ObjectiveTo investigate the clinical efficacy and mechanisms of Qigui Didang decoction in the treatment of kidney collateral stasis syndrome in patients with stage Ⅲ-Ⅳ diabetic kidney disease （DKD） in a real-world setting. MethodsPatients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome admitted to Beijing Aerospace General Hospital from January 2022 to December 2024 were selected for clinical study. According to treatment methods， patients were divided into the Qigui Didang decoction group （Qigui Didang decoction + conventional treatment） and the control group （conventional treatment alone）. A 1∶1 propensity score matching （PSM） method was used to reduce bias caused by confounding factors. Clinical efficacy， traditional Chinese medicine （TCM） symptom scores， renal function indicators， mRNA expression related to pathway mechanisms， glycolipid metabolism indices， and adverse reactions were compared between the two groups. ResultsA total of 120 patients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome were included， including 62 cases in the Qigui Didang Decoction group and 58 cases in the control group. Before matching， there were statistically significant differences between the two groups in DKD stage， baseline urinary albumin-to-creatinine ratio （UACR）， 24-hour urine total protein （24 h-UTP）， and estimated glomerular filtration rate （eGFR） （P<0.05）. After matching， 47 cases were included in each group， and there was no statistically significant difference in baseline data between the two groups. After matching， the total clinical effective rate of the Qigui Didang decoction group was significantly higher than that of the control group （χ²=4.681， P<0.05）. Compared with data before treatment， the scores of primary and secondary TCM symptoms in the Qigui Didang decoction group were significantly decreased （P<0.05）. Compared with data before treatment， serum creatinine （SCr）， 24 h-UTP， and UACR levels were significantly decreased， while eGFR was significantly increased in the Qigui Didang decoction group （P<0.05）. Compared with data before treatment， the mRNA expression of silent information regulator 1 （Sirt1） was significantly upregulated， while the mRNA expression of nuclear factor-kappa B （NF-κB） and tumor suppressor protein p53 （p53） was significantly downregulated in the Qigui Didang decoction group （P<0.05）. Compared with data before treatment， fasting plasma glucose （FPG）， 2-hour postprandial plasma glucose （2 hPG）， glycated hemoglobin A1c （HbA1c）， total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C） levels were decreased， while high-density lipoprotein cholesterol （HDL-C） levels were increased （P<0.05）. There was no statistically significant difference in adverse reactions between the two groups. ConclusionQigui Didang decoction combined with conventional treatment can significantly improve renal function， glycolipid metabolism， and TCM syndromes in patients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome， with good safety. The mechanism may be related to the regulation of the Sirt1/NF-κB/p53 signaling pathway.

ObjectiveTo investigate the clinical efficacy and mechanisms of Qigui Didang decoction in the treatment of kidney collateral stasis syndrome in patients with stage Ⅲ-Ⅳ diabetic kidney disease （DKD） in a real-world setting. MethodsPatients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome admitted to Beijing Aerospace General Hospital from January 2022 to December 2024 were selected for clinical study. According to treatment methods， patients were divided into the Qigui Didang decoction group （Qigui Didang decoction + conventional treatment） and the control group （conventional treatment alone）. A 1∶1 propensity score matching （PSM） method was used to reduce bias caused by confounding factors. Clinical efficacy， traditional Chinese medicine （TCM） symptom scores， renal function indicators， mRNA expression related to pathway mechanisms， glycolipid metabolism indices， and adverse reactions were compared between the two groups. ResultsA total of 120 patients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome were included， including 62 cases in the Qigui Didang Decoction group and 58 cases in the control group. Before matching， there were statistically significant differences between the two groups in DKD stage， baseline urinary albumin-to-creatinine ratio （UACR）， 24-hour urine total protein （24 h-UTP）， and estimated glomerular filtration rate （eGFR） （P<0.05）. After matching， 47 cases were included in each group， and there was no statistically significant difference in baseline data between the two groups. After matching， the total clinical effective rate of the Qigui Didang decoction group was significantly higher than that of the control group （χ²=4.681， P<0.05）. Compared with data before treatment， the scores of primary and secondary TCM symptoms in the Qigui Didang decoction group were significantly decreased （P<0.05）. Compared with data before treatment， serum creatinine （SCr）， 24 h-UTP， and UACR levels were significantly decreased， while eGFR was significantly increased in the Qigui Didang decoction group （P<0.05）. Compared with data before treatment， the mRNA expression of silent information regulator 1 （Sirt1） was significantly upregulated， while the mRNA expression of nuclear factor-kappa B （NF-κB） and tumor suppressor protein p53 （p53） was significantly downregulated in the Qigui Didang decoction group （P<0.05）. Compared with data before treatment， fasting plasma glucose （FPG）， 2-hour postprandial plasma glucose （2 hPG）， glycated hemoglobin A1c （HbA1c）， total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C） levels were decreased， while high-density lipoprotein cholesterol （HDL-C） levels were increased （P<0.05）. There was no statistically significant difference in adverse reactions between the two groups. ConclusionQigui Didang decoction combined with conventional treatment can significantly improve renal function， glycolipid metabolism， and TCM syndromes in patients with stage Ⅲ-Ⅳ DKD with kidney collateral stasis syndrome， with good safety. The mechanism may be related to the regulation of the Sirt1/NF-κB/p53 signaling pathway.

Triclosan (TCS) and triclocarban (TCC) are widely used synthetic broad-spectrum antibacterial agents that can enter the human body through the skin, gastrointestinal tract, and other pathways. More and more studies have found that exposure to TCS and TCC can affect human health, but currently, review reports on the health effects of human exposure to TCS and TCC are limited. Therefore, this study reviewed population studies on the relationship between TCS and TCC exposure and health effects by searching the PubMed database, summarized the associated health outcomes, and elucidated the biological mechanisms. A total of 56 studies were retrieved, among which cross-sectional studies (25 studies, 44.64%) and cohort studies (25 studies, 44.64%) accounted for a relatively large proportion, while case-control studies (6 studies, 10.72%) were relatively few. Studies on TCS exposure (48 studies, 85.71%) were far more prevalent than those on TCC exposure (2 studies, 3.57%). The remaining 6 studies involved both TCS and TCC exposure. The research results revealed that TCS exposure was associated with male and female abnormal reproductive functions, fetal growth restriction, abnormal behavior development in children, obesity, gestational diabetes mellitus (GDM), and immune-related diseases. Although the results of different studies show significant differences, they have indicated that exposure to TCS is a potential risk factor for these health problems. Due to the limited number of studies, the evidence for the relationship between TCC exposure and most of the aforementioned health effects is insufficient. Population studies and in vitro and in vivo studies have shown that exposure to TCS and TCC can interfere with the microbial homeostasis, the endocrine system, oxidative stress and immune function of the body, which are potential mechanisms causing adverse health effects. In the future, large-scale prospective cohort studies, as well as in vivo and in vitro studies, are still needed to further clarify the associations between TCS and TCC exposure and health effects, and to deeply explore its mechanism of action. These efforts will provide references for clarifying the human health hazards of TCS and TCC exposure and formulating targeted prevention and control strategies.

The disease-syndrome combination model of spleen deficiency with dampness pattern in ulcerative colitis（SDDP-UC） is an important experimental carrier for traditional Chinese medicine （TCM） research on the prevention and treatment of ulcerative colitis （UC）， and the quality of model construction and evaluation directly influences the scientific rigor and translational value of related research conclusions. However， this field still lacks methodological synthesis and a standardized consensus. Based on a comprehensive review of existing literature， this paper summarized isomorphic cues between the spleen deficiency with dampness pattern and UC across four dimensions， including energy metabolism， immune homeostasis， mucosal barrier， and intestinal microecology. The cues were mainly involved in impaired mitochondrial energy supply and glucose metabolic reprogramming， a lowered pro-inflammatory threshold of innate immunity with insufficient adaptive immune regulation， disruption of epithelial barrier gating accompanied by compromised repair capacity， and attenuation of the luminal hypoxia barrier with accumulation of toxic metabolites. A mutually reinforcing process between local "form damage" and systemic "Qi depletion" was further interpreted from a holistic perspective. Regarding modeling strategies， existing studies predominantly use rats as the carrier， apply combined interventions such as improper diet， external damp exposure， and fatigue-related dysregulation to establish the spleen deficiency with dampness pattern background， and subsequently superimpose chemical stimulation to induce UC-like colonic damage， with a total modeling period generally spanning three to four weeks. In terms of the evaluation system， a multidimensional framework integrating syndrome assessment， histopathology， mechanistic indices， and pharmacodynamic counter-verification was outlined. On this basis， current methodological bottlenecks of models were systematically identified， including syndrome drift risk and compounded stress dilemma in temporal sequencing， syndrome confounding from etiological simulation， cross-sectional evaluation bias related to modeling duration， inadequate disease-syndrome linkage and control design within the evaluation system， and limited controls with overly single-track decision logic in formula-based syndrome verification. To address the above issues， a construction and evaluation strategy emphasizing streamlining of core etiological factors， multi-node dynamic monitoring， integration of core disease-syndrome indicator clusters， and establishment of a formula-based syndrome verification system was proposed， providing a reference for the standardized construction and scientific evaluation of the SDDP-UC model.

Background/Aims: Dysregulated cholesterol metabolism is a hallmark of hepatocellular carcinoma (HCC) that drives tumor initiation and progression. However, clinical targeting of cholesterol metabolism has yielded limited benefits due to stringent feedback in tumor cells. Identifying a central mediator capable of restoring cholesterol homeostasis within the cell’s intrinsically fine-tuned regulatory framework is urgently needed. Methods: We integrated a proteomic dataset from patients with cholesterol-dysregulated HCC into a global cholesterol metabolic regulatory network to identify potential therapeutic targets for disrupted cholesterol homeostasis. The prognostic significance of the candidate targets was further validated in an independent cohort through immunohistochemistry. Functional and mechanistic studies were conducted in vitro using HCC cell lines and in vivo using mouse models. The pharmacological efficacy of the candidate agent was evaluated in both subcutaneous and orthotopic HCC mouse models. Results: ER lipid raft-associated 1 (ERLIN1), a pivotal regulator of cholesterol metabolism reprogramming, was identified as an independent favorable prognostic indicator in HCC. ERLIN1 constrains HCC progression both in vitro and in vivo by stabilizing the INSIG1–SCAP–SREBP2 axis and maintaining the metabolic balance of intracellular cholesterol. Under hypoxia, impaired factor-inhibiting hypoxia-1-dependent hydroxylation of ASB11 at asparagine residues 90 and 92 enhances ASB11-mediated ERLIN1 degradation. Pharmacological targeting of this axis using zoledronic acid (ZoA) attenuated HCC progression by weakening the ASB11–ERLIN1 interaction and restoring cholesterol homeostasis. Conclusions ERLIN1 represents a druggable metabolic vulnerability in cholesterol-dysregulated HCC. Targeting the ASB11–ERLIN1 axis with the clinically approved ZoA reestablishes cholesterol homeostasis and offers a promising therapeutic strategy to overcome the current limitations of cholesterol-targeted HCC therapies.

Current formulation of objective performance criteria （OPC） in traditional Chinese medicine （TCM） faces methodological challenges， including poor reporting quality， insufficient standardization of methods， limited comparability of study populations， and inadequate consideration of the genetic and environment particularities of ethnic minority populations. In response to these issues， this paper proposes optimization strategies for setting OPC in TCM， with particular attention to ethnic minority medicine. These include improving methodological techniques and statistical descriptions， ensuring transparency in meta-analyses and data sources； standardizing the estimation of point estimates and confidence intervals， and incorporating multidisciplinary expert consensus for value determination； introducing local real-world data from the same period， especially cohort study evidence， to compensate for the lack of high-quality randomized controlled trial data. Through process transparency and dynamic updating mechanisms， the credibility of OPC method can be enhanced， thereby providing methodological support for strengthening evidence-based research capacity in this field.

Objective To investigate the expression characteristics, prognostic value, and correlation with immune infiltration of vasoactive intestinal peptide receptor 2 (VIPR2) in esophageal adenocarcinoma (ESAD). Methods Transcriptome data of 80 ESAD and 10 normal tissues were retrieved from the TCGA database. Immune-related differential genes were identified by integrating the ImmPort database. Cox regression analysis was applied to evaluate the prognostic significance of VIPR2. GSVA and ssGSEA were employed to assess the association between VIPR2 and immune-cell infiltration. Functional enrichment was performed using GO, KEGG, and GSEA. Results VIPR2 expression was significantly downregulated in ESAD tissues (P<0.05). High VIPR2 expression was associated with prolonged overall survival (HR=0.246, P=0.047), serving as an independent prognostic factor. Fifteen immune-cell types, including CD8⁺ T cells, NK cells, and dendritic cells, showed significantly higher infiltration in the VIPR2-high group, whereas Th17-cell abundance was decreased (P<0.05). Enrichment analyses revealed that VIPR2 participated in multiple tumor-immune pathways and was positively correlated with PD-1 and CTLA-4 expression (P<0.01). Conclusion VIPR2 may serve as a potential biomarker in the prognostic assessment and could modulate the tumor-immune microenvironment in ESAD.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Periodontitis and diabetes have a close bidirectional relationship that is mutually exacerbated through mechanisms including inflammatory factor interplay and metabolic dysregulation. Research has shown that non-surgical periodontal therapy (NSPT), focused on scaling and root planing (SRP), effectively treats periodontitis, enhances glycemic control, and ameliorates systemic inflammation in diabetic patients. This review summarizes the glycemic improvement effects of diverse NSPT modalities (including SRP alone, SRP with adjunctive antimicrobials, and SRP with laser therapy) on patients with diabetes and periodontitis. SRP significantly reduces hemoglobin A1c (HbA1c) levels, while adjunctive antimicrobials and laser therapy considerably potentiate the glucose-lowering efficacy of SRP. Furthermore, we focus on elucidating the underlying regulatory mechanisms for NSPT-mediated glycemic control improvement, encompassing inflammation factor-mediated JNK/IKKβ pathway activation inducing insulin resistance; advanced glycation end products (AGEs)-triggered RAGE-ROS/NF-κB pathway dysregulation leading to pancreatic β-cell dysfunction; gut microbiota dysbiosis-driven TLR4-MyD88/TRIF signaling axis causing insulin resistance; flagellin from periodontal pathogens impairing insulin secretion; and lipopolysaccharide (LPS) of periodontal pathogens disrupting Th17/Treg balance with downstream STAT3/SOCS3 pathway inhibiting insulin signaling. These insights aim to provide novel references for targeted interventions and synergistic management of diabetes with periodontitis. Although current studies reveal potential benefits and partial mechanisms of NSPT, the following problems remain: unelucidated specific effector molecules and pathway networks for glycemic regulation by different NSPT regimens, significant interindividual variability in treatment response, and undetermined long-term stability of adjunctive therapy benefits. Future research should explore combined therapeutic strategies for synergistic efficacy, mechanistically dissect regulatory pathways, identify key targets, and advance precision management of diabetes-periodontitis comorbidities.