Renal fibrosis （RF）， characterized by glomerulosclerosis and tubulointerstitial fibrosis， is a central pathological process in chronic kidney disease （CKD）. The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3） inflammasome is closely linked to the occurrence and progression of RF. This review systematically elucidates the mechanisms of the NLRP3 inflammasome in RF， and summarizes the current research on the inhibition of NLRP3 inflammasome activation by single Chinese herbs， active components of traditional Chinese medicine， Chinese herbal compounds， and Chinese patent medicines for the prevention and treatment of RF. The existing studies have demonstrated that single Chinese herbs （Campanumoea lancifolia， Dioscorea zingiberensis）， active components of traditional Chinese medicine （morroniside， liquiritigenin， rosmarinic acid， magnoflorine， fucoidan， etc.）， Chinese herbal compounds （Bushen huoxue formula， Tongluo yishen decoction， Shizhi formula， Bixie fenqing drink）， and Chinese patent medicine （Suyin jiedu granule） can inhibit the activation of the NLRP3 inflammasome to counteract inflammatory damage. This affects multiple pathways（NLRP3/caspase-1/ gasdermin D， NLRP3/interleukin-1β/Smad， etc.） and related upstream and downstream targets of its activation， effectively reducing pyroptosis， mitigating oxidative stress， promoting mitochondrial autophagy， inhibiting fibroblast activation， and reducing excessive extracellular matrix deposition， thereby exerting anti-RF effects.

Myocardial injury is the leading cause of death in uremic patients.PINK 1/Parkin-mediated mitochondrial autophagy is involved in the progression of myocardial injury.In recent years,pathogenic turbidity has been gradually accepted as a representative of a new type of toxic pathogens by the researchers of traditional Chinese medicine(TCM).This paper sorts out literature about pathogenic turbidity,analyzes the etiological and pathogenic characteristics of pathogenic turbidity,and suggests that the pathogenesis of uremia-induced myocardial injury can be more comprehensively clarified from the perspective of healthy-qi deficiency resulting in latent pathogenic turbidity.In the patients with uremia,the down-regulation of PINK1/Parkin causes the weakening of mitochondrial autophagy,which leads to the elevation of levels of reactive oxygen species(ROS)and inflammatory factors,and eventually causes the injury of myocardial cell.The above pathogenic mechanism is similar to the process of traditional Chinese medicine(TCM)in which the deficiency of the healthy-qi(in particular kidney deficiency)results in the production of the pathogenic turbidity(showing as dampness,blood stasis,phlegm,toxin and so on)and then causes the pathogenic turbidity hide in vessels and collaterals and gradually injure the heart vessels,and eventually results in the deficiency of heart vessels.The mitochondrial autophagy mechanism mediated by the PINK1/Parkin pathway is suitalbe for explaining the TCM pathogenesis of uremia-induced myocardial injury,characterized by healthy-qi deficiency resulting in latent pathogenic turbidity,and also is suitable for interpretating the principle of supporting healthy-qi to eliminate pathogenic turbidity for treating uremia-induced myocardial injury.Under the guidance of the theory of health y-qi deficiency and turbid pathogens in TCM,the development of specific PINK 1/Parkin agonists may expand the approach for the treatment of uremia-induced myocardial injury.

Objective To analyze the current status and hotspots of domestic research on traditional Chinese medicine(TCM)in treating chronic refractory wounds(CRW)over the past 10 years using bibliometric and visualized analysis methods.Methods Articles about TCM therapy for CRW issued by the core periodicals in recent 10 years were retrieved from CNKI,Wanfang and VIP databases.The parameters of annual issued papers,authors,institutions and keywords of the articles were counted with the bibliometric methods.And then the statistical results were presented as visualized graphs by using VOSviewer and CiteSpace software.Results A total of 404 articles were included in the study,and 313 institutions and 1 340 scholars participated in the research on the treatment of CRW with TCM.However,there was limited collaboration between the authors and institutions.Research hotspots mainly focused on the efficacy of TCM external therapies for diabetic foot and pressure ulcers,and discussions on syndrome differentiation,treatment principles and methods about internal treatment by various medical experts.The development and application of Chinese patent medicines,exploration of TCM medication patterns,and the evidence-based medical research on TCM are future research trends in the treatment of CRW with TCM.Conclusion Research on TCM treatment of CRW has attracted significant attention in recent years,but academic barriers exist between the authors and institutions.In the future,it is necessary to promote multicenter research collaboration,strengthen the exploration of experiences in acupoint selection,and conduct higher-level research,thus to provide more compelling evidence and enhance the efficacy of TCM in treating CRW.

ObjectiveExploring the role of microRNA126 （miRNA126） in chronic kidney disease combined with atherosclerosis （CKD AS） by regulating the phosphatidylinositol-3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway and the mechanism of Shenshuai Xiezhuo decoction in the intervention of CKD AS rats with 5/6 nephrectomy combined with high-fat feeding. MethodA total of 60 SD rats were randomly divided into sham operation group， model group， losartan group， and low， medium， and high dose groups of Shenshuai Xiezhuo decoction. The CKD AS rat model was established by 5/6 nephrectomy combined with high-fat feeding for 10 weeks. The low， medium， and high dose groups （6.0， 12.0， 24.0 g·kg^-1·d^-1） of Shenshuai Xiezhuo decoction and the losartan group （20 mg·kg^-1·d^-1） were gavaged， and the corresponding intervention was carried out for eight weeks. Then， the rats were killed， and samples were collected for corresponding detection. Fully automated biochemical analyzers were used to detect kidney function and blood lipids in rats： blood creatinine （SCr）， blood urea nitrogen （BUN）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） levels. Hematoxylin-eosin （HE） and Masson staining of aortic tissue and pathological observation under a light microscope were carried out， and autophagosomes and autophagy lysosomes were observed by transmission electron microscopy. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to determine the mRNA levels of miRNA126， PI3K， Akt， and mTOR in rats， and Western blot was used to determine the protein expression levels of phosphorylated （p）-PI3K， PI3K， p-Akt， Akt， p -mTOR， mTOR， benzyl chloride 1 （Beclin-1）， and microtubule-associated protein light chain 3Ⅱ/Ⅰ （LC3Ⅱ/LC3Ⅰ）. ResultCompared with the sham operation group， the serum SCr， BUN， TC， TG， and LDL-C in the model group were significantly increased （P<0.01）. Compared with the model group， the SCr， BUN， TC， TG， and LDL-C were decreased in the losartan group and low， medium， and high dose groups of Shenshuai Xiezhuo decoction （P<0.05）. Compared with the sham operation group， thickening plaques， infiltration of mononuclear macrophages， a small number of foam cells， disordered arrangement of smooth muscle fibers in the tunica media， and increased collagen fibers were observed in the model group， and the lesions in the losartan group and Shenshuai Xiezhuo decoction groups were alleviated compared with those in the model group. Compared with the model group， the number of autophagosomes and autophagy lysosomes increased in the medium and high dose groups of Shenshuai Xiezhuo decoction. Compared with the sham operation group， the expression of miRNA126 in the aortic tissue of the model group was significantly decreased （P<0.01）， and the mRNA expressions of PI3K， Akt， and mTOR were significantly increased （P<0.01）. Compared with the model group， the expression of miRNA126 in the aortic tissue of rats in high， medium， and low dose groups of Shenshuai Xiezhuo decoction and losartan group was significantly increased （P<0.01）， while the mRNA expressions of PI3K， Akt， and mTOR were significantly decreased （P<0.01）. Compared with the sham operation group， the protein expressions of p-PI3K， PI3K， p-Akt， Akt， p-mTOR， and mTOR in the model group were significantly increased （P<0.01）， while the protein levels of Beclin-1， LC3Ⅰ， and LC3Ⅱ were significantly decreased （P<0.01）. Compared with the model group， the protein expressions of p-PI3K， PI3K， p-Akt， Akt， p-mTOR， and mTOR in the losartan group and low， medium， and high dose groups of Shenshuai Xiezhuo decoction were decreased （P<0.05）， while the protein levels of Beclin-1 and LC3Ⅱ/LC3Ⅰ were increased （P<0.05）. ConclusionThe expression of miRNA126 is decreased in the aortic tissue of CKD AS rats， and the PI3K/Akt/mTOR pathway is activated to inhibit autophagy flux. Shenshuai Xiezhuo decoction regulates the PI3K/Akt/mTOR signaling pathway through miRNA126， restores the autophagy of aortic endothelial cells， protects the damage of CKD vessels， reduces the formation of As plaques， and slows the development of cardiovascular complications.

Neurodegenerative diseases are often associated with inflammatory mechanisms, where persistent or excessive inflammatory responses can lead to neuronal damage and subsequent pathological changes. In acute neurological conditions such as stroke or traumatic brain injury, inflammation is a key factor that triggers acute neuronal injury and long-term sequelae. In chronic neurodegenerative diseases, including Alzheimer's disease, cognitive dysfunction, Parkinson's disease, and multiple sclerosis, the chronic activation of inflammation is closely related to gradual degeneration of neurons. Resolvin D1 (RvD1), an endogenous pro-resolving mediator, plays a crucial role in controlling the intensity and duration of inflammation by inhibiting excessive activation of immune cells, modulating the release of pro-inflammatory cytokines, and maintaining the integrity of the blood-brain barrier. This review focuses on the mechanisms of RvD1 in mediating inflammatory damage in major neurological diseases, aiming to provide theoretical support for a deeper understanding of disease mechanism, optimized therapeutic strategies, and enhanced outcome.

Objective: To identify confounding factors associated with dental caries prevention, as the basis for the development of subsequent health management plan for dental caries prevention in young children. Methods: From June to September 2019, a questionnaire survey was conducted among parents of young children enrolled in five kindergartens in the district of Shanggang Steel Community, Pudong New District, Shanghai, using the convenience sampling method. The survey included basic demographic characteristics on parents and children, as well as information factor, motivation factor, behavioral skills, and caries prevention behavior. Results: Among 718 parents surveyed, the median information factor score was 8 (7, 9), the median personal motivation factor score was 20 (19, 20), the median social motivation factor score was 9 (8, 10), the median behavioral skills score was 25 (24, 25), and the median caries prevention behavior score was 7 (5, 8). Motivation factor was positively associated with behavioral skills, both information factor and behavioral skills were positively associated with dental caries prevention (P<0.05). Personal motivation factor had a direct influence factor of 0.80 on behavioral skills and an indirect influence factor of 0.15 on dental caries prevention behavior; behavioral skills and information factor had a direct influence factor of 0.19 and 0.26 respectively on dental caries prevention. Conclusion The finding suggest that in addition to oral hygiene information and education for parents of young children, mental support should be a key component of any community-based dental caries prevention program.

OBJECTIVETo explore the effect of quercetin on the invasion, migration, proliferation and cell cycle of glioma U87 cells.

METHODSGlioma U87 cells were treated with 50, 100, or 150 µmol/L quercetin (Q(50), Q(100) and Q(150) groups, respectively) or with DMSO (Q(0) group). Transwell in vitro invasion and migration assays, Click-iT Edu test and flow cytometry were performed to evaluate the effect of quercetin on the invasion, migration, proliferation and cell cycle of U87 cells.

RESULTSAfter 36 h of quercetin treatment, the cells in Q(50), Q(100) and Q(150) groups showed invasive cell percentages (relative to Q(0) group) of 52.08%, 24.63%, and 13.13%, respectively (P<0.05). After quercetin treatment for 12 h, the migrating cell percentages (relative to Q(0) group) in Q(50), Q(100) and Q(150) groups were 49.46%, 26.78%, and 14.56%, respectively (P<0.05). After 24 h of quercetin treatment, the cell proliferation ratios in Q(0), Q(50), Q(100) and Q(150) groups were 25.21%, 18.38%, 16.74% and 15.24%; the cell percentages in phase G0/Gl were 71.14%, 72.71%, 69.29%, and 66.47%, phase S were 25.32%, 22.48%, 21.96%, and 23.32%, and phase G(2)/M were 3.53%, 4.80%, 8.75%, and 10.25% in the 4 groups, respectively, showing a significant difference between groups Q(100), Q(150) and group Q(0) in phase G(2)/M cell percentages (P<0.05).

CONCLUSIONSQuercetin can significantly inhibit the invasion, migration and proliferation of glioma U87 cells by blocking the cell cycle progression.

Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Glioma ; pathology ; Humans ; Quercetin ; pharmacology