Diabetic kidney disease （DKD） is a microvascular complication of diabetes， with a complex pathogenesis， in which mitochondrial dysfunction is considered to be the core of DKD development. Taking mitochondria as a target to regulate mitochondrial energy metabolism， mitochondrial oxidative stress， mitophagy， and mitochondrial dynamic function represents a promising strategy for the DKD prevention and treatment， with good prospects in clinical application. Traditional Chinese medicine （TCM） has great potential to mediate mitochondrial dysfunction in the DKD prevention and treatment. This article deeply explores the intrinsic relationship between various forms of mitochondrial dysfunction and DKD， and summarizes the current research status of various Chinese herbal compounds and Chinese herbal formulas in targeting mitochondrial dysfunction for the DKD prevention and treatment. This article aims to provide new targets and strategies for the DKD prevention and treatment， and the research and development of TCM.

ObjectiveTo explore the inhibitory effect and related molecular mechanisms of Saponin of Schizocapsa plantaginea HanceⅠ （SSPHⅠ） on human nasopharyngeal carcinoma HONE-1 cells. MethodsThe effect of SSPHⅠ on HONE-1 cell viability was detected using the CCK-8 assay. Its inhibitory effect on cell proliferation was evaluated through a colony formation assay. Changes in cell invasion ability were analyzed using the Transwell assay. Intracellular reactive oxygen species （ROS） levels were measured using the DHE fluorescent probe. The extent of intracellular content release was reflected by the LDH release assay. The rate of cell pyroptosis was detected using the Annexin-V/PI double staining method. Changes in the expression of proteins related to the classical pyroptosis pathway were examined by Western Blot. ResultsCCK-8 assay showed that treatment with SSPHⅠ for 24 hours reduced HONE-1 cell viability in a concentration-dependent manner， with an IC50 value of 3.383 μmol/L. In the colony formation assay， the number of HONE-1 cell colonies gradually decreased with increasing concentrations of SSPHⅠ （P<0.01）. The Transwell assay revealed that the number of cells migrating through the chamber was reduced following SSPHⅠ treatment （P<0.01）. DHE fluorescence probe detection indicated that intracellular ROS fluorescence intensity increased after SSPHⅠ treatment （P<0.001）. The LDH release assay showed that LDH activity in the cell supernatant increased with higher concentrations of SSPHⅠ （P<0.001）. Annexin-V/PI double staining demonstrated that the proportion of Annexin-V/PI-positive cells increased after SSPHⅠ treatment （P<0.001）. Western blot analysis showed that， compared with the control group， the protein expression levels of cleaved-Caspase-1 and GSDMD-N-terminal were upregulated in SSPHⅠ-treated cells （P<0.05）， and NLRP3 protein expression levels also increased （P<0.05）. ELISA results showed that the levels of IL-1β and IL-18 in the cells increased with higher concentrations of SSPHⅠ （P<0.05）. ConclusionSSPHⅠ can induce pyroptosis in nasopharyngeal carcinoma HONE-1 cells by regulating the ROS/NLRP3/Caspase-1 signaling axis， thereby exerting an anti-nasopharyngeal carcinoma effect. This suggests that SSPHⅠ may serve as a potential therapeutic agent for nasopharyngeal carcinoma.

Autosomal dominant polycystic kidney disease （ADPKD） is a systemic hereditary renal disorder and can affect multiple organs， and congenital hepatic fibrosis is one of the manifestations of liver involvement and is an important complication of ADPKD. Symptomatic management is currently the main treatment method for this disease， and disease-specific drugs such as tolvaptan have limited indications and cannot correct the underlying genetic defect. This article reports a case of ADPKD with congenital hepatic fibrosis， and sirolimus was identified as the individualized treatment regimen based on peripheral blood functional genomic analysis and drug sensitivity prediction platform. The patient achieved significant improvements in symptoms and quality of life after treatment， with a stable kidney volume. This case shows that functional genomics has a potential value in guiding individualized treatment of rare genetic disorders， which provides new treatment ideas and practice paths for similar patients.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Objective To explore latent classes of behavioural and psychological symptoms in the patients with Alzheimer's disease(AD)and to identify the factors influencing the latent classes and provide a basis for fomulating personalized nursing measures.Methods Convenience sampling was employed to recruit 361 AD inpatients from our hospital between November 2023 and May 2024 for this cross-sectional study.A general data questionnaire,the neuropsychiatric inventory questionnaire,Monteria cognitive assessment scale,activity of daily life scale,and mini-nutritional assessment scale were used in the survey.Latent class analysis was conducted to analyse the data acquired from the survey.Univariate analysis and multiple Logistic regression analysis were used to identify the factors influencing latent classes.Results Toally 346 patients finished the study.It was found that a 72.5%of AD patients developed behavioural and psychological symptoms.The symptoms were categorised into three classes:low symptom-apathy,middle symptom-emotional disturbance and high symptom-behaviour disorder.The course of disease,cognitive function,daily living ability and nutritional status were identified as the factors that influenced the latent classes(all P<0.05).Conclusion AD patients with low cognitive function,poor daily living ability,malnutrition and a course of disease over 5 years are at high risks of behavioural and psychological symptoms which are heterogeneous.Care providers are advised to propose personalised care strategies to improve the behavioural and psychological symptoms.

Ulcerative colitis(UC)is a chronic,recurrent intestinal inflammatory disorder.In recent years,the role of vitamin D in the treatment of UC has attracted widespread attention.Studies have demonstrated that vitamin D exerts therapeutic effects through multiple mechanisms including maintaining intestinal barrier,regulating immune cells and inflammatory factors,modulating gut microbiota,and regulating gene expression.Clinical studies have found that vitamin D supplementation can improve UC symptoms,alleviate inflammatory response,and enhance patients'quality of life.Additionally,there are differences in efficacies when vitamin D is combined with different drugs.This article reviewed the research progress on the mechanism and supplementation dosage of vitamin D in the treatment of UC,as well as its role in disease assessment and clinical significance.

Nanomaterials can be used in drug delivery systems to enhance drug targeting and efficacy, and reduce adverse reactions. At the same time, they can also be used in tissue engineering and regenerative medicine to promote bone tissue repair and regeneration. Nanozymes are special nanomaterials with the catalytic activity of biological enzymes, which can mediate efficient biochemical reactions and provide a new strategy for the diagnosis and treatment of orthopaedic diseases. In the treatment of tendon-related diseases, the enzymatic nanohybrid encapsulated by extracellular vesicles can effectively mimic catalase to remove reactive oxygen species, continuously release zinc ions, and induce immune regulation through extracellular vesicles. It can significantly promote functional recovery and matrix reconstruction, restore tendon morphology, and inhibit scar formation and adhesion around the tendon. In the treatment of bone and joint diseases, photothermal nanozymes with bionic characteristics can generate thermal energy under near-infrared radiation, enhance joint lubrication performance, reduce cartilage wear in early osteoarthritis, effectively remove reactive oxygen species and reactive nitrogen species, increase the production of hyaluronic acid inside and outside the cells, and help to restore the lubrication and function of articular cartilage. Hollow Prussian blue nanoenzyme prepared by template-free hydrothermal synthesis can inhibit osteoclast formation and bone resorption, inhibit intracellular reactive oxygen species production and mitogen-activated protein kinase and nuclear factor kappa-B signaling pathways, thereby improving osteoporosis. In the treatment of spinal diseases, Prussian blue nanozymes can not only remove excessive reactive oxygen species, maintain the normal Redox level of nucleus pulposus cells, but also escape lysosomal phagocytosis, achieve more effective mitochondrial targeting, and effectively alleviate intervertebral disc degeneration.

Objective:To investigate the impact of High Alcohol-Producing Klebsiella pneumoniae (HiAlc Kpn) on hepatocyte function and explore its regulatory mechanism from the perspective of epigenetic modifications. Methods:Using the HepG2 cell line as the research model, the study involved exposing the cells to alcohol and three different HiAlc Kpn strains in vitro, dividing them into a control group, alcohol-treated group, W8 group, 3-24 group, and 4-26 group. The effect of HiAlc Kpn on liver cell proliferation was investigated using the Incucyte live cell imaging system, and the apoptotic level of liver cells was determined using flow cytometry. The fluorescence confocal microscopy combined with live cell probes was used to detect lipid accumulation and intracellular ROS levels in liver cells. The amount of mitochondrial damage was determined using flow cytometry combined with the seahorse cell metabolism analyzer, and changes in protein levels undergoing global lactylation modification were investigated using Western blotting. Results:Compared with the control group, HiAlc Kpn strains W8, 3-24 and 4-26 could decrease the proliferation rate and increase the ratio of apoptosis of hepatocyte HepG2 cells. The results of high-content cell imaging showed that the fluorescence points of ROS enrichment in HepG2 cells were increased after HiAlc Kpn treatment. The lipid accumulation was significantly increased by oil red O and BODIPY staining. The number of oil droplets and fluorescence points was higher than those in the control group and alcohol treatment group. The results of flow cytometry showed that the ratio of JC-1 monomer/polymer was significantly increased after alcohol and three kinds of HiAlc Kpn were treated and the W8 treatment group was about six times higher than the control group ( P<0.05). Seahorse Energy Metabolism System′s mitochondrial pressure test results showed that the extracellular acidification degree and oxygen consumption rate were significantly reduced by the HiAlc Kpn 4-26 strain. Western blot analysis showed that the pan-lactylation modification level increased after high-concentration alcohol treatment and the increased rate of pan-lactylation modification in the 1 000 mmol/L alcohol group was about three times that of the control group. HiAlc Kpn W8 and 3-24 strains resulted in four or two-times pan-lactylation modification increases compared with the control group, and the differences were statistically significant ( P<0.05). Conclusion:HiAlc Kpn can induce lipid peroxidation in hepatic cells by regulating the increase in histone pan-lactylation modification levels, leading to mitochondrial damage, impaired cell proliferation capacity and increased apoptosis levels.