Esophageal cancer （EC） is a common malignant tumor of the digestive system with an extremely poor prognosis. MicroRNA （miRNA） is an important regulator in tumor occurrence and development， and can participate in malignant biological behaviors such as tumor cell proliferation， invasion， metastasis and apoptosis. Traditional Chinese medicine has the characteristics of accurate curative effects， wide range of effects， and few side effects. The review uses miRNA as the entry point to systematically elaborate on the mechanism of traditional Chinese medicine-mediated miRNA intervening in EC. The results showed that active ingredients of traditional Chinese medicine （including curcumin， Tussilago farfara polysaccharides， Atractylodes macrocephala polysaccharides and ophiopogonin B） and Dougen guanshitong oral liquid could up-regulate the expressions of miRNAs such as miRNA-532-3p （miR-532-3p）， miR-551b-3p， miR-99a， miR-34a， miR-199a-3p and miR-377； and the active ingredients/parts of traditional Chinese medicine （including chrysin and Actinidia arguta extract）， and Chinese herbal formulas （including Chaihu shugan san combined with Xuanfu daizhe decoction and Modified jupi zhuru decoction） could down-regulate the expressions of miRNAs such as miR-199a-3p， miR-451 and miR-21， which could regulate the expressions of signaling pathways （phosphoinositide 3-kinase/protein kinase B， etc.） or their downstream protein（zinc-finger and homeobox protein 1， etc.） or enzymes（thymidine kinase-1， etc.）， inhibit the proliferation， invasion and metastasis of EC cells and induce apoptosis， thereby ultimately achieving the purpose of preventing the disease from aggravating.

Reflux esophagitis is an inflammatory disease of esophageal mucosa damage caused by the reflux of gastric contents into the esophagus. Its incidence is on the rise， and it has become an important precancerous disease of esophageal cancer. Studies have shown that the continuous inflammatory response stimulates the esophageal mucosa， causing abnormal proliferation of esophageal epithelial cells and damage to esophageal mucosal tissue， which eventually leads to the occurrence of heterogeneous hyperplasia and even carcinogenesis. The nuclear transcription factor-kappa B （NF-κB） signaling pathway is one of the most classical inflammatory and cancer signaling pathways. It has been found that abnormal activation of the NF-κB signaling pathway is crucial to the development and prognosis of reflux esophagitis and esophageal cancer. It is widely involved in the proliferation， autophagy， apoptosis， and inflammatory response of esophageal epithelial cells and tumor cells， accelerating the transformation of reflux esophagitis to esophageal cancer and making it a potential target for the treatment of reflux esophagitis and esophageal cancer. Currently， there is no specific treatment for reflux esophagitis and esophageal cancer， and large side effects often appear. Therefore， finding a promising and safe drug remains a top priority. In recent years， traditional Chinese medicine scholars have conducted a lot of research on NF-κB signaling pathway， and the results indicate that NF-κB signaling pathway is an important potential target for traditional Chinese medicine to prevent and treat reflux esophagitis and esophageal cancer， but there is a lack of comprehensive and systematic elaboration. Therefore， this paper summarized the relevant studies in recent years， analyzed the relationship among NF-κB signaling pathway， reflux esophagitis， esophageal cancer， and transformation from inflammation to cancer， and reviewed the research literature on the regulation of the NF-κB signaling pathway in traditional Chinese medicine to prevent and treat reflux esophagitis and esophageal cancer， so as to provide new ideas for the prevention and treatment of reflux esophagitis and esophageal cancer.

OBJECTIVE To investigate the potential mechanism of procyanidin on rats with gingivitis by regulating phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt）/vascular endothelial growth factor （VEGF） signaling pathway. METHODS The rat model of gingivitis was constructed by sewing the neck of the first maxillary molar with silk thread+applying maltose on the gum+feeding with 20% sucrose solution and soft food. Forth-eight model rats were randomly divided into model group， procyanidin group （160 mg/kg）， 740Y-P group （PI3K/Akt signaling pathway activator， 0.02 mg/kg）， and procyanidin+ 740Y-P group （procyanidin 160 mg/kg+740Y-P 0.02 mg/kg）， with 12 rats in each group； another 12 rats were selected as control group； each medication group was treated with corresponding drugs intragastrically or/and intraperitoneally， once a day， for 7 consecutive days. Twenty-four hours after the last administration， the gingival index of rats was measured； the levels of interleukin- 18 （IL-18）， inducible nitric oxide synthase （iNOS） and alkaline phosphatase （ALP） in gingival crevicular fluid， as well as the levels of superoxide dismutase （SOD）， catalase （CAT） and reactive oxygen species （ROS） in gingival tissues of rats were detected； the pathological changes in gingival tissues were observed； the expression levels of PI3K/Akt/VEGF signaling pathway- related proteins in gingival tissues of rats were detected. RESULTS Compared with control group， the gingival tissues of rats in the model group had severe pathological damage，which was manifested as local tissue expansion and congestion， new capillaries， degeneration and loss of collagen fibers and disorder of arrangement， and a large number of inflammatory cell infiltration in the gingival sulcus wall. The gingival index， the levels of IL-18， iNOS， ALP in gingival crevicular fluid， the level of ROS in gingival tissues， the phosphorylations of PI3K and Akt， as well as the protein expression of VEGF in gingival tissues were significantly increased； the levels of SOD and CAT in gingival tissues of rats in model group were significantly decreased （P＜0.05）. Compared with model group， the pathological damage to the gingival tissues of rats in procyanidin group was reduced， and all quantitative indicators were significantly improved （P＜0.05）； 740Y-P could reverse the improvement effect of procyanidin on various indicators （P＜0.05）. CONCLUSIONS Procyanidin may alleviate gingival tissue damage， and improve gingival inflammation and oxidative stress in rats with gingivitis by inhibiting PI3K/Akt/VEGF signaling pathway.

Objective To investigate the effect of prunella vulgaris extract on inflammation,macrophage phenotype,and phagocytic ability in septic mice,and analyze whether Toll like receptor 4(TLR4)/nuclear factor-κB(NF-κB)signaling pathway involved in its mechanism.Methods C57BL/6 mice were divided into the control group,the model group and the prunella vulgaris extract low(25 mg/kg),medium(50 mg/kg)and high(100 mg/kg)dose groups.Except for the control group,all other groups of mice were injected intraperitoneally with lipopolysaccharide(LPS)to prepare sepsis model.Each group was given corresponding medication by gavage.After 24 hours of administration,serum tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,high mobility group protein B1(HMGB1),IL-10 levels,the proportion of M1 type(CD11b+F4/80+)and M2 type(CD206+F4/80+)macrophages in peritoneal macrophages,the phagocytotic capacity of macrophages,the expression of inducible nitric oxide synthase(iNOS)messenger RNA(mRNA)and arginase 1(Arg1)mRNA in peritoneal macrophages and expression levels of TLR4,NF-κB p65 and their phosphorylated proteins in macrophages were detected.Results Compared with the control group,serum TNF-α,IL-1β,HMGB1,proportion of M1 type macrophages in abdominal cavity,mean fluorescence intensity and phagocytotic capacity of macrophages,iNOS mRNA,TLR4,phosphorylated NF-κB p65(p-NF-κB p65)/NF-κB p65 protein expression were increased in the model group(P＜0.05).IL-10,proportion of M2 type macrophages and Arg1 mRNA expression were decreased(P＜0.05).Compared with the model group,serum TNF-α,IL-1β,HMGB1,proportion of M1 type macrophages in abdominal cavity,iNOS mRNA,TLR4,p-NF-κB p65/NF-κB p65 protein expression were decreased successively in the prunella vulgaris extract low,medium and high dose groups(P＜0.05).IL-10,proportion of M2 macrophages,mean fluorescence intensity and phagocytotic capacity of macrophages and Arg1 mRNA expression were increased successively(P＜0.05).Conclusion By inhibiting TLR4/NF-κB pathway,prunella vulgaris extract may inhibit the polarization of peritoneal macrophages into M1 type and promote their polarization to M2 type,enhance macrophage phagocytic ability and alleviate LPS induced inflammatory response in septic mice.

Objective To explore the effective components and possible targets and mechanism of Shenling Baizhu Powder in improving adipose tissue inflammation in children with obesity with the help of network pharmacology and molecular docking method;To conduct preliminary verification through animal experiments.Methods The active components and targets of Shenling Baizhu Powder were screened through the TCMSP database.GeneCards,OMIM,DisGeNET databases were used to obtain the disease targets.An active component-target network was constructed by taking the intersection of drug and disease targets.Protein-protein interaction networks were constructed and core targets were obtained for GO and KEGG pathway enrichment analysis.Molecular docking validation was performed to key components and core targets.Animal experiments were conducted by establishing a model of young obese rats induced by high fat diet,and Shenling Baizhu Powder were given for gavage.The contents of TG and TC in serum and mRNA expressions of TNF-α,IL-1β,INF-γ and Fas in rat adipose tissue of epididymis were detected.Results The key components of Shenling Baizhu Powder to improve the microinflammation of obesity in children were piperlonguminine,acacetin,luteolin,denudatin B,mandenol,inermine,etc.There were 515 common drug-disease targets,and the core targets were TP53,SRC,PIK3R1,HSP90AA1 and PIK3CA.The results of GO enrichment analysis included inflammatory response,positive regulation of MAPK cascade,membrane raft,protein serine/threonine/tyrosine kinase activity,etc.KEGG pathway enrichment analysis results included metabolic,immune,endocrine,cancer and related liver disease signaling pathways.The results of molecular docking showed that the key components could play a regulatory role on the core target.Animal experiments showed that Shenling Baizhu Powder could improve microinflammation and metabolic indexes of model rats.Conclusion Shenling Baizhu Powder can act on multiple targets through various active components and multiple signaling pathways,adjusting inflammatory response and immune process,alleviating insulin resistance,regulating glucose and lipid metabolism,thereby improving adipose tissue inflammatory in children with obesity.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Pancreatic cancer is one of the most destructive malignant tumors； the pathogenesis of this disease is complex and is closely related to genetic susceptibility， chronic pancreatitis， and gene mutations in signaling pathways. The phosphoinositide 3- kinase （PI3K）/protein kinase B （Akt） signaling pathway is a classical cancer signaling pathway that is aberrantly activated in pancreatic cancer cells. In recent years， it has been found that traditional Chinese medicine （TCM） monomers show special activity in the treatment of pancreatic cancer and can be potential drug for the treatment of pancreatic cancer. Based on PI3K/Akt signaling pathway， this paper summarizes the mechanism of TCM monomer intervening in pancreatic cancer and finds that TCM monomer of alkaloids （sinomenine， dictamnine， dauricine， etc.）， terpenoids （saikosaponin A， linderalactone， isoalantolactone， etc.）， phenols （6-gingerol， curcumin， pterostilbene， etc.）， flavonoids （fisetin， kaempferol， quercetin， etc.） and quinones （β-hydroxyisovaleryl shikonin， rhein， lucidone， etc.） can inhibit the proliferation， invasion and migration of pancreatic cancer cells， regulate autophagy and apoptosis， and then inhibit the pathological process of pancreatic cancer by inhibiting PI3K/Akt signaling pathway.

Colorectal cancer （CRC） is one of the leading causes of cancer-related deaths worldwide， with increasing incidence and mortality rates. The disease often develops covertly and lacks specific symptoms in its early stages， leading to late-stage diagnoses in most patients. It has become a prominent research topic in the field of digestive system tumors. The exact mechanisms underlying CRC are not yet clear and involve factors such as genetics， gene mutations， inflammatory responses， and aberrant activation of tumor-related signaling pathways. Nuclear factor-kappa B （NF-κB） is a crucial transcription factor that participates in various biological processes， including inflammatory responses， immune responses， cell proliferation， and apoptosis. Research suggests that NF-κB， serving as a molecular link between inflammation and cancer， is highly expressed in CRC. It promotes the occurrence and development of CRC by regulating the activity of target genes such as cell pro-inflammatory factors， chemokines， angiogenic factors， metastasis factors， and anti-apoptotic proteins. Currently， common treatments for CRC include surgery， radiation therapy， and chemotherapy drugs like 5-fluorouracil. However， these treatments have limitations such as significant adverse reactions， high metastasis rates， and the development of drug resistance. Therefore， the search for effective， low-adverse-reaction drugs to replace or supplement current treatments is essential. In recent years， traditional Chinese medicine （TCM） has shown some effectiveness in preventing and treating CRC. TCM has been found to inhibit the growth of CRC cells by modulating the NF-κB signaling pathway， playing a positive role in the occurrence and progression of CRC. Based on the asthenia in origin and sthenia in superficiality and deficiency-excess in complexity in CRC， this article summarized and analyzed the mechanisms and effects of TCM interventions targeting the NF-κB signaling pathway in CRC， and reviewed advances of 10 Chinese medicinal compound formulas and 37 Chinese medicinal monomer components of different types， including flavonoids， phenols， alkaloids， glycosides， and terpenoids with the effects of dispelling pathogenic factors， reinforcing healthy qi， and removing toxins in the prevention and treatment of CRC by targeting the NF-κB pathway. It is found that Chinese medicine can inhibit CRC cell proliferation， invasion， metastasis， angiogenesis， and inflammation by modulating the NF-κB signaling pathway， induce cell apoptosis， restore drug and radiation sensitivity， and counteract CRC. This article is expected to provide insights and references for the in-depth exploration and treatment of CRC mechanisms.

The development of liver inflammatory diseases is associated with autoimmunity and inflammatory response. As a negative feedback regulator of cell signal, suppressor of cytokine signaling 1 (SOCS1) plays a key role in the development and progression of inflammatory diseases. This article mainly introduces the mechanism of action of SOCS1 in autoimmunity and inflammatory response and briefly describes its role in the development and progression of liver inflammatory diseases such as viral hepatitis and nonalcoholic steatohepatitis. The analysis shows that the abnormal expression of SOCS1 in inflammatory response is associated with the regulation of cytokine receptor, Toll-like receptor, and hormone receptor signal, which leads to the development of inflammatory diseases. Therefore, SOCS1 has potential prospects as an auxiliary means for the diagnosis and treatment of liver inflammatory diseases.