Cancer has become a significant global public health issue， severely impacting public health and societal development. Despite advances in tumor treatment methods in recent years and a gradual decline in cancer mortality rates， drug-related adverse reactions and drug resistance remain substantial challenges. Traditional Chinese medicine （TCM） has demonstrated significant clinical efficacy in cancer treatment and small side effects， making it widely applied in the field of oncology. Xuefu Zhuyutang， derived from Yilin Gaicuo， is known for its abilities to invigorate blood circulation， dispel blood stasis， promote Qi flow， and alleviate pain. It was specifically formulated by the esteemed WANG Qingren of the Qing dynasty for the "blood stasis syndrome in the blood mansion" and is commonly used to treat Qi stagnation and blood stasis syndrome. Clinical studies have shown that Xuefu Zhuyutang， when combined with conventional Western medications， produces significant effects in the treatment of malignant tumors such as liver cancer， lung cancer， and cervical cancer. It substantially reduces the incidence of adverse reactions following Western treatments， including radiation esophagitis， radiation encephalopathy， radiation-induced oral mucositis， and edema. Additionally， it alleviates cancer-related pain and fever， blood hypercoagulability， and associated complications such as depression and anxiety， and also mitigates chemotherapy-induced side effects like hand-foot syndrome. Basic research has demonstrated its potential anti-tumor mechanisms， including the inhibition of Wnt/β-catenin signaling pathway activation， suppression of mitogen-activated protein kinase （MAPK） pathway activation， and anti-tumor angiogenesis. Pharmacological studies have revealed that its active components inhibit tumor cell proliferation and migration， induce tumor cell apoptosis， suppress tumor angiogenesis， enhance the cytotoxicity of natural killer cells against tumors， improve the tumor microenvironment， and regulate immune function. This paper reviewed the latest research progress on Xuefu Zhuyutang in the treatment of malignant tumors from four aspects： theoretical exploration， clinical studies， mechanisms of action， and pharmacological basis， aiming to provide insights and methods for the clinical diagnosis and treatment of malignant tumors.

Cancer has become a significant global public health issue， severely impacting public health and societal development. Despite advances in tumor treatment methods in recent years and a gradual decline in cancer mortality rates， drug-related adverse reactions and drug resistance remain substantial challenges. Traditional Chinese medicine （TCM） has demonstrated significant clinical efficacy in cancer treatment and small side effects， making it widely applied in the field of oncology. Xuefu Zhuyutang， derived from Yilin Gaicuo， is known for its abilities to invigorate blood circulation， dispel blood stasis， promote Qi flow， and alleviate pain. It was specifically formulated by the esteemed WANG Qingren of the Qing dynasty for the "blood stasis syndrome in the blood mansion" and is commonly used to treat Qi stagnation and blood stasis syndrome. Clinical studies have shown that Xuefu Zhuyutang， when combined with conventional Western medications， produces significant effects in the treatment of malignant tumors such as liver cancer， lung cancer， and cervical cancer. It substantially reduces the incidence of adverse reactions following Western treatments， including radiation esophagitis， radiation encephalopathy， radiation-induced oral mucositis， and edema. Additionally， it alleviates cancer-related pain and fever， blood hypercoagulability， and associated complications such as depression and anxiety， and also mitigates chemotherapy-induced side effects like hand-foot syndrome. Basic research has demonstrated its potential anti-tumor mechanisms， including the inhibition of Wnt/β-catenin signaling pathway activation， suppression of mitogen-activated protein kinase （MAPK） pathway activation， and anti-tumor angiogenesis. Pharmacological studies have revealed that its active components inhibit tumor cell proliferation and migration， induce tumor cell apoptosis， suppress tumor angiogenesis， enhance the cytotoxicity of natural killer cells against tumors， improve the tumor microenvironment， and regulate immune function. This paper reviewed the latest research progress on Xuefu Zhuyutang in the treatment of malignant tumors from four aspects： theoretical exploration， clinical studies， mechanisms of action， and pharmacological basis， aiming to provide insights and methods for the clinical diagnosis and treatment of malignant tumors.

Metabolic dysfunction-associated fatty liver disease （MAFLD） and its progressive form metabolic dysfunction-associated steatohepatitis （MASH） have become the leading causes of chronic liver diseases worldwide， and the incidence rate of MAFLD continues to rise， which is closely associated with metabolic disorders such as obesity and type 2 diabetes. The core pathogenesis of MAFLD involves insulin resistance， abnormal lipid metabolism， and chronic inflammation， which can progress to MASH and lead to liver fibrosis， liver cirrhosis， and even hepatocellular carcinoma （HCC）. At present， there are still limited effective pharmacotherapies for MAFLD. Based on the PRISMA guidelines， this article systematically reviews the role of statins in MAFLD. Studies have shown that statins not only improve blood lipid profiles and the levels of liver enzyme， but also bring good benefits to patients comorbid with cardiovascular disease or type 2 diabetes， and long-term use can also reduce the risk of HCC. However， the potential risks of hepatotoxicity and myopathy should be taken seriously， which， therefore， requires individualized medication and regular monitoring of liver function in clinical practice.

OBJECTIVE To explore the antidepressant mechanism of Wenyang jieyu granules （WYJYG） via the NOD-like receptor thermal protein domain associated protein 3 （NLRP3）/apoptosis-associated speck-like protein containing a CARD （ASC）/Caspase-1 pathway. METHODS A rat model of depression was established by chronic unpredictable mild stress combined with single-housing for 42 consecutive days.The experiment set up blank group， model group， MCC950 （NLRP3 inflammasome inhibitor） group （10 mg/kg）， fluoxetine group （positive control，2.08 mg/kg），low-dose WYJYG（3.78 g/kg） and high-dose WYJYG group （7.56 g/kg），with 10 rats in each group. From the 22nd day of the experiment， rats in the fluoxetine group， low-dose and high-dose WYJYG groups were intragastrically administered with the corresponding drugs and intraperitoneally injected with an equal volume of normal saline. Rats in the MCC950 group were intraperitoneally injected with MCC950 at the corresponding concentration and intragastrically administered with an equal volume of distilled water. Rats in the blank group and model group were given an equal volume of distilled water by gavage and an equal volume of normal saline by intraperitoneal injection. All interventions were performed once a day for 21 consecutive days. Behavioral tests were conducted once a week. After the last administration， the contents of ASC， ionized calcium binding adaptor molecule 1 （Iba1）， interleukin-1β （IL-1β）， and IL-18 in hippocampal tissues were detected. The protein expressions of NLRP3， cluster of differentiation 68 （CD68）， Caspase-1， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein were determined， and neuronal apoptosis was observed. RESULTS After the last administration， compared with the model group， the open-field activity time was significantly prolonged （ P ＜0.05）， and the latency to feed in a novel environment was significantly shortened （ P ＜0.05） in rats of the high-dose WYJYG group. In hippocampal tissue， the contents of ASC， Iba1， IL-1β， and IL-18， as well as the protein expression levels of NLRP3， Caspase-1， and CD68， and the positive rate of neuronal apoptosis were all significantly decreased/downregulated （ P ＜0.05）. Bcl-2 protein expression was significantly upregulated （ P ＜0.05）， and the density of neuronal apoptosis-positive cells was significantly reduced （ P ＜0.05）. CONCLUSIONS WYJYG play on antidepressant role by inhibiting the NLRP3/ASC/Caspase-1 pathway， reducing microglia-mediated neuroinflammation， and inhibiting hippocampal neurons apoptosis.

Objective To systematically evaluate the effects of liraglutide combined with metformin on glucose and lipid metabolism,sex hormones,reproductive function,and gastrointestinal reactions in patients with polycystic ovary syndrome(PCOS).Methods We searched databases such as PubMed,WanFang Medical Network,WanFang Database,China National Knowledge Infrastructure(CNKI),and VIP Journals to collect randomized controlled trials published from January 2011 to August 2022 on the treatment of polycystic ovary syndrome with liraglutide combined with metformin,using Revman 5.4 for the meta-analysis.Results A total of 16 case-control studies were included,involving 1436 patients.Compared to metformin alone,the combination of liraglutide and metformin significantly lowered fasting blood sugar,postprandial blood glucoseafter 2 hours,HbA1c,HOMA-IR,FINS,BMI,as well as LH,FSH,and total testosterone in patients with PCOS.It improved lipid levels,helped establish menstrual cycles,and increased the normal ovulation rate and natural conception rate in these patients.However,there was a significantly higher incidence of gastrointestinal reactions in the liraglutide plus metformin group,and the difference was statistically significant(P＜0.05).Conclusion The combination of liraglutide and metformin can improve glucose and lipid metabolism in patients with polycystic ovary syndrome(PC OS),reduce levels of LH,FSH,and total testosterone,help establish regular menstrual cycles,and increase ovulation and pregnancy rates,but it significantly increases gastrointestinal side effects.

Objective:To investigate the clinical efficacy and safety of ultrasound-guided thyroid injection of dexamethasone in the treatment of subacute thyroiditis (SAT).Methods:This is a randomized controlled study involving 32 patients with SAT who received treatment at Endocrinology Clinic of Heilongjiang Provincial Hospital between June 2022 and March 2023. The patients were randomly divided into an observation group and a control group ( n = 16 per group) using a random number table method. The observation group received ultrasound-guided injection of dexamethasone (5 mg per injection, once a week) into the thyroid lesion, while the control group was treated with oral prednisone acetate tablets (5 mg per dose, three times a day). Both groups were treated for 4 weeks. The clinical efficacy, time taken for body temperature to return to normal, time for pain resolution, time for goiter regression, time for thyroid function to normalize, as well as recurrence rates and adverse reactions, were compared between the two groups. Results:The response rate in the observation group was 100% (16/16), which was significantly higher than that in the control group [75% (12/16), χ2 = 4.57, P = 0.033]. The time taken for body temperature to return to normal, the time for goiter regression, and the time for goiter regression in the observation group were (3.5 ± 3.6) days, (7.4 ± 2.5) days, and (11.6 ± 7.4) days, respectively, which were significantly shorter than those in the control group [(6.1 ± 3.2) days, (9.9 ± 3.5) days, (16.9 ± 6.8) days, t = -2.16, -2.33, -2.11, all P < 0.05]. After 4 weeks of treatment, the observation group showed significantly lower body mass index, fasting blood glucose, and serum triglyceride levels compared to the control group ( t = -2.07, -2.46, -2.13, all P < 0.05). The recurrence rate in the observation group was 0%, which was significantly lower than that in the control group [25% (4/16), χ2 = 4.57, P = 0.033]. Conclusions:The efficacy and safety of ultrasound-guided local thyroid injection of dexamethasone for the treatment of SAT are superior to those of the oral treatment regimen.

Objective:To summarize the clinical and genetic characteristics of 23 children with pathogenic ACAN gene variants, enhance the understanding of this disorder, and explore possible regulatory mechanisms. Methods:A retrospective case series summary.The clinical characteristics and genetic analysis results of 23 children with ACAN gene variants treated in the Department of Endocrinology, Genetics and Metabolism, Children′s Hospital of Soochow University from January 2016 and September 2024 were analyzed retrospectively.Transcriptome sequencing was performed on peripheral blood samples from 3 of affected children and 3 age-matched healthy children as controls.Differentially expressed genes (DEGs) in the peripheral blood transcriptome profiles were identified.Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were conducted to explore the potential signaling pathways involved. Results:Among the 23 cases, there were 13 males and 10 females, aged from 2 years and 8 months to 12 years old, with 11 cases presenting advanced bone age.Thirteen cases were treated with growth hormone (GH), including 6 cases who received concomitant gonadotropin-releasing hormone analogue therapy.The treatment duration ranged from 3 to 70 months, resulting in varying degrees of height improvement in all treated patients.Transcriptomic analysis identified 811 DEGs, with 516 up-regulated and 295 down-regulated.GO and KEGG enrichment analyses revealed that the heterozygous ACAN variants were significantly associated with FcγR-mediated phagocytosis, nuclear factor-κB signaling pathway, the intestinal immune network for IgA production, rheumatoid arthritis, and systemic lupus erythematosus signaling pathways. Conclusions:The predominant clinical manifestations of patients with ACAN gene variants are short stature and advanced bone age.Although GH provocation tests may indicate normal GH levels, GH therapy can be effective in improving height.Immune-related factors may play a role in the pathogenesis of this disorder.

Cleidocranial dysplasia, a rare genetic disorder primarily caused by Runt-related transcription factor 2 (RUNX2) heterozygous mutation, serves as a representative model for investigating regulatory mechanisms of RUNX2 in bone remodeling and tooth eruption. As a master transcription factor governing mineralized tissue development, RUNX2 orchestrates bone remodeling and tooth eruption through diverse regulatory networks. It drives alveolar bone formation via transcriptional activation, integration of multiple signaling cascades, and epigenetic modifications, thereby generating the biomechanical force for tooth eruption. Concurrently, RUNX2 promotes osteoblastic secretion of osteoclastogenic factors and directly regulates osteoclast precursor differentiation, facilitating bone resorption at the coronal aspect of dental follicles to estavlish the eruption pathway. Furthermore, RUNX2 modulates eruption progression by participating in stress-induced biological signal transduction within dental follicle cells (DFCs), remodeling the DFCs microenvironment, and regulating DFCs senescence. RUNX2 also influences root development via the NOTUM-Wnt axis, providing auxiliary biomechanical conditions conducive to eruption. This review systematically delineates the pivotal role of RUNX2 in coordinating bone remodeling and tooth eruption. Future studies should leverage organoid models and multi-omics technologies to further elucidate the spatiotemporal regulatory networks of RUNX2, potentially advancing precision diagnostics and therapeutics for rare skeletal-dental developmental disorders.

Debates persist regarding the efficacy and safety of azvudine, particularly its real-world outcomes. This study involved patients aged ≥60 years who were admitted to 25 hospitals in mainland China with confirmed SARS-CoV-2 infection between December 1, 2022, and February 28, 2023. Efficacy outcomes were all-cause mortality during hospitalization, the proportion of patients discharged with recovery, time to nucleic acid-negative conversion (T _NANC), time to symptom improvement (T _SI), and time of hospital stay (T _HS). Safety was also assessed. Among the 5884 participants identified, 1999 received azvudine, and 1999 matched controls were included after exclusion and propensity score matching. Azvudine recipients exhibited lower all-cause mortality compared with controls in the overall population (13.3% vs. 17.1%, RR, 0.78; 95% CI, 0.67-0.90; P = 0.001) and in the severe subgroup (25.7% vs. 33.7%; RR, 0.76; 95% CI, 0.66-0.88; P < 0.001). A higher proportion of patients discharged with recovery, and a shorter T _NANC were associated with azvudine recipients, especially in the severe subgroup. The incidence of adverse events in azvudine recipients was comparable to that in the control group (2.3% vs. 1.7%, P = 0.170). In conclusion, azvudine showed efficacy and safety in older patients hospitalized with COVID-19 during the SARS-CoV-2 omicron wave in China.

OBJECTIVES: To investigate the effect of curcumin on lipid metabolism in non-small cell lung cancer (NSCLC) and its molecular mechanism. METHODS: The inhibitory effect of curcumin (0-70 μmol/L) on proliferation of A549 and H1299 cells was assessed using MTT assay, and 20 and 40 μmol/L curcumin was used in the subsequent experiments. The effect of curcumin on lipid metabolism was evaluated using cellular uptake assay, wound healing assay, triglyceride (TG)/free fatty acid (NEFA) measurements, and Oil Red O staining. Western blotting was performed to detect the expressions of PGC-1α, PPAR-α, and HIF-1α in curcumin-treated cells. Network pharmacology was used to predict the metabolic pathways, and the results were validated by Western blotting. In a nude mouse model bearing A549 cell xenograft, the effects of curcumin (20 mg/kg) on tumor growth and lipid metabolism were assessed by measuring tumor weight and observing the changes in intracellular lipid droplets. RESULTS: Curcumin concentration-dependently inhibited the proliferation of A549 and H1299 cells and significantly reduced TG and NEFA levels and intracellular lipid droplets. Western blotting revealed that curcumin significantly upregulated PGC-1α and PPAR‑α expressions in the cells. KEGG pathway enrichment analysis predicted significant involvement of the HIF-1 signaling pathway in curcumin-treated NSCLC, suggesting a potential interaction between HIF-1α and PPAR‑α. Western blotting confirmed that curcumin downregulated the expression of HIF-1α. In the tumor-bearing mice, curcumin treatment caused significant reduction of the tumor weight and the number of lipid droplets in the tumor cells. CONCLUSIONS Curcumin inhibits NSCLC cell proliferation and lipid metabolism by downregulating the HIF-1α pathway.
Curcumin/pharmacology* ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Animals ; Lipid Metabolism/drug effects* ; Carcinoma, Non-Small-Cell Lung/pathology* ; Lung Neoplasms/pathology* ; Mice, Nude ; Down-Regulation ; Mice ; Cell Proliferation/drug effects* ; Cell Line, Tumor ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; PPAR alpha/metabolism* ; Signal Transduction/drug effects* ; A549 Cells