Ulcerative colitis （UC） is a common digestive disease characterized by recurrence and remission alternation，which seriously affects the life quality and physical and mental health of patients. The pathogenesis of UC is complex，and studies have shown that the occurrence and development of UC are closely related to the transduction of multiple signaling pathways. The current western medicine treatment has many problems，such as single action target，more adverse reactions，poor patient tolerance，and easy recurrence after stopping the medicine. Traditional Chinese medicine has the advantages such as multi-targets，multi-pathways， and fewer adverse reactions， elucidating that the action mechanism of traditional Chinese medicine in the treatment of UC is the focus of current research. Therefore， this paper conducted a systematic review on how traditional Chinese medicine exerts therapeutic effects by regulating the signaling pathways related to UC in recent years，and it was found that traditional Chinese medicine can regulate nuclear factor-κB （NF-κB），adenylate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR），Janus tyrosine protein kinase （JAK）/signal transducer and activator of transcription （STAT），phosphatidylinositol 3-kinase （PI3K） /protein kinase B （Akt），NOD-like receptor thermoprotein structural domain-related protein 3 （NLRP3）/cysteine protease-1 （Caspase-1），nuclear respiratory factor 2 （Nrf2）/heme oxygenase-1 （HO-1）， and several other pathways，thereby inhibiting oxidative stress and cellular pyroptosis，regulating the Tregs/Th17 cellular balance， promoting autophagic response and M2-type macrophage polarization，restoring the diversity and abundance of intestinal flora，promoting the repair of intestinal mucosal barrier function，and alleviating the inflammatory damage of UC colonic tissues. The holistic concept and evidence-based treatment of traditional Chinese medicine were combined with the modern molecular mechanism research of traditional Chinese medicine， and the traditional Chinese medicine combinations with different mechanisms， following regulation， were formulated into compound formulas or pairs of medicines according to the pattern of evidence. It is expected to achieve better therapeutic efficacy and to provide ideas and references for the modification of classic compound formulae of traditional Chinese medicine in UC treatment and clinical translation.

Ulcerative colitis （UC）， a chronic relapsing inflammatory bowel disease， involves multifaceted pathological mechanisms such as intestinal barrier dysfunction， immune dysregulation， and oxidative stress. Current therapeutic strategies remain limited in efficacy and safety. In recent years， the adenosine monophosphate-activated protein kinase （AMPK） signaling pathway has emerged as a pivotal therapeutic target for UC due to its central role in energy metabolism， inflammatory regulation， and intestinal homeostasis. This article systematically reviewed the mechanisms by which traditional Chinese medicine （TCM） prevented and treated UC through the regulation of the AMPK signaling pathway， with a focus on elucidating AMPK's multidimensional regulatory network in inflammatory signaling crosstalk， alleviating oxidative stress， restoring intestinal immune balance， repairing the intestinal barrier， and modulating gut microbiota. Leveraging its unique advantages of multi-target engagement and low toxicity， TCM demonstrates promising potential in UC treatment and has become a focal area of research. By systematically summarizing and synthesizing the existing literature on TCM-mediated AMPK pathway modulation in UC， this review aims to provide a theoretical foundation for advancing mechanistic research and clinical interventions in UC.

Ulcerative colitis （UC）， a chronic， non-specific inflammatory bowel disease with typical symptoms such as abdominal pain， diarrhea， and bloody stools， demonstrates a high relapse rate and difficulty in curing. Sishenwan， first recorded in Internal Medicine Abstract （Nei Ke Zhai Yao）， are a classic prescription for treating diarrhea caused by deficiency of the spleen and kidney Yang. The core therapeutic principle of Sishenwan is warming and tonifying the spleen and kidney， and astringing the intestine and stopping diarrhea. In recent years， Sishenwan have demonstrated distinct advantages in the clinical treatment of UC. The pathogenesis of UC involves multiple factors， including immune dysregulation and gut microbiota imbalance. Although Western medicine is effective in the short term， its side effects， high relapse rate， and resistance associated with long-term use pose substantial challenges. Sishenwan have shown excellent clinical outcomes in the treatment of UC due to deficiency of the spleen and kidney Yang. Modern clinical studies indicate that Sishenwan， used alone or in combination with Western medicine or other Chinese medicine compound prescriptions， significantly improve the clinical efficacy in treating UC due to deficiency of the spleen and kidney Yang. Sishenwan effectively alleviate core symptoms such as mucus， pus， and blood in stools， and persistent abdominal pain， reduce Mayo scores and the relapse rate， and improve patients' quality of life. Research on the material basis reveals that Sishenwan contain multiple active ingredients such as psoralen， isopsoralen， and evodiamine. Mechanism studies indicate that Sishenwan inhibit the inflammatory cascade reactions by regulating the signal network through multiple targets. Sishenwan regulate cellular immunity and restore intestinal immune homeostasis. At the microecological level， Sishenwan promote the intestinal barrier repair through the "microbiota-metabolism-immunity" axis. The current research still needs to be deepened in aspects such as the mining of specific biomarkers for syndromes and the exploration of the collaborative mechanism of traditional Chinese and Western medicine. In the future， a full-chain system covering syndrome differentiation， targeting， and monitoring needs to be constructed for promoting the paradigm transformation of Sishenwan into precision drugs. This review systematically explains the treatment mechanism of Sishenwan regarding the combination of disease and syndrome and its multi-target regulatory characteristics， providing a theoretical basis and transformation direction for the treatment of UC with integrated traditional Chinese and Western medicine.

Ulcerative colitis （UC）， a chronic， non-specific inflammatory bowel disease with typical symptoms such as abdominal pain， diarrhea， and bloody stools， demonstrates a high relapse rate and difficulty in curing. Sishenwan， first recorded in Internal Medicine Abstract （Nei Ke Zhai Yao）， are a classic prescription for treating diarrhea caused by deficiency of the spleen and kidney Yang. The core therapeutic principle of Sishenwan is warming and tonifying the spleen and kidney， and astringing the intestine and stopping diarrhea. In recent years， Sishenwan have demonstrated distinct advantages in the clinical treatment of UC. The pathogenesis of UC involves multiple factors， including immune dysregulation and gut microbiota imbalance. Although Western medicine is effective in the short term， its side effects， high relapse rate， and resistance associated with long-term use pose substantial challenges. Sishenwan have shown excellent clinical outcomes in the treatment of UC due to deficiency of the spleen and kidney Yang. Modern clinical studies indicate that Sishenwan， used alone or in combination with Western medicine or other Chinese medicine compound prescriptions， significantly improve the clinical efficacy in treating UC due to deficiency of the spleen and kidney Yang. Sishenwan effectively alleviate core symptoms such as mucus， pus， and blood in stools， and persistent abdominal pain， reduce Mayo scores and the relapse rate， and improve patients' quality of life. Research on the material basis reveals that Sishenwan contain multiple active ingredients such as psoralen， isopsoralen， and evodiamine. Mechanism studies indicate that Sishenwan inhibit the inflammatory cascade reactions by regulating the signal network through multiple targets. Sishenwan regulate cellular immunity and restore intestinal immune homeostasis. At the microecological level， Sishenwan promote the intestinal barrier repair through the "microbiota-metabolism-immunity" axis. The current research still needs to be deepened in aspects such as the mining of specific biomarkers for syndromes and the exploration of the collaborative mechanism of traditional Chinese and Western medicine. In the future， a full-chain system covering syndrome differentiation， targeting， and monitoring needs to be constructed for promoting the paradigm transformation of Sishenwan into precision drugs. This review systematically explains the treatment mechanism of Sishenwan regarding the combination of disease and syndrome and its multi-target regulatory characteristics， providing a theoretical basis and transformation direction for the treatment of UC with integrated traditional Chinese and Western medicine.

Ulcerative colitis （UC） is a chronic and relapsing inflammatory bowel disease that primarily affects the mucosal layer of the rectum and colon. Its pathogenesis is complex and remains incompletely understood. Endoplasmic reticulum stress （ERS） plays a critical role in cellular responses to external stress and the maintenance of homeostasis， and its abnormal activation is closely associated with the development of various inflammatory diseases， particularly in the pathological process of UC. ERS maintains cellular homeostasis by activating the unfolded protein response （UPR）. However， when ERS is prolonged or excessive， UPR fails to alleviate the stress， leading to epithelial cell death and aggravating the progression of UC. Modulating ERS may serve as a key target for the prevention and treatment of UC， and it is one of the current research hotspots. Traditional Chinese medicine （TCM） has shown significant efficacy in regulating ERS， offering unique therapeutic advantages through multi-target and multi-pathway mechanisms. Recent studies have confirmed that TCM can alleviate ERS， inhibit apoptosis， regulate autophagy， reduce inflammatory responses， and maintain intestinal barrier function to prevent and treat UC. This review summarized the relationship between ERS and UC and discussed the intervention of TCM in regulating ERS for the treatment of UC， aiming to provide new insights and approaches for the treatment of UC with TCM.

Ulcerative colitis （UC） is a chronic and relapsing inflammatory bowel disease that primarily affects the mucosal layer of the rectum and colon. Its pathogenesis is complex and remains incompletely understood. Endoplasmic reticulum stress （ERS） plays a critical role in cellular responses to external stress and the maintenance of homeostasis， and its abnormal activation is closely associated with the development of various inflammatory diseases， particularly in the pathological process of UC. ERS maintains cellular homeostasis by activating the unfolded protein response （UPR）. However， when ERS is prolonged or excessive， UPR fails to alleviate the stress， leading to epithelial cell death and aggravating the progression of UC. Modulating ERS may serve as a key target for the prevention and treatment of UC， and it is one of the current research hotspots. Traditional Chinese medicine （TCM） has shown significant efficacy in regulating ERS， offering unique therapeutic advantages through multi-target and multi-pathway mechanisms. Recent studies have confirmed that TCM can alleviate ERS， inhibit apoptosis， regulate autophagy， reduce inflammatory responses， and maintain intestinal barrier function to prevent and treat UC. This review summarized the relationship between ERS and UC and discussed the intervention of TCM in regulating ERS for the treatment of UC， aiming to provide new insights and approaches for the treatment of UC with TCM.

Objective To observe the therapeutic effect of Suoquan Runchang Prescription for senile mice with constipation and its mechanism of action.Methods Senile Kunming mice were randomly divided into constipation group,Suoquan Runchang Prescription group,ISCK03[stem cell factor(SCF),receptor tyrosine kinase(c-Kit)signaling pathway inhibitor]group,Suoquan Runchang Prescription+ISCK03 group,and normal group,with 12 mice in each group.Except for the normal group,a constipation model was constructed by gavage of 150 mg/kg Compound Diphenoxylate Suspension in all groups of senile Kunming mice.After successful modeling,each group was treated for two weeks.At the end of the intervention,the fecal particles count and fecal water content were detected,the serum levels of interleukin(IL)-1β,IL-6,motilin,gastrin,5-hydroxytryptamine(5-HT),and vasoactive intestinal peptide(VIP)were detected by enzyme-linked immunosorbent assay(ELISA),and the changes in gastric emptying rate and small intestine propulsion rate were determined,the pathologic changes of colonic tissues were detected by hematoxylin-eosin(HE)staining,and protein expressions of SCF and c-Kit in the colonic tissues was detected by Western Blot.Results Compared with the normal group,the disrupted cellular structure,thinner muscle layer,damaged mucosal epithelium were seen in the constipation group,and the fecal particle count,fecal water content,serum motilin,gastrin and 5-HT levels,gastric emptying rate,small intestine propulsion rate,the protein expression levels of SCF and c-Kit in colonic tissues were decreased,and the serum IL-1 β,IL-6 and VIP levels were increased,the differences being statistically significant(P＜0.05).Compared with the constipation group,the colonic tissues damage were improved in Suoquan Runchang Prescription group,the fecal particle count,fecal water content,serum motilin,gastrin and 5-HT levels,gastric emptying rate,small intestine propulsion rate,protein expression levels of SCF and c-Kit in colonic tissues were elevated,the serum IL-1β,IL-6 and VIP levels were decreased,the difference being statistically significant(P＜0.05).The indexes mentioned above in mice of ISCK03 group versus to the results of Suoquan Runchang Prescription group(P＜0.05).Compared with Suoquan Runchang Prescription group,the colonic tissues damage showed aggravated in Suoquan Runchang Prescription+ISCK03 group,and the fecal particle count,fecal water content,serum motilin,gastrin and 5-HT levels,gastric emptying rate,small intestine propulsion rate,protein expression levels of SCF and c-Kit in colonic tissues were decreased,the serum IL-1β,IL-6 and VIP levels were increased,the difference being statistically significant(P＜0.05).Conclusion Suoquan Runchang Prescription can effectively improve constipation in senile mice,and its therapeutic effect maybe related to the up-regulation of SCF,c-Kit expression,thus promoting intestinal peristalsis.

Objective To investigate the therapeutic effects and mechanisms of Aurantii Fructus Immaturus(AFI)on slow-transit constipation(STC)in mice.Methods A STC model was established via intragastric administration of Loperamide Hydrochloride.Successfully modeled mice were randomized into a model group,low-and high-dose AFI groups,a high-dose AFI+Masitinib[tyrosine kinase(c-Kit)inhibitor]group,additionally,a normal group was set up.After intervention,intestinal transit rate,6-hour fecal pellet number,fecal water content,and colonic histomorphology(hematoxylin-eosin staining)were assessed.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of 5-hydroxytryptamine(5-HT),vasoactive intestinal polypeptide(VIP),substance P(SP),nitric oxide(NO),and nitric oxide synthase(NOS)activity in colon tissue.Quantitative real-time PCR(qRT-PCR)was used to evaluate mRNA expression of stem cell factor(SCF)and c-Kit in colon tissue,Western Blot was used to analyze relative protein expression of aquaporin 3(AQP3),aquaporin 8(AQP8),SCF,and c-Kit in colon tissue.Results Compared with the normal group,there was devere colonic damage observed in the colon tissue of the mice in the model group,the fecal pellet number,fecal water content,intestinal transit rate,colon tissue SP content,c-Kit and SCF gene and protein expression levels were reduced.The contents of 5-HT,VIP and NO,NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were increased,and the differences were statistically significant(P＜0.05).Compared with the model group,the colonic injury of mice in the low-and high-does AFI groups showed obvious improvement,the fecal pellet number,fecal water content,intestinal transit rate,colon tissue SP content,c-Kit and SCF gene and protein expression levels were increased,the contents of 5-HT,VIP and NO,NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were decreased(P＜0.05).Masitinib partially reversed the laxative effects of AFI(P＜0.05).Conclusion AFI enhances intestinal motility,alleviates colonic injury,and improves defecation in STC mice,potentially via activation of the SCF/c-Kit pathway.

Objective:To investigate the efficacy of venetoclax-based combined regimen in treatment of adult patients with acute myeloid leukemia (AML).Methods:The data of 50 adult AML (non-acute promyelocytic leukemia) who received venetoclax-based combined regimen in the First Affiliated Hospital of Xiamen University, Dongguan People's Hospital, the First Hospital of Longyan City, Jieyang People's Hospital from December 2018 to May 2021 were retrospectively analyzed. Different doses venetoclax combined with demethylation drugs or low-dose chemotherapy regimen were used to analyze the therapeutic efficacy. The related factors influencing efficacy were analyzed by using logistic regression.Results:The composite complete remission (CR) rate of 50 AML patients was 62.0% (31/50), the overall response rate (ORR) was 76.0% (38/50); 28 patients achieved effectiveness [CR and partial remission (PR)] after the first cycle and could achieve effectiveness by 3 courses of treatment at the latest. Among 50 patients, 28 cases were newly diagnosed AML, the composite CR rate was 60.8% (17/28), ORR was 78.6% (22/28); 22 cases were recurrent and relapsed, the composite CR rate was 63.6% (14/22), ORR was 72.7% (16/22); and there was no statistically significant difference of ORR between the both groups ( χ2 = 0.23, P = 0.743). Logistic regression multivariate analysis showed age was the only independent influencing factor for the treatment effectiveness ( OR = 8.451, 95% CI 1.306-54.697, P = 0.025). The median duration time of patients receiving venetoclax treatment regimen was 4.5 months (1.1-15.0 months); 16 cases who had treatment effectiveness finally relapsed, the median time of maintaining effectiveness was 5 months (1.1-11.0 months). Additionally, the common treatment-related adverse reactions included bone marrow suppression after treatment, followed by some gastrointestinal reactions like nausea, vomiting and stomachache. In addition, no patient stopped medication for more than 1 week due to bone marrow suppression related complications. Conclusion:Venetoclax-based combined regimen shows a good short-term efficacy in treatment of AML. It is also effective and tolerable for elderly patients receiving reduced dose therapy.

Objective: To investigate clinicopathological features and prognostic factors of gastric neuroendocrine tumors (G-NEN). Methods: Clinical and pathological data of patients with G-NEN diagnosed by pathological examination in Chinese PLA General Hospital from January 2000 to June 2018 were retrospectively analyzed in this case-control study. Patients with complicated visceral lesions, other visceral primary tumors, mental disorders and incomplete clinicopathological data were excluded. Finally, 240 hospitalized patients who met the inclusion criteria were enrolled. Physical examination information, tumor characteristics and pathological characteristics of patients were summarized. The Cox regression models were used to analyze the risk factors affecting G-NEN and the survival conditions were described by Kaplan-Meier survival curves and log-rank test. Results: In 240 patients with G-NEN, the mean age was (60.3±10.1) years; 181 were male (75.4%) and 59 females (24.6%); mean tumor diameter was (4.2±2.8) cm; 51 cases (21.2%) were neuroendocrine tumor (NET), 139 cases (57.9%) neuroendocrine carcinoma (NEC), 50 cases (20.8%) mixed neuroendocrine carcinoma (MANEC); 28 cases (11.7%) were G1 low grades, 34 cases (14.2%) G2 medium grades, and 178 cases (74.2%) G3 high grades; tumor infiltration depth T1 to T4 were 44 cases (18.3%), 27 cases (11.2%), 60 cases (25.0%) and 109 cases (45.4%) respectively; 163 cases (67.9%) developed lymphatic metastasis and 46 patients (19.2%) distant metastasis; tumor stage from stage I to stage IV were 55 cases (22.9%), 42 cases (17.5%), 94 cases (39.2%) and 53 cases (22.1%) respectively. Of the 240 G-NEN patients, 223 cases (92.9%) were followed up. The median survival time of the patients was 39.2 (95% CI: 29.1 to 47.5) months. Univariate survival analysis showed that age ≥ 60 years, tumor diameter ≥ 4.2 cm, tumor grade G3, lymphatic metastasis, distant metastasis, and tumor stage III-IV were risk factors for G-NEN patients. Multivariate survival analysis revealed that lymphatic metastasis (HR=1.783, 95%CI: 1.007-3.155, P=0.047) and distant metastasis (HR=2.288, 95% CI: 1.307-4.008, P=0.004) were independent risk factors of the prognosis. Further analysis of the G3 subgroup of G-NEN showed that the 5-year survival rate of NET-G3 was 76.19%, which was significantly higher than that of NEC-G3 and MANEC-G3 (15.60% and 24.73%, P=0.012). Conclusions Most G-NEN patients are in advanced stage at diagnosis. Lymphatic metastasis and distant metastasis indicate poor prognosis. The prognosis of high proliferation NET-G3 patients is better as compared to those of NEC-G3 and MANEC-G3. This classification is worth further attention.