homogenates.CONCLUSION Biological matrices,oxidants and alkaline environment can affect the stability of salvianolic acid B.This experimental exhibits important significance for the development and application of salvianolic acid B-related products.

Aim To investigate the anti-acute lung injury(ALI)effect of Sterculiae Lychnophorae Semen(SLS)and its mechanism.Methods The main ac-tive components of SLS and their core targets and path-ways of action against ALI were obtained by network pharmacology methods.Subsequently,molecular doc-king technology and in vitro cellular experiments were applied for validation.Results A total of 19 core tar-gets were obtained,including HSP90AA1,CASP3,TNF,MAPK8 and MAPK14.The mechanisms may in-volve signaling pathways such as cancer,PI3K/Akt and MAPK.Molecular docking confirmed that the key targets of SLS formed a better binding activity with the relevant active ingredients.The in vitro results showed that SLS was able to protect the PM2.5-contaminated BEAS-2B cells,inhibit their NO,IL-1β and TNF-αlevels,and reduce the expression of p-p38 MAPK and p-JNK proteins.Conclusions The study successfully predicts the active ingredients,targets and signaling pathways of SLS against ALI,and in vitro experiments demonstrate that SLS might protect BEAS-2B cells from PM2.5 stimulus-induced inflammation and apoptosis by inhibiting the over-activation of p38 MAPK and JNK signaling pathways.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Aim To investigate the anti-acute lung injury(ALI)effect of Sterculiae Lychnophorae Semen(SLS)and its mechanism.Methods The main ac-tive components of SLS and their core targets and path-ways of action against ALI were obtained by network pharmacology methods.Subsequently,molecular doc-king technology and in vitro cellular experiments were applied for validation.Results A total of 19 core tar-gets were obtained,including HSP90AA1,CASP3,TNF,MAPK8 and MAPK14.The mechanisms may in-volve signaling pathways such as cancer,PI3K/Akt and MAPK.Molecular docking confirmed that the key targets of SLS formed a better binding activity with the relevant active ingredients.The in vitro results showed that SLS was able to protect the PM2.5-contaminated BEAS-2B cells,inhibit their NO,IL-1β and TNF-αlevels,and reduce the expression of p-p38 MAPK and p-JNK proteins.Conclusions The study successfully predicts the active ingredients,targets and signaling pathways of SLS against ALI,and in vitro experiments demonstrate that SLS might protect BEAS-2B cells from PM2.5 stimulus-induced inflammation and apoptosis by inhibiting the over-activation of p38 MAPK and JNK signaling pathways.

Aim To investigate the antagonistic effect of Schizandrin A(SchA)on oxidative stress-induced endothelial dysfunction and its mechanism of action.Methods Human umbilical vein endothelial cells(HUVECs)were selected as the research subjects,and the effects of SchA on cell viability were detected by MTT assay;the content of ROS in the cells was detec-ted by flow cytometry;the content of MDA and CAT in the cells,and the content of NO and ET-1 in the cell supernatant were detected by kit assay;and the expres-sion of SOD1,p-eNOS/eNOS proteins,and ET-1 in the cell supernatant were detected by Western blot.Immu-nofluorescence experiments were performed to detect Nrf2 entry into the nucleus of cells.Results SchA re-versed the LPS-or hypoxia-induced increase in ROS and MDA content as well as the decrease in SOD1 and CAT content in HUVECs by activating the Nrf2/Keap1/HO-1 signaling pathway.SchA inhibited the decrease of p-eNOS and eNOS protein expression in HUVECs cells,as well as NO content in cell culture medium and the increase of ET-1 content induced by LPS.The Nrf2 inhibitor ML385 reversed the antagonis-tic effects of SchA on oxidative stress and endothelial dysfunction.Conclusions SchA antagonized LPS and hypoxia-induced oxidative stress,and SchA amelio-rated oxidative stress-induced endothelial dysfunction by up-regulating the Nrf2/Keap1/HO-1 signaling path-way.

AIM To investigate the stability of salvianolic acid B.METHODS HPLC was adopted in the content determination of salvianolic acid B,after which the chemical stability in different pH of buffer solutions,oxidation stability in different concentrations of H2O2,and biological stability in artificial gastric fluid,artificial intestinal fluid and biological matrices were analyzed,and its degradation kinetics was fitted.RESULTS Salvianolic acid B was stable in acidic and weakly acidic buffer solutions and artificial gastric fluid,which demonstrated poor stability in neutral and alkaline buffer solutions,artificial intestinal fluid,H2O2 and biological matrices.The degradation process of this constituent accorded with the first-order kinetic model in ileum homogenate,and the second-order kinetic model in pH 7.4 buffer solution,artificial intestinal fluid,H2O2 and stomach,duodenum,jejunum,colon homogenates.CONCLUSION Biological matrices,oxidants and alkaline environment can affect the stability of salvianolic acid B.This experimental exhibits important significance for the development and application of salvianolic acid B-related products.

Objective To explore the clinical and genetic characteristics of children with holocarboxylase synthetase(HLCS)deficiency.Methods A retrospective analysis was conducted on the clinical data of 3 children with HLCS deficiency who were admitted to Children's Hospital Affiliated to Zhengzhou University from December 2014 to January 2024.Relevant literature indexed in CNKI,Wanfang Data,PubMed and other databases was reviewed to summarize the clinical characteristics and HLCS gene mutations of children with HLCS deficiency.Results All 3 children were male,with onset age of 4-6 months.The main clinical manifestations included shortness of breath,vomiting,diarrhea,and poor mental state,and partial cases were complicated by growth retardation and neurological symptoms.Laboratory tests showed metabolic acidosis in all cases,blood amino acid and acylcarnitine profiles as well as urinary organic acid analysis suggested multiple carboxylase deficiency.Genetic testing revealed compound heterozygous mutation in the HLCS gene of all 3 children,among which the c.1892delT(p.L631X)mutation was previously unreported.According to the guidelines of the American College of Medical Genetics and Genomics(ACMG),the c.1892delT(p.L631X)mutation was rated as pathogenic mutation(PVS1+PM2_supporting+PM3).Biotin supplementation was effective in all cases.Literature review included 27 English literatures and 29 Chinese literatures,reporting a total of 133 children with HLCS deficiency caused by HLCS gene mutation.Common clinical manifestations included metabolic acidosis,skin lesions,vomiting,feeding difficulties,dyspnea,diarrhea,and neurological symptoms,etc.Conclusions Blood amino acid and acylcarnitine profiles,urine organic acid analysis,and gene testing are helpful for the diagnosis of HLCS deficiency.Timely biotin supplementation leads to a good prognosis.The mutation of HLCS gene is considered as the genetic etiology of HLCS deficiency in 3 children,among which the c.1892delT(p.L631X)mutation is a newly discovered mutation.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Aim To investigate the antagonistic effect of Schizandrin A(SchA)on oxidative stress-induced endothelial dysfunction and its mechanism of action.Methods Human umbilical vein endothelial cells(HUVECs)were selected as the research subjects,and the effects of SchA on cell viability were detected by MTT assay;the content of ROS in the cells was detec-ted by flow cytometry;the content of MDA and CAT in the cells,and the content of NO and ET-1 in the cell supernatant were detected by kit assay;and the expres-sion of SOD1,p-eNOS/eNOS proteins,and ET-1 in the cell supernatant were detected by Western blot.Immu-nofluorescence experiments were performed to detect Nrf2 entry into the nucleus of cells.Results SchA re-versed the LPS-or hypoxia-induced increase in ROS and MDA content as well as the decrease in SOD1 and CAT content in HUVECs by activating the Nrf2/Keap1/HO-1 signaling pathway.SchA inhibited the decrease of p-eNOS and eNOS protein expression in HUVECs cells,as well as NO content in cell culture medium and the increase of ET-1 content induced by LPS.The Nrf2 inhibitor ML385 reversed the antagonis-tic effects of SchA on oxidative stress and endothelial dysfunction.Conclusions SchA antagonized LPS and hypoxia-induced oxidative stress,and SchA amelio-rated oxidative stress-induced endothelial dysfunction by up-regulating the Nrf2/Keap1/HO-1 signaling path-way.

Objective To explore the therapeutic mechanism of Liuwei Buqi(LWBQ)Formula for chronic obstructive pulmonary disease(COPD)in rat models.Methods SD rat models of COPD established by cigarette smoking combined with intratracheal lipopolysaccharide(LPS)instillation and hormone injection were treated with LWBQ Formula by gavage with or without intraperitoneal injection of MCC950 for 3 weeks,starting at the 5th week of modeling.After the treatments,the rats were examined for lung pathologies,lung function,total cell count and white blood cell count in bronchoalveolar lavage fluid(BALF),and serum levels of IL-6,TNF-α,IL-18 and NO.The mRNA expressions of NLRP3,ASC,caspase-1,GSDMD-N,IL-1β,and IL-18 in the lung tissue were detected with qRT-PCR.Results Compared with the normal control rats,the COPD rat models had severe lung pathologies and showed significantly decreased lung function,increased total cell and leukocyte subset counts in BALF,and increased serum levels of IL-6,TNF-α,IL-18 and NO and mRNA expressions of pyroptosis-related proteins in the lung tissue.Treatment of the rat models with LWBQ Formula significantly improved lung pathology and lung function,reduced total cell and leukocyte counts in BALF,and decreased serum levels of the inflammatory factors and expressions of pyroptosis-related proteins in the lung tissue.The combined treatment with MCC950 further improved lung pathology and function in spite of a significant difference,but BALF cell counts,serum inflammatory factor levels and pulmonary expressions of pyroptosis-related proteins were all significantly reduced following the treatment.Conclusion LWBQ Formula can delay the progression of COPD in rats possibly by inhibiting lung tissue pyroptosis via regulating the NLRP3/caspase-1/GSDMD pathway to reduce inflammatory response and lung damage.