ObjectiveTo observe the clinical efficacy and safety of Yuyin Lidan granules （YYLD） in preventing the recurrence of common bile duct stones （CBDS） in patients with liver and gallbladder dampness-heat syndrome following endoscopic retrograde cholangiopancreatography （ERCP）. MethodsThis randomized， parallel， controlled trial enrolled postoperative CBDS-ERCP patients who met the inclusion and exclusion criteria. Sixty-four patients were randomly assigned to an observation group or a control group， with 32 cases in each. Both groups received conventional Western medical treatment after ERCP， while the observation group additionally received YYLD for 8 weeks. The follow-up period lasted for 1 year. The efficacy indicators included bile bilirubin levels， traditional Chinese medicine （TCM） syndrome scores， clinical efficacy rate， pancreatitis and inflammation markers， postoperative liver function， and CBDS recurrence rate at 1-year follow-up， which were used to jointly evaluate the clinical efficacy and safety of both groups. ResultsA total of 56 patients completed the study and were included in the final analysis， i.e.， 29 in the observation group and 27 in the control group. Baseline characteristics were comparable between the two groups. Compared with pre-treatment and with the control group after treatment， the bile bilirubin level in the observation group significantly decreased （P<0.05）. After treatment， the clinical cure and marked improvement rates were higher in the observation group than in the control group， showing a statistically significant difference in overall clinical efficacy （P<0.05）. Compared with pre-treatment， the primary and secondary symptoms in the observation group， as well as the primary symptom and the secondary symptom of nausea and vomiting in the control group （weeks 4 and 8）， were significantly reduced （P<0.05）. Compared with the control group after treatment， the observation group showed significant reductions in the primary symptom of loose stools/constipation （day 5 and week 4） and in three secondary symptoms， i.e.， bitter taste and sticky dry mouth， abdominal distension and poor appetite （throughout the treatment period）， and general heaviness and fatigue （day 5 and week 4）， with statistical differences （P<0.05）. Compared with pre-treatment， both groups showed decreased lipase and urinary amylase levels （P<0.05）. However， no significant between-group differences were observed in pancreatitis or inflammation-related indices after treatment. Compared with pre-treatment， all liver function indicators in the observation group and alanine aminotransferase （ ALT ）， γ-glutamyl transferase （ γ-GT ）， alkaline phosphatase （ALP）， and conjugated bilirubin in the control group significantly decreased at weeks 4 and 8 （P<0.05）. Compared with the control group after treatment， only serum total bilirubin and unconjugated bilirubin were significantly reduced in the observation group during the treatment period （P<0.05）. ConclusionYYLD combined with conventional Western medical treatment can effectively regulate bilirubin metabolism （in bile and serum）， improve TCM clinical symptoms， and prevent CBDS recurrence after ERCP in patients with liver and gallbladder dampness-heat syndrome. This regimen is safe and effective and is worthy of further clinical research and promotion.

OBJECTIVE To investigate the effects of quercetin （QUE） on intervertebral disc degeneration in rats with lumbar intervertebral disc herniation （LDH） and explore its mechanism based on the forkhead box protein O3/silent information regulator 1 （FOXO3/Sirt1） pathway. METHODS A rat model of LDH was established. The successfully modeled rats were randomly divided into LDH group （gavaged with and intraperitoneally injected with an equal volume of normal saline）， QUE-L group （gavaged with 50 mg/kg QUE+intraperitoneally injected with an equal volume of normal saline）， QUE-H group （gavaged with 100 mg/kg QUE+ intraperitoneally injected with an equal volume of normal saline）， and QUE-H+EX-527 （a Sirt1 inhibitor） group （gavaged with 100 mg/kg QUE+intraperitoneally injected with 1 mg/kg EX-527）， with 12 rats in each group. Additionally， 12 healthy normal rats were selected as the control group （gavaged with and intraperitoneally injected with an equal volume of normal saline）. All rats were administered the corresponding agents once daily for consecutive 8 weeks. After the final administration， the pain threshold and serum levels of inflammatory factors in rats were measured； pathological damage of lumbar intervertebral disc tissue was observed， the apoptosis of nucleus pulposus cells in lumbar intervertebral disc tissue was assessed， and the expression levels of matrix metalloproteinase-3 （MMP-3）， phospholipase A2 （PLA2）， as well as apoptosis-related proteins and FOXO3/Sirt1 pathway- related proteins in intervertebral disc tissue were determined. RESULTS Compared with LDH group， pathological damage of intervertebral disc tissue were improved significantly in QUE-L group and QUE-H group； paw withdrawal mechanical threshold， paw withdrawal thermal latency， the serum levels of transforming growth factor-β1 and interleukin-10 （IL-10） as well as the expression levels of B-cell lymphoma-2 （Bcl-2）， FOXO3 and Sirt1 were significantly increased or prolonged （P＜0.05）. Serum levels of tumor necrosis factor-α and IL-1β， histopathological score of intervertebral disc tissue， apoptotic rate of nucleus pulposus cells， positive expressions of MMP-3 and PLA2 in intervertebral disc tissue and expression levels of Bcl-2 associated X protein were significantly decreased （P＜0.05）. Compared with the QUE-H group， the QUE-H+EX-527 group presented aggravated pathological damage of intervertebral disc tissue， and the trends of all the above indicators were significantly reversed（P＜0.05）. CONCLUSIONS QUE can ameliorate intervertebral disc degeneration in LDH rats， and its mechanism may be related to the activation of the FOXO3/Sirt1 pathway.

It is considered that "turbid pathogen damaging the clear， and the loss of clarity and harmony regulation" is the core pathogenesis of esophageal precancerous lesions， with turbid pathogen persisting throughout the disease course. Turbid pathogen encompasses qi turbidity， phlegm turbidity， stasis turbidity， and toxin turbidity， closely related to dietary indiscretion， emotional disharmony， spleen-stomach deficiency， and kidney deficiency failing to consolidate. Turbid pathogen undergoes a dynamic evolution process of qi constraint generating turbid→ phlegm-stasis transforming into toxin→turbidity toxin harming the healthy qi， corresponding to the pathological alterations of hypoxia， inflammation and immunosuppression within the tumor microenvironment. The overall therapeutic principle is to remove turbidity and restore clarity. In the early stage， targeting the hypoxic tumor microenvironment， the suggested treatment method is opening constraint and dispersing the block， regulating qi and remove turbidity， with emphasis on soothing liver and regulating stomach， raising the clear and directing the turbid downward. In the middle stage， targeting inflammatory microenvironment， the treatment aims to clear toxin and dissipate nodules， resolve stasis and eliminate turbid， emphasizing phlegm-stasis elimination， turbid-toxin resolution， and concurrent stomach qi protection. In the late stage， corresponding to immunosuppressive microenvironment， the method of boosting qi， nourishing yin， reinforcing healthy qi， and eliminating turbidity can be used， with focus on spleen-stomach tonification， kidney essence replenishment， and healthy qi reinforcement to expel pathogenic factors.

The development of traditional Chinese medicine (TCM) diagnosis and treatment has undergone multiple paradigms, evolving from sporadic experiential practices to systematic approaches in syndrome differentiation and treatment and further integration of disease and syndrome frameworks. TCM is a vital component of the medical system, valued alongside Western medicine. Treatment based on syndrome differentiation embodies both personalized treatment and holistic approaches; however, the inconsistency and lack of stability in syndrome differentiation limit clinical efficacy. The existing integration of diseases and syndromes primarily relies on patchwork and embedded systems, where the full advantages of synergy between Chinese and Western medicine are not fully realized. Recently, driven by the development of diagnosis and treatment concepts and advances in analytical technology, Western medicine has been rapidly transforming from a traditional biological model to a precision medicine model. TCM faces a similar need to progress beyond traditional syndrome differentiation and disease-syndrome integration toward a more precise diagnosis and treatment paradigm. Unlike the micro-level precision trend of Western medicine, precision diagnosis and treatment in TCM is primarily reflected in data-driven applications that incorporate information at various levels, including precise syndrome differentiation, medication, disease management, and efficacy evaluation. The current priority is to accelerate the development of TCM precision diagnosis and treatment technology platforms and advance discipline construction in this area.

Biomolecular condensates are formed through phase separation of biomacromolecules such as proteins and RNAs. These condensates exhibit liquid-like properties that can futher transition into more stable material states. They form complex internal structures via multivalent weak interactions, enabling precise spatiotemporal regulations. However, the use of inconsistent and non-standardized terminology has become increasingly problematic, hindering academic exchange and the dissemination of scientific knowledge. Therefore, it is necessary to discuss the terminology related to biomolecular condensates in order to clarify concepts, promote interdisciplinary cooperation, enhance research efficiency, and support the healthy development of this field.

Background: Diabetic nephropathy (DN) is the most common and serious complication of diabetes mellitus. Shionone (SH), an important triterpenoid compound in the root extract of Aster, might exert a protective effect in DN mice and high glucose cultivated glomerular podocytes. The current study aimed to unravel the underlying mechanism by which SH mitigates DN. We postulate that SH stimulates the expression of sestrin-2 (SESN2), a pivotal stress-inducible protein in the anti-inflammasome machinery. Methods: We utilized high-fat diet combined with streptozotocin (55 mg/kg intraperitoneal) for DN mice model, and high glucose (30 mM, 48 hours) cultured glomerular podocytes for DN cell model to evaluate the effect of SH. We also preformed experimentation on SESN2 deficiency models (SESN2 knockout mice and SESN2 siRNA in cells) to further prove our hypothesis. Results: The results demonstrated that SH effectively suppressed glomerular fibrosis, induced adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, and inhibited NLR family pyrin domain containing 3 (NLRP3) activation. Furthermore, our findings revealed that SH exerted its anti-inflammatory effect through Sesn2-dependent nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and subsequent activation of its downstream target heme oxygenase-1 (HO-1). Conclusion In summary, our findings suggest that SH serves as a promising therapeutic agent for the treatment of DN-related glomerular fibrosis. SH enhances the expression of SESN2, attenuates α-smooth muscle actin accumulation, and suppresses NLRP3-related inflammation through the Nrf2/HO-1 signaling pathway.

Background: Diabetic nephropathy (DN) is the most common and serious complication of diabetes mellitus. Shionone (SH), an important triterpenoid compound in the root extract of Aster, might exert a protective effect in DN mice and high glucose cultivated glomerular podocytes. The current study aimed to unravel the underlying mechanism by which SH mitigates DN. We postulate that SH stimulates the expression of sestrin-2 (SESN2), a pivotal stress-inducible protein in the anti-inflammasome machinery. Methods: We utilized high-fat diet combined with streptozotocin (55 mg/kg intraperitoneal) for DN mice model, and high glucose (30 mM, 48 hours) cultured glomerular podocytes for DN cell model to evaluate the effect of SH. We also preformed experimentation on SESN2 deficiency models (SESN2 knockout mice and SESN2 siRNA in cells) to further prove our hypothesis. Results: The results demonstrated that SH effectively suppressed glomerular fibrosis, induced adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, and inhibited NLR family pyrin domain containing 3 (NLRP3) activation. Furthermore, our findings revealed that SH exerted its anti-inflammatory effect through Sesn2-dependent nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and subsequent activation of its downstream target heme oxygenase-1 (HO-1). Conclusion In summary, our findings suggest that SH serves as a promising therapeutic agent for the treatment of DN-related glomerular fibrosis. SH enhances the expression of SESN2, attenuates α-smooth muscle actin accumulation, and suppresses NLRP3-related inflammation through the Nrf2/HO-1 signaling pathway.

Background: Diabetic nephropathy (DN) is the most common and serious complication of diabetes mellitus. Shionone (SH), an important triterpenoid compound in the root extract of Aster, might exert a protective effect in DN mice and high glucose cultivated glomerular podocytes. The current study aimed to unravel the underlying mechanism by which SH mitigates DN. We postulate that SH stimulates the expression of sestrin-2 (SESN2), a pivotal stress-inducible protein in the anti-inflammasome machinery. Methods: We utilized high-fat diet combined with streptozotocin (55 mg/kg intraperitoneal) for DN mice model, and high glucose (30 mM, 48 hours) cultured glomerular podocytes for DN cell model to evaluate the effect of SH. We also preformed experimentation on SESN2 deficiency models (SESN2 knockout mice and SESN2 siRNA in cells) to further prove our hypothesis. Results: The results demonstrated that SH effectively suppressed glomerular fibrosis, induced adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, and inhibited NLR family pyrin domain containing 3 (NLRP3) activation. Furthermore, our findings revealed that SH exerted its anti-inflammatory effect through Sesn2-dependent nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and subsequent activation of its downstream target heme oxygenase-1 (HO-1). Conclusion In summary, our findings suggest that SH serves as a promising therapeutic agent for the treatment of DN-related glomerular fibrosis. SH enhances the expression of SESN2, attenuates α-smooth muscle actin accumulation, and suppresses NLRP3-related inflammation through the Nrf2/HO-1 signaling pathway.

Background: Diabetic nephropathy (DN) is the most common and serious complication of diabetes mellitus. Shionone (SH), an important triterpenoid compound in the root extract of Aster, might exert a protective effect in DN mice and high glucose cultivated glomerular podocytes. The current study aimed to unravel the underlying mechanism by which SH mitigates DN. We postulate that SH stimulates the expression of sestrin-2 (SESN2), a pivotal stress-inducible protein in the anti-inflammasome machinery. Methods: We utilized high-fat diet combined with streptozotocin (55 mg/kg intraperitoneal) for DN mice model, and high glucose (30 mM, 48 hours) cultured glomerular podocytes for DN cell model to evaluate the effect of SH. We also preformed experimentation on SESN2 deficiency models (SESN2 knockout mice and SESN2 siRNA in cells) to further prove our hypothesis. Results: The results demonstrated that SH effectively suppressed glomerular fibrosis, induced adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, and inhibited NLR family pyrin domain containing 3 (NLRP3) activation. Furthermore, our findings revealed that SH exerted its anti-inflammatory effect through Sesn2-dependent nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and subsequent activation of its downstream target heme oxygenase-1 (HO-1). Conclusion In summary, our findings suggest that SH serves as a promising therapeutic agent for the treatment of DN-related glomerular fibrosis. SH enhances the expression of SESN2, attenuates α-smooth muscle actin accumulation, and suppresses NLRP3-related inflammation through the Nrf2/HO-1 signaling pathway.

Objective:To systematically evaluate the authentic feeling of mental experience among patients with inflammatory bowel disease (IBD) in the process of dietary management, aiming to provide insights for maintaining the psychological well-being of patients with IBD and strengthening their dietary management.Methods:The qualitative studies related to dietary management in patients with IBD from China National Knowledge Infrastructure, Wanfang, VIP, China Biomedical Database, PubMed, Web of Science, Embase, Cochrane Library, CINAHL and PsyINFO were searched from inception to January 31st 2025. Quality evaluation criteria for qualitative research of Joanna Briggs Institute, Australia, 2016 edition was used for literature evaluation. Meta integration method was used to integrate and analyze the literature findings.Results:A total of 11 articles were included in the review, from which 22 research findings were extracted and categorized into 7 groups, culminating in 3 integrated outcomes: IBD patients experienced complex emotions, IBD patients faced multiple pressures and IBD patients had ambivalent coping.Conclusions:IBD patients manifest profound psychological complexities throughout dietary management processes. Future healthcare professionals can implement multifaceted psychological intervention strategies to relieve psychological distress, promote positive emotion, overcome negative coping, and ultimately enhance the competence of dietary self-management among IBD patients.